Hydrocyanic acid and its compounds

Hydrocyanic acid (hydrocyanic acid) was first synthesized by the Swedish scientist Karl Scheele in 1782. Hydrocyanic acid was first used as a poisonous substance on July 1, 1916 on the river. Somme by French troops against German troops. It was not possible to obtain a pronounced combat effect, since the relative density of HCN vapor in the air is less than 1. Attempts to make hydrocyanic acid vapor heavier by adding arsenic trichloride, tin chloride and chloroform also did not lead to the creation of combat concentrations of toxic vapors in the atmosphere.

The acid itself and its salts are widely used in agriculture (as pest control agents for fruit trees), in industry (for extracting gold and silver from ores), in the chemical synthesis of nitrile rubber, synthetic fibers, plastics, etc.

As an OV, it is unlikely to be used. It is possible to use hydrocyanic acid derivatives as diversion agents.

Currently, various groups of chemical compounds are known that contain a CN group in the molecule.

250. Boiling point of hydrocyanic acid

Among them: nitriles - hydrocyanic acid, cyanide, potassium cyanide, cyanogen chloride - CI-CN, propionitrile - C3H7-CN, etc.); isonitriles - phenylisonitrile chloride; cyanates - phenyl cyanate; isocyanates - methyl isocyanate, phenyl isocyanate; thiopianates - thiocyanate potassium; isothiocyanates - methylisothiocyanate. The least toxic (LD50 over 500 mg/kg) are representatives of cyanates and thiocyanates. Isocyanates and isothiocyanates are irritating and asphyxiant. A general toxic effect (due to the elimination of the CN- ion from the parent substance in the body) is exhibited by nitriles and, to a lesser extent, isonitriles. In addition to hydrocyanic acid itself and its salts, cyanogen chloride, cyanogen bromide, as well as propionitrile, which is only 3-4 times inferior in toxicity to potassium cyanide, is distinguished by high toxicity.

Hydrocyanic acid occurs in plants in the form of heteroglycosides. About 2000 plant species contain CN-containing glycosides. For example, in the form of amygdalin, HCN is found in the seeds of bitter almonds, in the seeds of peaches, apricots, plums, cherries, etc.

Physico-chemical and toxic properties

Hydrocyanic acid is a colorless transparent liquid with a smell of bitter almonds. boiling point + 25.7 ° C, freezing point 13.4 ° C. The relative density of its vapor in air is 0.93. Hydrocyanic acid vapors are poorly absorbed by activated carbon, but are well absorbed by other porous materials.

When interacting with alkalis, HCN forms salts (potassium cyanide, sodium cyanide, etc.), which are not much inferior in toxicity to hydrocyanic acid itself. When a hydrogen atom is replaced by halogens, halandtions (cyanogen chloride, cyanogen bromide, cyanogen chloride) are formed. Hydrocyanic acid and cyamides interact with sulfur (non-toxic rhodomides are formed), as well as with aldehydes and netons (low-toxic cyanhydrides are formed). These reactions underlie the detoxification of the poison. In aqueous solutions, the acid and its salts dissociate to form the CN- ion. Hydrocyanic acid is a weak acid and can be displaced from its salts by other, even the weakest, acids (for example, carbonic).

The main route of penetration of hydrocyanic acid vapors into the body is inhalation. The average lethal concentration is 2 mg × min / l, fatal poisoning with hydrocyanic acid salts is possible when they enter the body with contaminated water or food. In case of poisoning by mouth, lethal doses for humans are: HCN - 1 mg / kg; KCN - 2.5 mg/kg; NaCN - 1.8 mg/kg.

Mechanism of toxic action and pathogenesis of intoxication

As is known, at this stage, the chain of cytochromes (cytochromes B, C1, C, A, and A3) is the carrier of protons and electrons. The successive transfer of electrons from one cytochrome to another leads to the oxidation and reduction of the iron contained in them (Fe3 + "Fe2 +"). The final link in the cytochrome chain is cytochrome oxidase. It was found that the enzyme includes 4 units of heme "A" and 2 units - "A3". It is from cytochrome oxidase that electrons are transferred to oxygen delivered to the tissues by blood. It has been established that cyan ions (CN-) dissolved in the blood reach the tissues, where they interact with the ferric form of cytochrome A3 iron of cytochrome oxidase (cyanides do not interact with Fe2+). By combining with cyanide, cytochrome oxidase loses its ability to transfer electrons to molecular oxygen.

Due to the failure of the final link of oxidation, the entire respiratory chain is blocked and tissue hypoxia develops. Oxygen with arterial blood is delivered to the tissues in sufficient quantities, but they are not absorbed by them and passes unchanged into the venous bed. At the same time, the processes of formation of macroergs (ATP, etc.) are disrupted. Glycolysis is activated, i.e., the exchange from aerobic is rebuilt to anaerobic.

Clinic of defeat

As a result of tissue hypoxia, which develops under the influence of hydrocyanic acid, the functions of the central nervous system are primarily impaired. Acting in large doses, substances first cause excitation of the central nervous system, and then its depression.

Under the action of ultra-high doses of the toxicant develops lightning fast form of poisoning. The victim loses consciousness a few seconds after exposure. Seizures develop. Blood pressure after a short rise falls. After a few minutes, breathing and cardiac activity stop.

At slow flow In the development of intoxication, several periods can be distinguished.

Period of initial phenomena characterized by slight irritation of the mucous membranes of the upper respiratory tract and conjunctiva of the eyes, an unpleasant bitter taste and burning sensation in the mouth. There is a smell of bitter almonds. Salivation, nausea, sometimes vomiting, dizziness, headache, pain in the heart area, tachycardia (sometimes bradycardia), and increased respiration are observed. Coordination of movements is disturbed, weakness is felt, a feeling of fear arises. These signs appear almost immediately after exposure to the poison. There is practically no hidden period.

Dyspnoetic period characterized by the development of excruciating shortness of breath. There is a pronounced increase in the frequency and depth of breathing. The initial excitation of respiration, as intoxication develops, is replaced by its oppression. Breathing becomes irregular - with a short inhalation and a long exhalation. Increased pain and tightness in the chest. Consciousness is oppressed. Severe bradycardia, dilated pupils, exophthalmos, vomiting are observed. The skin and mucous membranes acquire a pink color. In mild cases, hydrocyanic acid poisoning is limited to these symptoms. After a few hours, all manifestations of intoxication disappear.

The dyspnoetic period is replaced period of seizures. Convulsions are clonic-tonic in nature with a predominance of the tonic component. Consciousness is lost. Breathing is rare, but there are no signs of cyanosis. The skin and mucous membranes are pink. The initially observed slowing of the heart rate, an increase in blood pressure and an increase in cardiac output are replaced by a drop in blood pressure, increased heart rate, and its arrhythmia. Acute cardiovascular failure develops. Possible cardiac arrest. Corneal, pupillary and other reflexes are reduced. Muscle tone is significantly increased.

Following a short convulsive period, if death does not occur, develops paralytic period. It is characterized by a complete loss of sensation, the disappearance of reflexes, muscle relaxation, involuntary defecation and urination. Breathing becomes rare, superficial. Blood pressure drops. The pulse is frequent, weak filling, arrhythmic. A coma develops, in which the victim, if death does not occur from respiratory arrest and cardiac activity, can be for several hours, and sometimes even days. The body temperature of those affected in the paralytic period is lowered.

