How potassium cyanide is neutralized. What happens to a person who drinks potassium cyanide?

Of all the poisons, potassium cyanide has the most notorious reputation. In detective stories, the use of this cyanide by criminals is a very popular way to get rid of unwanted persons. Obviously, the wide popularity of the poison is also associated with its availability at the turn of the 19th and 20th centuries, when the powder could easily be bought at a pharmacy.

Meanwhile, potassium cyanide is not the most dangerous and toxic substance - in terms of lethal dose it is inferior to such prosaic poisons as nicotine or botulinum toxin. So what is potassium cyanide, where is it used and how does it affect the human body? Does his fame correspond to the real state of affairs?

What is potassium cyanide

The poison belongs to the group of cyanides - derivatives of hydrocyanic acid. The formula of potassium cyanide is KCN. The substance was first obtained by the German chemist Robert Wilhelm Bunsen in 1845, and he also developed an industrial method for its synthesis.

In appearance, potassium cyanide is a colorless crystalline powder, highly soluble in water. The reference books describe that potassium cyanide has a specific smell of bitter almonds. But this characteristic is not always correct - approximately 50% of people are able to smell this smell. It is believed that this is due to individual differences in the olfactory apparatus. Potassium cyanide is not a very stable compound. Since hydrocyanic acid is weak, the cyano group is easily displaced from the compound by salts of stronger acids. As a result, the cyano group evaporates, and the substance loses its toxic properties. Cyanides also oxidize when exposed to moist air or in solutions with glucose. The latter property allows the use of glucose as one of the antidotes for poisoning with hydrocyanic acid and its derivatives.

Why does a person need potassium cyanide? It is used in the mining and processing industry and in galvanic production. Since noble metals are not able to be oxidized directly by oxygen, solutions of potassium or sodium cyanide are used to catalyze the process. Chronic potassium cyanide poisoning can occur among people not involved in production. Thus, in the early 2000s, there were cases of toxic emissions from mining and processing enterprises in Romania and Hungary into the Danube River, as a result of which people living in the vicinity of the floodplain suffered. Workers of special laboratories who come into contact with poison as a reagent are at risk of getting a chronic disease.

In household conditions, cyanide can be found in reagents for darkrooms and in jewelry cleaning products. Small amounts of potassium cyanide are used by entomologists in insect stains. There are also artistic paints (gouache, watercolor), which contain cyanides - “Prussian blue”, “Prussian blue”, “milori”. There they are combined with iron and give the dye a rich azure color.

What contains potassium cyanide in nature? You won’t find it in its pure form, but a compound with a cyano group, amygdalin, is found in the seeds of apricots, plums, cherries, almonds, and peaches; elderberry leaves and shoots. When amygdalin is broken down, hydrocyanic acid is formed, which acts similarly to potassium cyanide. Fatal poisoning can be obtained from 1 g of amygdalin, which corresponds to approximately 100 g of apricot kernels.

Effect of potassium cyanide on humans

How does potassium cyanide affect the human body? The poison blocks the cellular enzyme - cytochrome oxidase, which is responsible for the absorption of oxygen by the cell. As a result, oxygen remains in the blood and circulates there bound to hemoglobin. Therefore, in case of cyanide poisoning, even venous blood has a bright scarlet color. Without access to oxygen, metabolic processes inside the cell stop and the body quickly dies. The effect is equivalent to that of a poisoned person simply suffocating due to lack of air.

Potassium cyanide is poisonous if ingested, or if the powder and solution vapors are inhaled; can also penetrate the skin, especially if it is damaged. The lethal dose of potassium cyanide for humans is 1.7 mg/kg body weight. The drug belongs to the group of potent toxic substances, its use is controlled with all possible rigor.

The effect of cyanide is weakened in combination with glucose. Laboratory workers who are forced to come into contact with this poison while working hold a piece of sugar under their cheek. This allows you to neutralize microscopic doses of toxin that accidentally enter the blood. Also, the poison is absorbed more slowly on a full stomach, which allows the body to reduce its harmful effects through oxidation by glucose and some other blood compounds. A small amount of cyanide ions, about 140 mcg per liter of plasma, circulates in the blood as a natural metabolic metabolite. For example, they are part of vitamin B12 - cyanocobalamin. And the blood of smokers contains twice as much of them.