Inhibition of tissue respiration leads to a change in the cellular, gas and biochemical composition of the blood. The content of erythrocytes in the blood increases due to the reflex contraction of the spleen and the release of cells from the depot. The color of venous blood becomes bright scarlet due to the excess content of oxyhemoglobin (HbO). The arterio-venous difference in oxygen sharply decreases. The content of CO2 in the blood decreases due to less formation and increased excretion during hyperventilation of the lungs. Such dynamics of the gas composition initially leads to gaseous alkalosis, which is then replaced by metabolic acidosis. Underoxidized metabolic products accumulate in the blood: the content of lactic acid increases, the content of ketone bodies (acetone, acetoacetic and b-hydroxybutyric acids) increases, the sugar content increases (hyperglycemia).

The duration of the course of the entire poisoning, as well as individual periods of intoxication, varies considerably (from several minutes to many hours). It depends on the amount of poison that has entered the body, the previous state of the body and other reasons.

Consequences of intoxication

The severity, nature of complications and consequences of poisoning largely depend on the duration of the hypoxic state in which the poisoned remains. Particularly frequent are violations of the functions of the nervous system. After transferring acute poisoning, headaches, increased fatigue, and impaired coordination of movements are observed for several weeks. Speech is difficult. Sometimes paralysis and paresis of individual muscle groups develop. Possible mental disorders.

There are persistent changes in the functions of the cardiovascular system due to myocardial ischemia. Respiratory system disorders are manifested by the functional lability of the respiratory center and its rapid exhaustion under increased loads.

Features of the action of halogen derivatives of hydrocyanic acid

Cyanogen chloride (CICN) as a poisonous substance was first used during the First World War in October 1916 by French troops. Cyanogen chloride is a colorless transparent liquid that boils at 12.6°C and freezes at -6.5°C. It has an irritating odor (the smell of chlorine). Vapor density in air 2.1.

Cyanogen bromide (BrCN) first used during the First World War (1916) by the Austro-Hungarian troops in the form of a mixture of 25% cyanogen bromide, 25% bromoacetone and 50% benzene. Cyanogen bromide is a colorless or yellow crystalline substance, very volatile, with a pungent odor. Boiling point 61.3ºС, melting point 52°С. The vapor density in air is 7.

Both compounds (especially C1CN) are similar in toxicity to hydrocyanic acid.

Cyanogen chloride and cyanogen bromide, acting like HCN, also have an irritating effect. They cause lacrimation, irritation of the mucous membranes of the nose, nasopharynx, larynx and trachea. In high concentrations, it can cause toxic pulmonary edema.

Medical protection measures:

Special sanitary and hygienic measures:

• use of respiratory protective equipment in the focus of chemical contamination;
• participation of the medical service in conducting chemical reconnaissance, conducting an examination of water and food for TCV contamination;
• a ban on the use of water and food from unverified sources.

Special treatment measures:

• the use of antidotes and means of pathogenetic and symptomatic therapy;
• preparation and conduct of the evacuation.

Medical protective equipment

Antidotes used for cyanide poisoning are divided into 2 groups:

1) methemoglobin formers;

2) linking the CN group.

1) Methemoglobin formers:

As you know, once in the body, cyanides do not interact with hemoglobin iron, which is in a divalent state, and, having penetrated into the tissues, they bind to the ferric iron of cytochrome oxidase, which loses its physiological activity. If a poisoned person is quickly introduced in the required amount of a methemoglobin former, then the resulting methemoglobin (ferric iron) will enter into chemical interaction with poisons, binding them and preventing them from entering the tissues. Moreover, the concentration of free toxicants in the blood plasma will decrease, and conditions will arise for the destruction of the reversible bond of the cyan ion with cytochrome oxidase.

The cyan-methemoglobin complex formed is an unstable compound. After 1-1.5 hours, this complex begins to gradually disintegrate. However, since the process of dissociation of CNMtHb is extended in time, the slowly released cyan-ion has time to be eliminated. Nevertheless, with severe intoxication, a relapse of intoxication is possible. Among the methemoglobin-forming agents - cyanide antidotes, include: sodium nitrite, amyl nitrite, 4-dimethylaminophenol, anticyan, methylene blue. It should be remembered that methemoglobin is not able to bind with oxygen, so it is necessary to use strictly defined doses of drugs that change no more than 25-30% of blood hemoglobin.

The most available methemoglobin former is sodium nitrite (NaNO2). When helping the poisoned, sodium nitrite is administered intravenously (slowly) in the form of a 1-2% solution in a volume of 10-20 ml, under the control of blood pressure.

amyl nitrite designed for first aid. An ampoule with amyl nitrite (1 ml), which is in a cotton-gauze wrapper, should be crushed and placed under a gas mask. It can be reapplied if necessary. Currently, the antidote properties of the drug tend to be explained not so much by its ability to methemoglobin formation (which is weakly expressed), but by increased cerebral blood flow, which develops as a result of the vasodilating effect of the substance.

Antician is another substance that can be used as an antidote. In case of hydrocyanic acid poisoning, the first injection of anticyan in the form of a 20% solution is made in a volume of 1.0 ml intramuscularly or 0.75 ml intravenously. When administered intravenously, the drug is diluted in 10 ml of 25-40% glucose solution or isotonic sodium chloride solution. The rate of administration is 3 ml per minute. If necessary, after 30 minutes, the antidote can be re-introduced at a dose of 1.0 ml, but only intramuscularly. After another 30 minutes, a third administration at the same dose can be carried out, if there are indications for this.

4-dimethylaminophenol hydrochloride is produced in ampoules in the form of a 15% solution, administered intravenously at the rate of 3-4 mg / kg of the patient's weight mixed with a glucose solution. Does not cause collapse.

Has a partial methemoglobin-forming effect methylene blue. The main effect of this drug is its ability to activate tissue respiration. The drug is administered intravenously as a 1% solution in a 25% glucose solution ( chromosmon) 50 ml.

2) Linking CN-group:

Sodium thiosulfate(Na2S2O3). As already mentioned, one of the ways of transformations of cyanides in the body is the formation of rhodanium compounds when interacting with endogenous sulfur-containing substances. The resulting thiocyanates excreted from the body with urine are about 300 times less toxic than cyanides.

The true mechanism for the formation of rhodanide compounds has not been fully established, but it has been shown that with the introduction of sodium thiosulfate, the rate of the process increases by 15-30 times, which justifies the expediency of using the substance as an antidote for cyanide poisoning. The drug is administered intravenously as a 30% solution of 50 ml. Sodium thiosulfate potentiates the action of other antidotes. It is advisable to start the provision of emergency care with methemoglobin formers, and then switch to the introduction of other drugs.

Glucose. The antidote effect of the drug is associated with the ability of substances containing an aldehyde group in the molecule to form stable, low-toxic compounds, cyanohydrins, with hydrocyanic acid. The substance is administered intravenously in the amount of 20-25 ml of a 25-40% solution. In addition to the ability to bind the toxicant, glucose has a beneficial effect on respiration, cardiac function and increases diuresis.

Preparations containing cobalt. Cobalt is known to form strong bonds with the cyan ion. In animal experiments, hydroxycobalamin (vitamin B12) has been shown to be effective in the treatment of potassium cyanide poisoning. The drug is very effective, slightly toxic, but expensive, which required the search for other compounds. Among the agents tested were cobalt acetate, gluconate, glutamate, histidinate, and dicobalt salt of ethylenediaminetetraacetate (EDTA). The last drug, which is used in some countries in clinical practice, turned out to be the least toxic and effective. In our country, cobalt preparations are not used as antidotes.

In the process of helping the poisoned, the use of other means of pathogenetic and symptomatic therapy is also envisaged. Hyperbaric oxygen therapy has a positive effect.

Mechanisms of toxic action of hydrocyanic acid

Cyanides inhibit redox processes in tissues, disrupting the last stage of the transfer of protons and electrons by a chain of respiratory enzymes from oxidized substrates to oxygen.

As is known, at this stage, the chain of cytochromes (cytochromes b, C1, C, a and a3) is the carrier of protons and electrons. The successive transfer of electrons from one cytochrome to another leads to the oxidation and reduction of the iron present in them (Fe3+ « Fe2+). The final link in the cytochrome chain is cytochrome oxidase. It has been established that the enzyme includes 4 units of heme "a" and 2 units - "a3". It is from cytochrome oxidase that electrons are transferred to oxygen delivered to the tissues by blood. It has been established that cyan-ions (CN-) dissolved in the blood reach the tissues, where they interact with the trivalent form of iron of cytochrome a3 cytochrome oxidase (cyanides do not interact with Fe2+). By combining with cyanide, cytochrome oxidase loses its ability to transfer electrons to molecular oxygen.

Due to the failure of the final oxidation link, the entire respiratory chain is blocked and tissue hypoxia. Oxygen with arterial blood is delivered to the tissues in sufficient quantities, but they are not absorbed by them and passes unchanged into the venous bed. At the same time, the processes of formation of macroergs (ATP, etc.) are disrupted. Glycolysis is activated, that is, the exchange from aerobic to anaerobic is rebuilt.

In addition to the direct action of cyanides on tissues, a significant role in the formation of acute symptoms of damage, has reflex mechanism.

The body has specialized structures, the sensitivity of which to the developing deficiency of macroergs is much greater than all other tissues. The most studied of these formations is the carotid glomerulus (glomus caroticum). The carotid glomerulus is located at the bifurcation of the common carotid artery into the internal and external. About 20 ml of blood per 1 g of tissue flows through it per minute (0.6 ml through the brain). It consists of two types of cells (according to Hess): type I, mitochondria-rich glomus cells, and type II, capsular cells. The endings of Hering's nerve, which connects the structure with the CNS, penetrate the bodies of type II cells and come into contact with type I cells. M.L. Belenky showed that reflexes from the glomus arise with changes in PaO2, pH, and other metabolic parameters, which are noted even with minimal violations of the conditions necessary for the implementation of the process of oxidative phosphorylation. The strongest stimulating agent of this structure is potassium cyanide. It was concluded that the main physiological role of the carotid glomerulus is to signal the CNS about an impending energy metabolism disorder. There is an assumption that the starting link of the reflex reactions formed in the glomus is a decrease in the level of ATP in type I cells. A decrease in the level of ATP provokes the release of chemicals by glomus cells, which excite the endings of Hering's nerve. The sensitivity of glomus to a number of neuroactive compounds, for example, N-cholinomimetics, catecholamines, is well known (Anichkov S.V.). However, it is also known that none of them changes the sensitivity of the structure to cyanide.

Hydrocyanic acid

The action of adequate stimuli on the glomus is accompanied by CNS excitation, increased blood pressure, bradycardia, increased and deepened respiration, release of catecholamines from the adrenal glands and, as a result, hyperglycemia, etc. That is, all those reactions that are noted in the early stages of intoxication with substances of general toxic action. No matter how the toxicants disrupt the mechanisms of energy supply, the reaction of the body is largely the same. Manifestations of intoxication are effects that form first as a result of excitation and overexcitation of specialized regulatory systems (for example, glomus), and then - a violation of bioenergetics directly in the tissues, and, first of all, quickly responding to a shortage of macroergs (the brain).

Study question 5.Clinic, prevention and general principles of medical care for hydrocyanic acid lesions in the outbreak and at the stages of medical evacuation

Hydrocyanic acid (hydrogen cyanide) - HCN is a weak oxygen-free acid, very volatile. It is a mobile colorless liquid with a faint smell of bitter almonds.

Boils at 25.6°. Easily soluble in water, alcohol and ether.

Prussic acid vapor is lighter than air. Hydrocyanic acid and its salts (cyanides) - sodium cyanide (NaCN), potassium cyanide (KCN), ammonium cyanide (NH4 CN) and many others are widely used in various industries and agriculture.

Thus, cyanides are used to extract gold and silver from ore for cyanidation of steel, in hardening and liquid cementation of metals, in electroplating silvering, gilding, cadmium plating, zinc plating, etc., in the production of pharmaceuticals, in photography, lithography.

Hydrocyanic acid and cyanides are used to control agricultural pests, to kill barn pests and ground squirrels, for deratization (on ships), in railway cars, as artificial fertilizer, etc. It should be noted that cyanides are usually unstable compounds: in air , especially in the presence of moisture, they easily decompose with the release of hydrocyanic acid due to its displacement by carbon dioxide. Therefore, hydrocyanic acid is released as a gas in all processes where salts of hydrocyanic acid are used, in the processing of various metals, minerals and acids contaminated with cyanide.

Under production conditions, hydrocyanic acid poisoning most often occurs as a result of inhalation of gaseous hydrogen cyanide, as well as its salts, which are in an aerosol state. Under production conditions, it is also possible for hydrocyanic acid and its compounds to enter the body through the digestive organs. When entering the stomach, cyanides decompose under the influence of hydrocyanic acid of gastric juice with the release of free hydrochloric acid, which is rapidly absorbed.

Routes of entry into the body

In the presence of high concentrations of hydrogen cyanide in the air, it can enter the body not only through the respiratory tract and gastrointestinal tract, but also through the skin, which can also cause severe poisoning.

The absorption of hydrocyanic acid through the skin is facilitated by the high air temperature of industrial premises and severe physical stress, causing skin flushing and increased sweating.

Hydrocyanic acid is most quickly absorbed by the mucous membrane of the respiratory tract, and most slowly by the skin.

Cyanides that have entered the body may be in an unchanged state in the blood and organs for some time. They soon undergo transformations, of which the most famous is the transformation of hydrocyanic acid into non-toxic thiocyanate compounds by the addition of sulfur. The mechanism of formation of rhodanide compounds is not yet sufficiently clear, but there is reason to believe that it is associated with compounds containing sulfhydryl groups (glutathione, cysteine).

Hydrocyanic acid can be excreted unchanged from the body through the lungs (the exhaled air has the smell of bitter almonds), salivary and sweat glands, and is also partially eliminated in the form of rhodanide compounds through the kidneys and intestines.

Various cyanide compounds, entering the body through the respiratory organs, stomach, skin, decompose in it with the release of free hydrocyanic acid. Thus, the toxicity of these compounds is due to the toxic effect of this acid.

The high toxicity inherent in hydrocyanic acid is explained by the affinity of the CN molecule for the ferric iron of the respiratory enzyme (cytochrome oxidase) of cells. As a result, the blockade of the specified enzyme occurs, which leads to a sharp difficulty in the transfer of oxygen to cells and, thus, to direct "suffocation" of tissues - tissue hypoxia.

Pathogenesis and symptoms of hydrocyanic acid poisoning

In the pathogenesis of the development of acute cyanide intoxication and, in particular, the development of tissue hypoxia, the functional state of the higher parts of the central nervous system is also of great importance.

A sharp decrease in the ability of cells to utilize oxygen that occurs during acute poisoning with hydrocyanic acid leads to a significant increase in the oxygen content in the venous blood and a decrease in the arteriovenous difference in oxygen; in severe cases of poisoning, it almost completely disappears. As a result, venous blood in appearance is very similar to arterial blood. This explains the pink color of the skin and mucous membranes, as well as the scarlet color of the organs in people who died from hydrocyanic acid poisoning.