Symptoms of potassium cyanide poisoning

What are the symptoms of potassium cyanide poisoning? The effect of the poison manifests itself very quickly - when inhaled almost instantly, when ingested - after a few minutes. Cyanide is absorbed slowly through the skin and mucous membranes. Signs of potassium cyanide poisoning depend on the dose received and individual sensitivity to the poison.

In acute poisoning, disorders develop in four stages.

Prodromal stage:

The second stage is dyspnoetic, during which the signs of oxygen starvation increase:

pressure in the chest increases;
the pulse slows down and weakens;
general weakness increases;
dyspnea;
the pupils are dilated, the conjunctiva of the eyes turns red, the eyeballs protrude;
a feeling of fear arises, turning into a stunned state.

When a lethal dose is received, the third stage begins - convulsive:

The fourth stage is paralytic, leading to death from potassium cyanide:

the victim is unconscious;
breathing slows down greatly;
the mucous membranes turn red, a blush appears;
Sensitivity and reflexes are lost.

Death occurs within 20–40 minutes (if the poison gets inside) from respiratory and cardiac arrest. If the victims do not die within four hours, then, as a rule, they survive. Possible consequences - residual impairment of brain activity due to oxygen starvation.

In chronic cyanide poisoning, the symptoms are largely due to intoxication with thiocyanates (rodanides) - substances of the second class of danger into which cyanides are converted in the body under the influence of sulfide groups. Thiocyanates cause pathology of the thyroid gland, have a harmful effect on the liver, kidneys and provoke the development of gastritis.

First aid for poisoning

The victim needs the prompt administration of potassium cyanide antidotes, of which there are several. Before introducing a specific antidote, it is necessary to alleviate the patient’s condition - remove the poison from the stomach by lavage:

Then give a sweet warm drink.

If the victim is unconscious, then only a medical professional can help him. In case of respiratory arrest, artificial ventilation is performed.

If there is a possibility of potassium cyanide getting on clothing, it is necessary to remove it and wash the patient’s skin with water.

Treatment

Measures are taken to maintain vital functions - a breathing tube and an intravenous catheter are inserted. Potassium cyanide is a poison for which there are several antidotes. They are all used because they have different mechanisms of action. The antidote is effective even in the last stages of poisoning.

In this case, they focus on ensuring that the level of methemoglobin in the blood does not exceed 25–30%.

Solutions of substances that easily release sulfur neutralize cyanide in the blood. A 25% sodium thiosulfate solution is used.
Glucose solution 5 or 40%.

To stimulate the respiratory center, the drugs “Lobelin” or “Cititon” are administered.

To summarize, we can say the following. The toxic effect of potassium cyanide on humans is to block the mechanism of cellular respiration, resulting in death from suffocation and paralysis very quickly. Antidotes - amyl nitrite, sodium thiosulfate, glucose - can help. They are administered intravenously or inhaled.

To prevent chronic poisoning in production, it is necessary to follow general safety measures: avoid direct contact with poison, use protective equipment, and regularly conduct medical examinations.

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Poisoning a person can happen accidentally or intentionally. Many have heard of such a poison as potassium cyanide. It acts on humans quite quickly and cyanide poisoning often results in severe consequences or death. This toxic substance is used only in production (jewelry making, mining of precious metals); it is not often found in everyday life.

How to determine potassium cyanide

Potassium cyanide, or potassium cyanide, is a substance that is a compound of hydrocyanic acid and potassium hydroxide. It is very toxic. However, it should be noted that this toxic substance is not particularly resistant to decay. That is, under certain conditions (concentrated glucose solution, high environmental humidity), oxidation and decomposition of a dangerous compound occurs.

Is it possible to detect this poison? This is quite difficult, since it does not have any special distinctive features, and when it gets into food and drinks it is not distinguishable.

Characteristics of potassium cyanide:

Type of this substance. It appears as small colorless crystals. Looks like regular refined sugar;
Solubility. Poison crystals dissolve well in water. At the same time, the liquid does not change its color and consistency;
Smell. We can say that potassium cyanide has no smell at all. Although some people, due to their genetic predisposition, can detect a slight almond aroma.

How can you get poisoned?

Potassium cyanide can be found in some plant foods:

Almonds, cassava;
Fruit tree seeds (cherry, apricot, peach, plum).

If these products are consumed in large quantities, symptoms of mild intoxication may occur.