The most severe cases of acute poisoning, resulting from the direct action of high concentrations of hydrocyanic acid vapors, can proceed at lightning speed: after 2-3 deep breaths, an attack of general convulsions occurs, often accompanied by an involuntary cry, loss of consciousness and death occurs a few minutes after the poison from paralysis respiration, and then the heart (with greatly dilated pupils). In industrial conditions, this kind of lightning-fast poisoning is very rare.

As a rule, the cases of acute poisoning that occur here are characterized by a slower and more sluggish course. In these cases of acute hydrocyanic acid poisoning, it is customary to distinguish between the prodromal, dyspnoetic, convulsive and paralytic stages.

During the first stage, there are sensations of scratching in the throat, a feeling of bitterness in the tongue, numbness of the mouth and throat, a metallic taste in the mouth, salivation, general weakness, a sharp headache, dizziness, staggering, difficulty speaking, nausea, vomiting, urge to defecate, feeling chest tightness, palpitation, rush of blood to the head. Breathing quickens and then becomes deeper. If the victim at this stage goes out into the fresh air, the symptoms may quickly disappear.

With the intensification of the phenomena of intoxication, a dyspnoetic stage develops. General weakness increases, the feeling of embarrassment and pain in the region of the heart increase, the pulse slows down. Shortness of breath gradually increases, taking on a painful character and accompanied by a violation of the rhythm of breathing: sometimes there are separate short breaths in combination with long exhalations.

At the same time, there is dilated pupils, protrusion of the eyeballs, a feeling of fear, a stunned state.

The convulsive stage is characterized by the appearance of strong convulsions (usually tonic), reduction of the chewing muscles with a bite of the tongue. There is involuntary defecation and urination, the patient loses consciousness.

During the paralytic stage, there is a complete loss of consciousness, sensation and reflexes, convulsions cease, breathing becomes increasingly rare, shallow and irregular, and finally stops. Cardiac arrest sometimes occurs only a few minutes after respiratory arrest.

The rate of development of intoxication depends on the route of penetration of the poison into the body. So, with the inhalation route of hydrocyanic acid, the clinical picture of poisoning develops quickly (the latent period is calculated in minutes), and with the skin route there is a rather long latent period - sometimes from 40 minutes to 1.5 hours.

Diagnosis of poisoning with hydrocyanic acid and its derivatives

The clinical diagnosis of acute cyanide intoxication is aided by the presence of two characteristic features: the smell of bitter almonds and the pink color of the skin of the poisoned person, with the simultaneous development of pronounced shortness of breath. The presence of the smell of bitter almonds eliminates carbon monoxide poisoning. The appearance of a pink coloration of the skin excludes intoxication with nitrobenzene (mirban oil), in which there is also the smell of bitter almonds from the mouth, but as a result of the intensive formation of methemoglobin, a grayish-blue color of the skin appears.

The differential diagnosis facilitates the detection of Heinz bodies in the erythrocytes of this intoxication.

After acute cyanide intoxication, persistent and deep pathological changes in the central nervous system can develop.

There are described cases of development of parkinsonism after hydrocyanic acid poisoning, persistent organic disorders of the cerebellar nature, prolonged cerebellar spasmodic syndrome that occurred after a coma caused by cyanide poisoning, hemiplegia after inhalation poisoning with hydrocyanic acid.

Until recently, the issue of chronic cyanide intoxication was considered unresolved, and many authors denied this possibility.

However, studies have found that in the presence of cyanide compounds in the air of industrial enterprises ranging from several ten-thousandths to several thousandths of a milligram per 1 liter, conditions are created for the occurrence of chronic intoxication.

Clinical observations have confirmed that under the influence of long-term exposure to low concentrations of cyanide compounds (of the order of thousandths of a milligram per 1 liter), people complain of headache, dizziness, memory loss, lack of appetite, sometimes weakening of sexual function, constricting pain in the chest, palpitations, shortness of breath

An objective study of the patients revealed: hypotension, bradycardia, heart tone disturbances, progressive weight loss, enlargement of the thyroid gland, disorders of gastric secretion, instability of the autonomic nervous system, a tendency to increase the number of erythrocytes and hemoglobin, disorders of carbohydrate, nitrogen and sulfur metabolism.

Cyanic compounds in the air of industrial premises, with prolonged exposure, cause disturbances in redox processes in the body of workers, resulting in a decrease in the blood levels of glutathione (total and oxidized) and catalase. There are indications that with chronic exposure to hydrocyanic acid, an important role in the picture of poisoning is played by the inhibition of thyroid hormone production, which, however, is caused not by hydrocyanic acid, but by the rhodanide compounds formed from it in the body, which do not have time to be excreted in urine and feces.

Some cyanides also have a pronounced local effect. Thus, in persons in contact with solutions of potassium cyanide, subacute and chronic eczema occurs, sometimes with deep ulcerations on the fingers (ulcers with ridged edges).

First aid and treatment for poisoning with hydrocyanic acid and other cyanides

The effectiveness of first aid for acute cyanide poisoning depends on the speed and clear sequence of the necessary measures. To stop the further intake of poison, first of all, the victim should be removed from the contaminated atmosphere and clothing should be removed from him, which can be a source of poison entering the body. Appropriate antidote therapy is used to release the respiratory enzyme (cytochrome oxidase) of the cells from the cyan molecule and prevent further entry of this poison from the blood into the tissues. First of all, methemoglobin formers are used, since methemoglobin contains ferric iron, to which cyanide molecules have a high affinity. Methemoglobin circulating in the blood binds cyanide compounds before they enter the tissues from the blood, and also promotes the extraction of cyan from the cytochrome oxidase of cells. As a result, cyanmethemoglobin is formed in the blood. Inhalation of amyl nitrite (2-3 drops from a piece of cotton wool, gauze or handkerchief)1, intravenous administration of freshly prepared 1-2% sodium nitrite solution (5-10 ml) or intravenous infusion of chromosmon (50 ml) are used as methemoglobin-forming agents.

Unfortunately, cyanmethemoglobin is an unstable compound. It easily breaks down, and cyan is split off rather quickly. Therefore, after the introduction of methemoglobin-forming agents, it is recommended that approximately 5 minutes later, 20 ml of a 30% solution of sodium hyposulfite be administered intravenously, which causes the neutralization of cyanides by the formation of thiocyanates, excreted from the body mainly by the kidneys. If the patient's condition does not improve in the near future, it is necessary to re-introduce the above antidotes in the same order and in the same dosage.

The effectiveness of the use of amyl nitrite, sodium nitrite or their combinations with sodium thiosulfate for the treatment of acute cyanide poisoning has been repeatedly confirmed by experimental studies and clinical observations.

Dozens of cases are described in the literature when, using the above drugs, it was possible to save people who were fatally poisoned by cyanides.

Recently, a number of other drugs have been proposed for the treatment of acute cyanide intoxications. So, a case of acute poisoning with gaseous hydrocyanic acid is described, when, after unsuccessful use of nitrites, methylene blue and sodium thiosulfate, a good effect was obtained after a double injection of pituitary adrenotropic hormone (ACTH) at a dose of 25 mg.

Experimental studies have shown that for the prevention and treatment of acute cyanide intoxication, cortisone, vitamin, complexing compounds of cobalt - EDTA CaNa2, rhodanese and ethanethiosulfonate, 6,8-dithiocaprylic acid, cysteine ​​can be used.

However, the effect of these drugs, studied in experiments on animals, has not been tested in cases of poisoning in humans.

Of great importance is the use of agents that stimulate the respiratory center (lobelia subcutaneously 0.01 g, intravenously 0.003 g, cytiton 1 ml subcutaneously or intravenously), as well as inhalations of carbogen. These funds not only restore breathing, but also enhance pulmonary ventilation, promoting the release of hydrocyanic acid through the lungs.

It is rational to alternate carbogen inhalations every 15-20 minutes with inhalation of 100% oxygen, since oxygen dissolved in plasma in an increased amount can contribute to a more vigorous oxidation of hydrocyanic acid and its conversion into low-toxic cyanic acid.

According to experimental studies, inhalation of oxygen at atmospheric pressure does little to change the course of poisoning, but its inhalation at a slight increase in pressure (25 cm of water column) significantly delays the onset of initial respiratory arrest and increases the animal's resistance to cyanide by 2.5 times.

When breathing stops, artificial respiration is immediately started, which must be carried out for a long time (hours). With the development of cardiovascular insufficiency, 1 ml of a 20% camphor solution or a 10% caffeine solution, or a 10% solution of corazole, cordiamine, or a 5% solution of ephedrine, or an adrenaline solution (1: 1000) subcutaneously (1 ml) or intravenously ( 0.5 ml).

In cases of ingestion of cyanides through the mouth, along with the use of the above therapy, it is necessary to prescribe emetics (0.5 ml of a 1% solution of apomorphine subcutaneously), abundant gastric lavage with 0.04% potassium permanganate or 1% hydrogen peroxide to oxidize hydrocyanic acid.

When providing first aid, it is necessary to create conditions for the patient to rest completely and apply heat. All patients with acute cyanide intoxication are subject to hospitalization. Victims should be transported in a supine position and only after removing them from a coma. Patients who have undergone severe intoxication should be under medical supervision for a long time after discharge from the hospital.

Prevention of poisoning with hydrocyanic acid and other cyanides

Their rational employment and appropriate therapy for the consequences of poisoning, if they occur, are necessary.

In the prevention of poisoning with hydrocyanic acid, it is especially important to ensure the sealing of equipment and equipment from which this poison can be released, the installation of local exhaust devices at cyanide baths, the mechanization of loading and unloading parts from cyanide furnaces during cyanidation of steel, thorough ventilation of all rooms and control of the air environment. before entering them (for example, after deratization, disinsection with hydrocyanic acid or other cyanide compounds). When working with the danger of exposure to HCN and its compounds, it is necessary to use a gas mask.

Since hydrocyanic acid is extremely toxic, it is necessary in the relevant industries to pay special attention to the prevention of accidents and to use special devices for constant monitoring of the air in hazardous areas and automatic signaling of dangerous concentrations. All workers are required to strictly observe personal hygiene measures, must be well acquainted with the dangerous effects of cyanides and trained in first aid for victims, in particular artificial respiration techniques.

The maximum permissible concentration in the air of hydrocyanic acid and its salts in terms of HCN is 0.0003 mg/l.

Contraindications for employment with cyanide exposure

Contraindications for employment associated with cyanide exposure are organic disorders of the central nervous system, mental illness, pronounced endocrine-vegetative disorders, as well as diseases of the respiratory and cardiovascular systems that prevent wearing a gas mask.

Drugs and poisons [Psychedelics and toxic substances, poisonous animals and plants] Petrov Vasily Ivanovich

Hydrocyanic acid

Hydrocyanic acid

Until now, hydrocyanic acid is considered the most important representative of cyanides. This light, volatile liquid with a characteristic smell of bitter almonds is a very strong poison: in an amount of 0.05 g, it already causes fatal poisoning in humans. Hydrocyanic acid, obtained for the first time in its pure form in the 80s of the 18th century by the Swedish pharmacist and chemist Karl Scheele (it is claimed that Scheele himself became a victim of this poison during one of the experiments), now attracts the close attention of many specialists.

Cyanic compounds were used already in ancient times, although, of course, their chemical nature was not known then. So, the ancient Egyptian priests knew how to make an essence from peach leaves, with which they killed the guilty people. In Paris, in the Louvre, on a papyrus roll there is a warning saying: “Do not pronounce the name of Iao under pain of punishment with a peach,” and in the temple of Isis an inscription was found: “Do not open - otherwise you will die from a peach.”

Now we know that hydrocyanic acid, which is formed in the process of enzymatic transformations of certain substances of plant origin, was the active component here. A number of prominent chemists of the past studied the structure, methods of production and use of cyanides. So, in 1811, Gay-Lussac showed for the first time that hydrocyanic acid is a hydrogen compound of a radical consisting of carbon and nitrogen, and Bunsen in the middle of the 19th century. developed a method for the industrial production of potassium cyanide. It has been many years since potassium cyanide and other cyanides were of value as means of intentional poisoning and when forensic experts showed particular interest in these fast-acting poisons.

History knows cases of the use of cyanides for the mass destruction of people. For example, during the First World War, the French army used hydrocyanic acid as a poisonous substance, in the Nazi extermination camps the Nazis used poisonous gases cyclones (cyanoformic acid esters), American troops in South Vietnam used toxic organic cyanides against the civilian population. It is also known that in the United States the death penalty has been used for a long time by poisoning convicts with hydrocyanic acid vapors in a special chamber.

Due to their high reactivity and ability to interact with numerous compounds of various classes, cyanides are widely used in many industries, agriculture, and scientific research, and this creates many opportunities for research. Thus, hydrocyanic acid and a large number of its derivatives are used in the extraction of precious metals from ores, in galvanoplastic gilding and silvering, in the production of aromatic substances, chemical fibers, plastics, rubber, organic glass, plant growth stimulants, herbicides. Cyanides are also used as insecticides, fertilizers and defoliants.

Hydrocyanic acid is released in the gaseous state in many industrial processes, and is also formed when cyanides come into contact with other acids and moisture. There may also be cyanide poisoning due to the consumption of large amounts of seeds of almonds, peaches, apricots, cherries, plums and other plants of the Rosaceae family or tinctures from their fruits. It turned out that they all contain amygdalin glycoside, which decomposes in the body under the influence of the emulsin enzyme to form hydrocyanic acid, benzaldehyde and 2 glucose molecules.

The largest amount of amygdalin is found in bitter almonds, in the refined grains of which it is about 3%. Somewhat less amygdalin (up to 2%) in combination with emulsin is found in apricot seeds. Clinical observations have shown that the death of the poisoned usually occurred after eating about 100 peeled apricot seeds, which corresponds to about 1 g of amygdalin. Like amygdalin, hydrocyanic acid is cleaved off by plant glycosides such as linamarin, found in flax, and laurocerazine, found in the leaves of the laurel cherry tree. There are a lot of cyanide substances in young bamboos and their shoots (up to 0.15% of wet weight). In the animal world, hydrocyanic acid is found in the secretion of the skin glands of millipedes.

The toxicity of cyanide to different animal species is different. Thus, high resistance to hydrocyanic acid was noted in cold-blooded animals, while many warm-blooded animals are very sensitive to it. As for man, he seems to be more resistant to hydrocyanic acid than some of the higher animals. This is confirmed, for example, by an experiment carried out at great risk to himself by the famous English physiologist Barcroft, who in a special chamber, together with a dog, was exposed to hydrocyanic acid at a concentration of 18:6000. The experiment continued until the dog fell into a coma and had convulsions. The experimenter at that time did not notice any signs of poisoning. Only after 10-15 minutes. after removing the dying dog from the cell, he had impaired attention and nausea.