Industries and industries that use cyanide:

Causes of potassium cyanide poisoning:

Violation of safety precautions and rules of use when working with toxic substances at work;
Failure to comply with the rules for handling rodent poison;

Industrial accidents;
Eating tassels of fruiting plants(more often in children). Canned compotes with pits, as well as frozen cherries, tend to accumulate this dangerous substance. Therefore, it is not recommended to store these stocks longer than 12 months;
Intentional use for the purpose of suicide (recently practically not registered).

Ways of penetration of poison into the body:

Airborne - inhalation of poison vapors;
Food – penetration into the body with food and drinks;
Contact household, that is, poisoning with potassium cyanide through the skin and mucous membranes.

The effect of potassium cyanide on the human body

The speed of action of potassium cyanide on the body directly depends on the route of its penetration. If the poison enters the air, the body’s reaction is lightning fast. When this substance is inhaled, it quickly penetrates the blood, from which it spreads throughout the body. When penetrated by other routes, pathological signs increase gradually.

Cyanide disrupts the functioning of the body at the cellular level.

Cyanide has a negative effect on humans. As soon as the toxic substance has entered the body, it begins to block the cells. That is, the body's cells lose the ability to absorb oxygen, which is so necessary for life and activity.

Oxygen enters the cells, but they cannot absorb it, which is why hypoxia develops, and then asphyxia. First of all, brain cells, which vitally need oxygen to function, are affected.

Symptoms of potassium cyanide poisoning

In the clinical picture of poisoning, there are 4 stages, which depend on the concentration of the poison that has entered the body.

The first stage is prodromal. This is a mild poisoning, which is manifested by the following pathological signs:

The second stage is dyspneic. It develops with further contact with the toxic substance. The dyspnoetic stage is characterized by the presence of the following symptoms of cyanide poisoning:

The victim's anxiety;
Feeling of fear of death;
Bradycardia (pulse becomes rare);
Impaired coordination of movements;
Dizziness;
Redness of the skin, perspiration;
Trembling limbs (tremor);
The eyeballs are bulging, the pupils are dilated. Their reaction to light is preserved;
Severe shortness of breath, tachypnea.

The third stage is convulsive:

Vomit;
Convulsions;
Loss of consciousness;
The bullet is weak, thread-like;
Body temperature is sharply increased;
Reduced blood pressure.

At this stage of intoxication, immediate qualified medical assistance is required.

Fourth stage paralytic:

Bright blush;
Stopping seizures;
There is no sensitivity of the skin;
Paresis and paralysis, including the respiratory center;
Lack of breathing.

First aid and treatment after poisoning

In case of poisoning with potassium cyanide, it is necessary to call an ambulance team, which will ensure hospitalization of the patient. Before doctors arrive, first aid should be provided to the victim to alleviate his condition:

Antidotes are:

5 or 40% glucose solution;
2% sodium nitrite solution;
1% solution of methylene blue;
25% sodium thiosulfate solution;
Amyl nitrite. This solution is applied to a cotton swab and the victim is allowed to breathe.

The victim is hospitalized in the intensive care unit, where appropriate treatment is carried out:

Consequences and complications

When working with cyanide, chronic poisoning may develop, which appears:

Severe headaches;
Dizziness;
Irritability;
Decreased memory;
Sleep disturbance;
Unpleasant sensations and pain in the heart area.

With a long course of chronic intoxication, severe pathologies of various systems (nervous, cardiovascular, digestive, excretory) develop.

Complications of cyanide poisoning include:

Persistent memory impairment (difficulty remembering new information, disappearance of certain moments of the past from memory);
In severe poisoning, severe brain damage is observed, which is manifested by a decrease in intellectual and cognitive abilities;
Chronic headaches;
Nervous breakdowns and depression;
Changes in blood pressure;
Change in heart rate;
Coma and convulsions are early complications that are life-threatening for the victim;
In severe cases, death.

Death from potassium cyanide: lethal dose and causes of death

Death from potassium cyanide is very real. This is a very toxic substance, which even in small doses has extremely negative effects.

17 milligrams of potassium cyanide per 1 kilogram of human weight is a lethal dose.

When this concentration enters the body, death occurs in a matter of minutes. In this case, the person does not even have time to provide first aid to the victim.

Why does death occur from potassium cyanide poisoning? Death occurs when there is a high concentration of the toxic substance in the body, as well as when medical care is not provided in a timely manner. In this case, a paralytic stage quickly occurs, which often ends in the death of the patient. Many organs and systems stop working.