There are many data indicating the formation of cyanides in the human body under physiological conditions. Cyanides of endogenous origin are found in biological fluids, in exhaled air, and in urine. It is believed that their normal level in blood plasma can reach 140 mcg / l.

Cyanides can penetrate into the internal environment of the body with poisoned food and water, as well as through damaged skin. Inhalation exposure to volatile cyanides, primarily hydrocyanic acid and cyanogen chloride, is very dangerous. Back in the 60s of the 19th century, attention was drawn to the fact that venous blood flowing from the tissues and organs of cyanide-poisoned animals acquires a scarlet, arterial color. Later it was shown that it contains about the same amount of oxygen as arterial blood. Consequently, under the influence of cyanide, the body loses the ability to absorb oxygen.

Thus, the course of the normal process of tissue respiration is inhibited. Thus, by blocking one of the iron-containing respiratory enzymes, cyanides cause a paradoxical phenomenon: there is an excess of oxygen in cells and tissues, but they cannot assimilate it, since it is chemically inactive. As a result, a pathological condition is rapidly formed in the body, known as tissue, or histotoxic, hypoxia, which is manifested by suffocation, convulsions, paralysis. When non-lethal doses of poison enter the body, the case is limited to a metallic taste in the mouth, redness of the skin and mucous membranes, dilated pupils, vomiting, shortness of breath and headache.

On the other hand, if the animal organism is adapted to a low level of oxygen metabolism, then its sensitivity to cyanides is sharply reduced. At the beginning of this century, the outstanding Russian pharmacologist N.P. Kravkov established a curious fact: during hibernation, hedgehogs tolerate such doses of potassium cyanide, which are many times higher than the lethal ones. N. P. Kravkov explained the resistance of hedgehogs to cyanide by the fact that under conditions of hibernation at low body temperature, oxygen consumption is significantly reduced and animals tolerate the inhibition of its uptake by cells better.

The ability of CN ions to reversibly inhibit tissue respiration and thereby lower the level of metabolic processes unexpectedly turned out to be very valuable for the prevention and treatment of radiation injuries. This is due to the fact that in the mechanism of the damaging effect of ionizing radiation on cellular structures, the leading role is played by the products of water radiolysis, which oxidize many macromolecules, including tissue respiration enzymes. Cyanides, reversibly blocking these enzymes, protect them from the action of these biologically active substances formed under the influence of radiation. In other words, the cyanide-enzyme complex becomes relatively resistant to radiation. After radiation exposure, it dissonates due to a decrease in the concentration of CN ions in the biophase due to their neutralization in the blood and excretion from the body. Amygdalin is the most commonly used cyanide radioprotective agent.

Many historically famous personalities have been poisoned or committed suicide by cyanide.

Goering German (1893-1946) - Nazi war criminal, commander-in-chief of the air force during the fascist dictatorship in Germany, Reich Marshal. The International Military Tribunal at Nuremberg sentenced him to death by hanging.

The execution of Nazi criminals was scheduled for 16 October. On the evening of October 15, Colonel Andrews, who was in charge of guarding the prison where the convicts were, ran into the journalists' room and announced in confusion that Goering had died. Having somewhat calmed down, Andrews said that the guard guard, who was on duty at the door of Goering's cell, suddenly heard a strange wheezing. He immediately called the duty officer and the doctor. When they entered the cell, Goering was in his death throes. The doctor found small pieces of glass in his mouth and pronounced him dead from cyanide poisoning.

After some time, the Austrian journalist Bleibtrey declared publicly that it was he who helped Goering to die. Allegedly, before the start of the meeting, he made his way into the hall and, using chewing gum, attached an ampoule of poison to the dock. The sensation brought Bleibtrego a lot of money, although it was deceitful from beginning to end - at that time the meeting room was better guarded than any other place in Europe. A few years later, Obergruppenführer Bach-Zelewski, released from prison, said the same thing as the Austrian journalist. But he attributed the transfer of the poison to Goering to himself. Perhaps they are both lying. M. Yu. Raginsky believes that the poison was transferred to Goering through an American security officer for a substantial bribe. And it was handed over by his wife Goering, who came to her husband a few days before the appointed date for the execution of the sentence.

Himmler Heinrich (1900–1945) – Nazi war criminal, chief of the Gestapo, Minister of the Interior and commander of the reserve army in Germany.

On May 20, 1945, Himmler decided to flee. On May 23, he was detained by the British and placed in camp 031 near the city of Lüneburg.

The British found an ampoule of potassium cyanide in Himmler's clothes. They didn't stop there. A doctor was called, who examined the arrested man for the second time. Himmler opened his mouth, and the doctor saw something black between his teeth. He pulled Himmler towards the light, but then the former Reichsführer SS snapped his teeth - he cracked open the hidden capsule. After a few seconds, Himmler expired.

Hitler Adolf (pseudonym, real name Schicklgruber) (1889-1945) - leader of the National Socialist Party, head of the German state in 1933-1945.

His death is presented in two main versions.

According to the first version, based on the testimony of Hitler's personal valet Linge, the Fuhrer and Eva Braun shot themselves at 15.30. When Linge and Bormann entered the room, Hitler was allegedly sitting on a sofa in the corner, a revolver lying on the table in front of him, blood flowing from his right temple. The dead Eva Braun, who was in the other corner, dropped her revolver on the floor.

Another version (accepted by almost all historians) says: Hitler and Eva Braun were poisoned by potassium cyanide. Before his death, Hitler also poisoned two beloved sheep dogs.

Rasputin(New) Grigory Efimovich (1864/186 5-1916) - a favorite of Nicholas II and his wife Alexandra Feodorovna.

In 1916, another conspiracy was drawn up against Rasputin. Its main participants were Prince Felix Yusupov, Grand Duke Dmitry Pavlovich, the famous politician Vladimir Purishkevich and military doctor S. S. Lazavert. The conspirators lured Rasputin to the Yusupov Palace in St. Petersburg, agreeing to kill him there and throw his body into the river, under the ice. For the murder, cakes stuffed with poison were prepared, and bottles of potassium cyanide, which were going to be mixed into wine.

Upon Rasputin's arrival at the palace, he was received by the host, while Purishkevich, Grand Duke Dmitry Pavlovich and Dr. Lazavert were waiting upstairs in another room.

Purishkevich, describing in his diary the murder of the tsar's favorite as a feat performed by the conspirators to save Russia, nevertheless pays tribute to Rasputin's courage:

“Another good half an hour passed, which was utterly painful for us, when at last we clearly heard the clapping of two corks one after another, the clink of glasses, after which the interlocutors who had been talking before that downstairs suddenly fell silent.

We froze in our poses, descending a few more steps down the stairs. But ... another quarter of an hour passed, and peaceful conversation and even sometimes laughter from below did not stop.

“I don’t understand anything,” I whispered to him, spreading my arms and turning to the Grand Duke. “What is he, bewitched, or something, that even potassium cyanide does not work on him!”

... We went up the stairs and the whole group again went to the office, where after two or three minutes Yusupov again inaudibly entered, upset and pale.

“No,” he says, “impossible! Imagine, he drank two glasses of poison, ate a few pink cakes, and, as you can see, nothing; Absolutely nothing, and after that minutes, at least fifteen! I can’t imagine how we should be, especially since he was already worried why the countess did not come out to him for so long, and I hardly explained to him that it was difficult for her to disappear unnoticed, because there were few guests upstairs ...; he is now sitting on the sofa gloomy, and, as I see, the effect of the poison affects him only in that he has incessant belching and some salivation ... "

Five minutes later, Yusupov appeared in the office for the third time.

“Gentlemen,” he told us quickly, “the situation is still the same: the poison either doesn’t work on him, or it’s not good for hell; Time is running out, we can't wait any longer."

"But how to be?" - said Dmitry Pavlovich.

“If you can’t use poison,” I answered him, “you need to go for broke, in the open, we all go down together, or leave it to me alone, I will put him down either from my “co-vage”, or I will crush his skull with brass knuckles. What do you say to that?"

“Yes,” Yusupov remarked, “if you put the question this way, then, of course, you will have to stop at one of these methods.”

In the United States, a type of execution is used that evokes a clear analogy with the "gas chambers" of the Nazis.

The execution technology is as follows: “The convict is tied to a chair in a sealed chamber. A stethoscope is attached to the chest, connected to headphones in an adjacent witness room and used by a doctor to monitor the progress of the execution. Cyanide gas is supplied to the cell, poisoning the convict when inhaled. Death occurs as a result of suffocation caused by the suppression of respiratory enzymes by the cyanide gas, which ensures the delivery of oxygen by the blood to the cells of the body.

Although unconsciousness sets in quickly, the entire procedure may take longer if the condemned tries to delay death by holding or slowing his breathing. As with the use of other methods of execution, regardless of whether the convicted person is unconscious or not, the vital organs can continue to function for a long time.

In Mississippi, on September 2, 1983, a certain Jimmy Lee Gray was executed by gassing. During the execution, his body convulsively twitched for 8 minutes in a row; he sighed 11 times with his mouth wide open, without ceasing to beat his head on the crossbar behind the back of the chair. According to eyewitnesses, Lee Gray did not look dead at the end of the execution procedure, when the prison administration invited them to leave the witness room, separated from the execution room by thick glass.

From the book Drugs and Poisons [Psychedelics and Toxic Substances, Poisonous Animals and Plants] author Petrov Vasily Ivanovich

Hydrocyanic acid Until now, hydrocyanic acid is considered the most important representative of cyanides. This light, volatile liquid with a characteristic smell of bitter almonds is a very strong poison: in an amount of 0.05 g, it already causes death in humans.

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Hydrocyanic acid (hydrogen cyanide, HCN) is a colorless volatile liquid with a specific smell of bitter almonds. Easily soluble in water and organic solvents.

Source: depositphotos.com

This compound is often found, because it is part of the seeds of almonds, peaches, apricots, cherries, plums and other plants of the Rosaceae family or tinctures from their fruits. All the kernels of the stones of these plants contain the glycoside amygdalin, which is metabolized in the body to form hydrocyanic acid. The largest amount of amygdalin is found in bitter almonds, about 3%, somewhat less (up to 2%) is present in apricot kernels.

There is evidence of the presence of cyanides (hydrocyanic acid salts) in the human body under physiological conditions. Cyanides of endogenous origin are found in some biological fluids, in exhaled air, and in urine. It is believed that their normal level in blood plasma can reach 140 mcg / l.

Hydrocyanic acid and its salts (sodium cyanide (NaCN), potassium cyanide (KCN), ammonium cyanide (NH4CN) and others) are widely used in industry and agriculture. Hydrogen cyanide is an essential component in the production of synthetic rubbers, acrylic polymers, chemical fibers, plastics, fragrances, plexiglass, and pesticides. Cyanides are used for the extraction of gold and silver from ore, for hardening and liquid carburizing of metals, for galvanoplastic cadmium plating, zinc plating, etc., in the production of pharmaceuticals, in photography, and lithography.

In agriculture, hydrocyanic acid and its derivatives are used to control rodents, plant pests, for the purpose of disinfection.

Hydrogen cyanide is extremely toxic: when taken orally at a dose of 50 mg or when inhaled at a concentration of more than 0.4 mg / l, it causes poisoning, resulting in death. If the concentration of a substance in the air exceeds 11 mg / l, then intoxication with hydrocyanic acid vapor is possible even percutaneously. In this case, the penetration of the poison inside is facilitated by the high air temperature of the industrial premises and severe physical stress, which cause increased blood circulation in the upper layers of the skin.

The widespread use of hydrocyanic acid and its compounds in production conditions, along with its specific characteristics and high toxicity, leads to a high risk of acute or chronic intoxication. Most often, poisoning occurs in the following cases:

• inhalation of hydrocyanic acid vapors or its contact with the skin in case of violation of safety regulations at the workplace (0.2-0.3 mg / l for 5-10 minutes);
• ingress of concentrated aerosols into the gastrointestinal tract;
• inhalation of vapors or contact of substances on the skin when working with herbicides without personal protective equipment;
• eating peach, apricot, cherry, almond, etc. seeds in large quantities;
• the use of homemade tinctures, wines, liqueurs, prepared on the bones of the fruits of the listed plants.

Once in the body, acid and its compounds significantly reduce the activity of tissue respiration enzymes - cytochromes and the catalase enzyme, which stimulates the breakdown of hydrogen peroxide. As a result, acute hypoxia develops, when arterial and venous blood are supersaturated with oxygen, but its absorption by tissues at an adequate level is not possible due to blocking of key enzymes. Stopping the degradation of hydrogen peroxide leads to its accumulation and damage to the cells and tissues of the body. The central nervous system is most sensitive to tissue hypoxia.

Symptoms of poisoning

According to the intensity of the lesion, lightning-fast and protracted forms of hydrocyanic acid poisoning are distinguished.

The lightning-fast form develops within a few minutes when a large amount of toxin enters the body:

• instant loss of consciousness;
• superficial abnormal breathing;
• thready arrhythmic pulse;
• tonic and clonic convulsions;
• death, as a rule, from paralysis of the respiratory center.

With this form of poisoning, it is not possible to provide specialized medical care due to the rapid and transient symptoms.

With a delayed form, clinical manifestations of intoxication develop in the range from 15 to 60 minutes, while it can proceed in mild, moderate and severe degrees.

Mild degree of poisoning

It is characterized by the following symptoms:

• unpleasant taste in the mouth, a feeling of bitterness;
• severe muscle and general weakness;
• dizziness, headache;
• numbness of the oral mucosa;
• increased salivation;
• nausea, vomiting;
• dyspnea.

After the cessation of the action of the poison, the phenomena stop on their own after 1-3 days.

Source: depositphotos.com

Average degree of poisoning

With moderate intoxication, the initial manifestations are similar to those with a mild degree, and later the symptoms increase, join:

• psycho-emotional arousal, a feeling of fear of death;
• staining of the mucous membranes and skin in an intense scarlet color;
• decrease in heart rate (HR);
• increased blood pressure (BP);
• superficial unproductive breathing;
• the smell of bitter almonds from the mouth;
• incoming short-term neurological symptoms: confusion, convulsions, disorientation.

With timely assistance, the condition returns to normal, complaints disappear after 4-6 days.

Severe degree of poisoning

Severe poisoning develops sequentially, passing through several stages: the stage of initial phenomena, respiratory failure, convulsive and paralytic stages.