The causes of death are:

Brain damage. Paralysis of the respiratory center occurs. In this case, respiratory arrest is of central origin;
Hypoxia of brain and heart tissue;
Respiratory and cardiac arrest are the leading causes of death.

It is impossible to avoid death when a lethal dose is administered.

In all other cases, in order to save the patient, it is necessary to provide him with assistance and administer antidotes as quickly as possible.

Potassium cyanide (potassium cyanide, calcium cyanide) is a salt of hydrocyanic acid. It is a colorless crystalline powder, very similar in appearance to sugar. Potassium cyanide has good solubility and is one of the strongest organic poisons. 1.7 mlg. per 1 kg of weight is a lethal dose for humans. Information about the appearance of such a substance was received from the Swedish pharmacist - Karl Scheele back in 1762.

Receipt

You can receive it in several ways.
1. During the chemical reaction of hydrocyanic acid with potassium powder.
2. In the laboratory method, a chemical reaction of ammonia, chloroform and caustic potash occurs.

Application

Potassium cyanide is used in the separation of silver or gold from ore. All this happens using the cyanidation method. Also, potassium cyanide has found application in galvanizing products using the galvanic method.

The product easily decomposes in open air; immediate decomposition occurs when potassium cyanide reacts with carbon dioxide and water. In the process of such instant decomposition, hydrocyanic acid and potassium nitrate (which is sometimes used in the food industry) are formed.

In an aqueous solution, it gradually hydrolyzes with the release of HCN (hydrolysis constant 2.54.10-5 at 25 °C); When boiling water solutions, it decomposes into NH3 and HCOOC. According to chemistry Holy KCN is a typical representative of alkali metal cyanides. Above 634 °C it is oxidized by oxygen or PbO to KNCO. In humid air interaction. with CO2, giving K2CO3 and HCN. Forms complexes with transition metals, e.g. K4.

Get KCN interaction. HCN with excess KOH. KCN is a reagent for the extraction of Ag and Au from ores, a complexometric reagent. analysis for the determination of Ag, Ni and Hg, a component of electrolytes for the purification of Pt from Ag and for galvanic. gilding and silvering. It is also used to produce nitriles, potassium cyanate KNCO. Highly toxic, causes suffocation due to paralysis of tissue respiration. KCN powders and solutions irritate the skin. MPC 0.0003 mg/l (in terms of HCN).

For questions regarding purchasing potassium cyanide and receiving detailed advice on product properties, delivery conditions and concluding a contract, please contact our managers.

“I took out a box of potassium cyanide from the supply and put it on the table next to the cakes. Dr. Lazavert put on rubber gloves, took several crystals of poison from it, and ground it into powder. Then he removed the top of the cakes and sprinkled the filling with enough powder, he said, to kill an elephant. There was silence in the room. We watched his actions excitedly. All that remains is to put the poison in the glasses. We decided to put it in at the last moment so that the poison would not evaporate...”

This is not an excerpt from a detective novel, and the words do not belong to a fictional character. Here are the memoirs of Prince Felix Yusupov about the preparation of one of the most famous crimes in Russian history - the murder of Grigory Rasputin. It happened in 1916. If until the middle of the 19th century arsenic was the main assistant of poisoners, then after the introduction of the Marsh method into forensic practice (see the article “Mouse, Arsenic and Kale the Detective”, “Chemistry and Life”, No. 2, 2011) arsenic was used less and less. But potassium cyanide, or potassium cyanide (potassium cyanide, as it was called before), began to be used more and more often.

What it is...

Potassium cyanide is a salt of hydrocyanic acid, or hydrocyanic acid, Н–СN; its composition is reflected by the formula KCN. Hydrocyanic acid in the form of an aqueous solution was first obtained by the Swedish chemist Carl Wilhelm Scheele in 1782 from the yellow blood salt K4. The reader already knows that Scheele developed the first method for the qualitative determination of arsenic (see “Mouse, Arsenic and Kale the Detective”). He also discovered the chemical elements chlorine, manganese, oxygen, molybdenum and tungsten, obtained arsenic acid and arsine, barium oxide and other inorganic substances. Over half of the organic compounds known in the 18th century were also isolated and described by Karl Scheele.

Anhydrous hydrocyanic acid was obtained in 1811 by Joseph Louis Gay-Lussac. He also established its composition. Hydrogen cyanide is a colorless volatile liquid that boils at 26°C. The root “cyan” in its name (from the Greek - azure) and the root of the Russian name “cyanic acid” are similar in meaning. This is no coincidence. CN – ions form blue compounds with iron ions, including the composition KFe. This substance is used as a pigment in gouache, watercolor and other paints under the names “Prussian blue”, “milori”, “Prussian blue”. You may be familiar with these paints from gouache or watercolor sets.

Detective authors unanimously claim that hydrocyanic acid and its salts have “the smell of bitter almonds.” Of course, they did not sniff hydrocyanic acid (neither did the author of this article). Information about the “smell of bitter almonds” was gleaned from reference books and encyclopedias. There are other opinions. The author of “Chemistry and Life” A. Kleshchenko, who graduated from the Faculty of Chemistry of Moscow State University and is familiar with hydrocyanic acid first-hand, in the article “How to poison a hero” (“Chemistry and Life”, 1999, No. 2) writes that the smell of hydrocyanic acid is not similar to almond.

Crime writers have fallen victim to a long-standing misconception. But on the other hand, the directory “Harmful Chemicals” was also compiled by specialists. One could, after all, get prussic acid and smell it. But something is scary!

It remains to be assumed that the perception of odors is an individual matter. And what reminds one of the smell of almonds has nothing in common with almonds for another. This idea is confirmed by Peter MacInnis in the book “Silent Killers. World History of Poisons and Poisoning": "Detective novels always mention the aroma of bitter almonds, which is associated with sodium cyanide, potassium cyanide and hydrogen cyanide (hydrogen cyanide), but only 40-60 percent of ordinary people are able to even smell this specific smell." Moreover, residents of central Russia, as a rule, are not familiar with bitter almonds: its seeds, unlike sweet almonds, are not eaten and are not sold.

...and why do they eat it?

We'll get back to almonds and their smell later. And now - about potassium cyanide. In 1845, the German chemist Robert Bunsen, one of the authors of the spectral analysis method, obtained potassium cyanide and developed a method for its industrial production. If today this substance is in chemical laboratories and in production under strict control, then at the turn of the 19th and 20th centuries, potassium cyanide was available to anyone (including attackers). Thus, in Agatha Christie’s story “The Hornet’s Nest,” potassium cyanide was bought at a pharmacy supposedly to kill wasps. The crime was foiled only thanks to the intervention of Hercule Poirot.

Entomologists used (and still use) small amounts of potassium cyanide in insect stains. Several poison crystals are placed at the bottom of the stain and filled with plaster. Cyanide reacts slowly with carbon dioxide and water vapor, releasing hydrogen cyanide. The insects inhale the poison and die. The stain filled in this way lasts for more than a year. Nobel laureate Linus Pauling told how he was supplied with potassium cyanide for making stains by the caretaker of a dental college. He also taught the boy how to handle this dangerous substance. This was in 1912. As we can see, in those years the storage of the “king of poisons” was treated quite frivolously.

Why does potassium cyanide become so popular among real and fictional criminals? The reasons are not difficult to understand: the substance is highly soluble in water, does not have a pronounced taste, the lethal (fatal) dose is small - on average 0.12 g is enough, although individual susceptibility to the poison, of course, varies. A high dose of potassium cyanide causes almost instantaneous loss of consciousness, followed by respiratory paralysis. Add to this the availability of the substance at the beginning of the 19th century, and the choice of Rasputin’s murderous conspirators becomes clear.

Hydrocyanic acid is just as poisonous as cyanides, but is inconvenient to use: it has a specific odor (it is very weak in cyanides) and cannot be used unnoticed by the victim; moreover, due to its high volatility, it is dangerous for everyone around, not just for the one for whom it is intended. But it also found use as a poisonous substance. During the First World War, hydrocyanic acid was used by the French army. In some US states it was used to execute criminals in “gas rooms”. It is also used to treat carriages, barns, and ships infested with insects - the principle is the same as that of young Pauling’s stain.

How does it work?

It’s time to figure out how such a simple substance acts on the body. Back in the 60s of the 19th century, it was established that the venous blood of animals poisoned with cyanide has a scarlet color. This is characteristic, if you remember, of arterial blood rich in oxygen. This means that an organism poisoned by cyanide is unable to absorb oxygen. Hydrocyanic acid and cyanide somehow inhibit the process of tissue oxidation. Oxyhemoglobin (a combination of hemoglobin with oxygen) circulates throughout the body in vain, without giving oxygen to the tissues.