1. Initial stage. Symptoms are nonspecific, similar to those of mild or moderate poisoning. This condition is short-term, it quickly passes into the stage of shortness of breath.
2. Dyspnoetic stage (stage of shortness of breath). The leading signs are acute tissue hypoxia: the scarlet color of the visible mucous membranes and skin, severe weakness, a state of stupor, and increasing pain in the region of the heart. Objectively: the pupils are dilated, the victim is restless, the pulse is quickened, arrhythmic, the breathing is unproductive, frequent, the breath is shortened, there is a persistent smell of bitter almonds from the mouth.
3. Convulsive stage. The deterioration of the general condition progresses, shortness of breath increases, the pulse becomes rare, and blood pressure rises. Clonic and tonic convulsions develop with the reduction of the chewing muscles and, often, biting the tongue, when frequent rhythmic muscle contractions turn into a long persistent generalized muscle spasm; the victim is unconscious. This condition lasts from several minutes to several hours, transforming into the terminal paralytic stage.
4. paralytic stage. Convulsions stop, a coma develops, respiratory arrest occurs, a critical drop in blood pressure and cessation of cardiac activity.

First aid for hydrocyanic acid poisoning

1. Evacuate the victim from the place of contamination (break contact with the poison).
2. Provide access to fresh air (open windows, doors, unfasten tight clothing).
3. If the casualty is unconscious, lay him on his side or on his back with his head turned to one side to prevent aspiration of vomit in case of vomiting.
4. When using hydrogen cyanide inside - rinse the stomach (drink 1-1.5 liters of warm water, a weak solution of potassium permanganate or 1% hydrogen peroxide, press on the root of the tongue, causing vomiting).
5. Take a sorbent (Enterosgel, Polyphepan, Polysorb).
6. In the presence of symptoms of clinical death (lack of consciousness, breathing, pulse on the carotid arteries and pupillary response to light), immediately proceed to basic cardiopulmonary resuscitation of the victim by performing an indirect heart massage. Artificial ventilation of the lungs by mouth-to-mouth or mouth-to-nose should not be performed, as this can lead to the development of poisoning in the rescuer.

When is medical assistance required?

Medical attention is needed in 100% of cases of hydrocyanic acid poisoning. Since it is not always possible to assess the degree of impact and the severity of the lesion at the initial stage, the victim must be under round-the-clock medical supervision.

Hydrocyanic acid antidotes are Glucose, Sodium thiosulfate, Ethyl nitrite, Methylene blue with Tetrathiosulfate (co-administration), Amyl nitrite with Thiosulfate (co-administration). The co-administration of sodium nitrite with thiosulfate most strongly counteracts hydrocyanic acid.

After the introduction of the antidote, measures are taken to maintain the most important life support systems. When stabilization is achieved, further treatment is symptomatic.

Possible consequences

The consequences of hydrocyanic acid poisoning can be persistent, sometimes irreversible changes in the central nervous system (parkinsonism, symptoms of cerebellar damage, emotional disorders, toxic encephalopathy, muscle paresis and paralysis), astheno-neurotic conditions, toxic pneumonia, acute heart failure.

Prevention

Since the bulk of hydrocyanic acid poisoning is industrial in nature, preventive measures are primarily aimed at optimizing production processes:

• compliance with safety requirements at the workplace;
• prevention of violations of the technological process;
• mandatory use of personal protective equipment (gloves, respirator, gas mask, protective clothing).

Poisoning in everyday life can be avoided by remembering the high danger of eating large quantities of seeds and seeds of apricots, cherries, almonds, peaches, etc., and products made from them.

Many people know the taste of spicy, tasty apricot kernels. But not everyone understands that this seemingly harmless natural product contains an unsafe component - hydrocyanic acid.

Let's try to understand in order what effect hydrocyanic acid has on the body, its properties and precautionary methods.

Hydrocyanic acid in combination with compounds represent a group of cyanides, which are natural insecticides. This substance is able to protect plants from harmful insects and microorganisms. Cyanides are found in many edible and inedible fruits and leaves of plants. By itself, the substance has no color, and tastes like bitter almonds. Hydrocyanic acid is a highly toxic substance of high volatility and low density.

In the bones of fruit trees, it occurs naturally and is part of low-toxic glycosides as long as the seeds are dry and intact. If these conditions are violated, chemical reactions begin to occur that contribute to the release of hydrocyanic acid.

Moisture that affects fruit seeds: cherries, plums, apricots, mountain ash, apples, almonds, forms hydrocyanic acid. Since all of the above plants are rosaceous, they contain glycosides that release a toxic substance.

Grapes, for example, do not belong to this family, so it does not tend to release hydrocyanic acid, and wines are made from grapes, and from all fruits containing a strong acid in the whole, the drink will be poisonous.

What plants contain hydrocyanic acid

Probably everyone is interested in how much hydrocyanic acid is present in each of the fruits. So, its specific gravity in these "poisonous" fruits is as follows:

Thus, the apple tree will interfere with the least concentrated content of the toxic substance, therefore, it can be poisoned much less often than, for example, almonds.

What dose is lethal to the body

According to scientists and the results of long-term experiments, it was possible to find out that the human body and the body of warm-blooded animals are more susceptible to the effects of this substance. in the body of cold-blooded creatures, its compounds are destroyed naturally and do not lead to poisoning.

Scientists were able to find out that the lethal or most dangerous dose of poison can be the use of bitter almonds in the amount of 40 grams if you eat more than 100 apricot kernels, or 60 grams of those kernels that contain amygdalin.

If we translate these data into a pure hydrocyanic acid concentrate, then it is most dangerous when consumed from 1 mg per kilogram.

Do not forget that cooked wine from fruits and berries that have not been separated from the seeds is very dangerous, it can cause not only acute poisoning, but also lead to death.

If we talk about compotes and jams, things are different. With a high concentration of sugar in these dishes, hydrocyanic acid is neutralized, since it is its antidote.

With an excessive concentration of this substance (from 0.24 to 0.97 mg per liter), intoxication of this substance occurs in the human body, causing acute poisoning.

In case of poisoning as a result of the use of apricot kernels or other seeds, energy decline occurs and the function of the respiratory tract is disturbed. This negatively affects the work of the central nervous system, especially the brain.

Lack of energy greatly affects the functioning of the nervous system, which leads to a change in the structure of its cells. It also happens that poisoning and death occurs regardless of the saturation of oxygen in the blood. This is evidenced by the pleasant reddish color of the skin of victims of poisoning in a fatal outcome.

Energy starvation of the brain occurs due to the action of the poison, which stimulates the release of blood cells from the spleen. Scientists say that this process occurs due to a reflex effect on the spleen. Simply put, the body mistakenly believes that the lack of energy occurs due to lack of oxygen, so it tries to restore homeostasis on its own.

Nevertheless, the rest of the organs and systems of the body are quite coping with their functions. As practice shows, after opening the bodies of people poisoned by hydrocyanic acid, there is no change in the functioning of the heart, liver, kidneys, which cannot be said about disorders of the nervous system. if the poison acts in the body for a long time, then later changes occur in the work of the heart and other organs due to the formation of oxygen starvation.

The accumulation of oxygen in the blood leads to a violation of blood pressure. In addition, if severe poisoning occurs, venous blood becomes externally similar to arterial blood, that is, it acquires a scarlet hue.

Although hydrocyanic acid is not a strongly acidic substance, it is capable of reacting with many compounds present in the body. But, given that these reactions do not develop so quickly, and the process of the effect of the poison on the body occurs very quickly, a person may die.

Summing up, it is worth saying that the kernels of rosaceae should not be eaten. Compotes and jams are best prepared from pitted berries and fruits. An exception is grapes, which are used to make wine whole, since their pits do not contain hydrocyanic acid.

Such very simple precautions will help maintain your health and the health of those close to you.