The reason for this phenomenon was discovered by the German biochemist Otto Warburg in the late 20s of the twentieth century. During tissue respiration, oxygen must accept electrons from the substance undergoing oxidation. The process of electron transfer involves enzymes collectively called “cytochromes”. These are protein molecules containing a non-protein hemin fragment associated with an iron ion. The cytochrome containing the Fe 3+ ion accepts an electron from the substance being oxidized and turns into the Fe 2+ ion. This, in turn, transfers an electron to the next cytochrome molecule, oxidizing to Fe 3+. Thus, the electron is transferred along the chain of cytochromes, like a ball that “a chain of basketball players passes from one player to another, inexorably bringing him closer to the basket (oxygen).” This is how English biochemist Stephen Rose described the work of tissue oxidation enzymes. The last player in the chain, the one who throws the ball into the oxygen basket, is called cytochrome oxidase. In oxidized form it contains the Fe 3+ ion. This form of cytochrome oxidase serves as a target for cyanide ions, which can form covalent bonds with metal cations and prefer Fe 3+.

By binding cytochrome oxidase, cyanide ions remove the molecules of this enzyme from the oxidative chain, and the transfer of electrons to oxygen is disrupted, that is, oxygen is not absorbed by the cell. An interesting fact was discovered: hibernating hedgehogs are able to tolerate doses of cyanide many times greater than lethal ones. And the reason is that at low temperatures, the absorption of oxygen by the body slows down, like all chemical processes. Therefore, a decrease in the amount of enzyme is easier to tolerate.

Readers of detective stories sometimes get the idea that potassium cyanide is the most poisonous substance on Earth. Not at all! Nicotine and strychnine (substances of plant origin) are tens of times more toxic. The degree of toxicity can be judged by the mass of toxin per 1 kg of laboratory animal weight, which is required to cause death in 50% of cases (LD 50). For potassium cyanide it is 10 mg/kg, and for nicotine - 0.3. Next come: dioxin, a poison of artificial origin - 0.022 mg/kg; tetrodotoxin secreted by puffer fish - 0.01 mg/kg; batrachotoxin secreted by the Colombian tree frog - 0.002 mg/kg; ricin contained in castor bean seeds - 0.0001 mg/kg (a clandestine terrorist laboratory for the production of ricin was uncovered by British intelligence services in 2003); β-bungarotoxin, venom of the South Asian bungaros snake, - 0.000019 mg/kg; tetanus toxin - 0.000001 mg/kg.

The most toxic is botulinum toxin (0.0000003 mg/kg), which is produced by bacteria of a certain type that develop under anaerobic conditions (without air access) in canned food or sausage. Of course, they have to get there first. And from time to time they get there, especially in home-made canned goods. Homemade sausage is now rare, but at one time it was often the source of botulism. Even the name of the disease and its causative agent comes from the Latin botulus- "sausage". During its life, the botulinum bacillus releases not only toxin, but also gaseous substances. Therefore, swollen cans should not be opened.

Botulinum toxin is a neurotoxin. It disrupts the functioning of nerve cells that transmit impulses to the muscles. The muscles stop contracting and paralysis occurs. But if you take a toxin in low concentration and target certain muscles, the body as a whole will not be harmed, but the muscle will be relaxed. The drug is called “Botox” (botulinum toxin), it is both a medicine for muscle spasms and a cosmetic product for smoothing wrinkles.

As we see, the most poisonous substances in the world were created by nature. Extracting them is much more difficult than obtaining the simple compound KCN. It is clear that potassium cyanide is both cheaper and more accessible.

However, the use of potassium cyanide for criminal purposes does not always give a guaranteed result. Let's see what Felix Yusupov writes about the events that took place in the basement on the Moika on a cold December night in 1916:

“...I offered him eclairs with potassium cyanide. He refused at first.

“I don’t want it,” he said, “it’s too sweet.”

However, he took one, then another. I looked in horror. The poison should have taken effect immediately, but, to my amazement, Rasputin continued to talk as if nothing had happened. Then I offered him our homemade Crimean wines...

I stood next to him and watched his every move, expecting that he was about to collapse...

But he drank, smacked, savored the wine like real experts. Nothing changed in his face. At times he raised his hand to his throat, as if he had a spasm in his throat. Suddenly he stood up and took a few steps. When I asked what was wrong with him, he replied:

Nothing. Tickling in the throat.

The poison, however, had no effect. The “old man” calmly walked around the room. I took another glass of poison, poured it and gave it to him.

He drank it. No impression. The last, third glass remained on the tray.

In desperation, I poured it for myself, so as not to let Rasputin go away from the wine...”

All in vain. Felix Yusupov went up to his office. “...Dmitry, Sukhotin and Purishkevich, as soon as I entered, rushed towards me with questions:

Well? Ready? Is it over?

The poison didn’t work,” I said. Everyone fell silent in shock.

Can't be! - Dmitry cried.

Elephant dose! Did he swallow everything? - asked the others.

That’s it, I said.”

But still, potassium cyanide had some effect on the old man’s body: “He hung his head, breathed intermittently...

Are you feeling unwell? - I asked.

Yes, my head is heavy and my stomach burns. Come on, pour a little. Maybe he’ll feel better.”

Indeed, if the dose of cyanide is not so large as to cause instant death, at the initial stage of poisoning there is a scratching in the throat, a bitter taste in the mouth, numbness of the mouth and pharynx, redness of the eyes, muscle weakness, dizziness, staggering, headache, palpitations, nausea, vomit. Breathing is somewhat rapid, then becomes deeper. Yusupov noticed some of these symptoms in Rasputin. If at this stage of poisoning the flow of poison into the body stops, the symptoms disappear. Obviously, the poison was not enough for Rasputin. It is worth understanding the reasons, because the organizers of the crime calculated the “elephant” dose. By the way, about elephants. Valentin Kataev in his book “Broken Life, or Oberon’s Magic Horn” describes the case of an elephant and potassium cyanide.

In pre-revolutionary times, in the Odessa circus-tent of Lorberbaum, the elephant Yambo fell into a rage. The behavior of the enraged elephant became dangerous, and they decided to poison it. What do you think? “They decided to poison him with potassium cyanide, put in cakes, which Yambo was a big fan of,” writes Kataev. And further: “I didn’t see this, but I vividly imagined how a cab driver drives up to Lorberbaum’s booth and how attendants bring cakes into the booth, and there is a special medical commission there... with the greatest precautions, wearing black gutta-percha gloves, they stuff the cakes with tweezers crystals of potassium cyanide..." Isn't it very reminiscent of the manipulations of Dr. Lazovert? It should only be added that a high school boy paints an imaginary picture for himself. It is no coincidence that this boy later became a famous writer!

But let's return to Yambo:

“Oh, how vividly my imagination painted this picture... I moaned half asleep... Nausea rose to my heart. I felt poisoned by potassium cyanide... I felt like I was dying... I got out of bed and the first thing I did was grab the Odessa Leaflet, confident that I would read about the death of an elephant. Nothing like this!

The elephant that ate cakes filled with potassium cyanide turns out to be still very much alive and, apparently, is not going to die. The poison had no effect on him. The elephant only became even more violent.”

You can read about further events that happened with the elephant and with Rasputin in books. And we are interested in the reasons for the “inexplicable nonsense,” as Odessa Leaflet wrote about the case of the elephant. There are two such reasons.

First, HCN is a very weak acid. Such an acid can be displaced from its salt by a stronger acid and evaporate. Even carbonic acid is stronger than hydrocyanic acid. Carbonic acid is formed when carbon dioxide is dissolved in water. That is, under the influence of moist air containing both water and carbon dioxide, potassium cyanide gradually turns into carbonate:

KCN + H 2 O + CO 2 = HCN + KHCO 3

If the potassium cyanide used in the cases described was kept in contact with moist air for a long time, it might not work.

Secondly, the salt of weak hydrocyanic acid is subject to hydrolysis:

KCN + H 2 O = HCN + KOH.

The released hydrogen cyanide is able to attach to a molecule of glucose and other sugars containing a carbonyl group:

CH 2 OH-CHON-CHON-CHON-CHON-CH=O + HC≡N →
CH 2 OH-CHON-CHON-CHON-CHON-CHON-C≡N

Substances formed as a result of the addition of hydrogen cyanide to the carbonyl group are called cyanohydrins. Glucose is a product of the hydrolysis of sucrose. People who work with cyanide know that to prevent poisoning they should hold a piece of sugar against their cheek. Glucose binds cyanide in the blood. That part of the poison that has already penetrated into the cell nucleus, where tissue oxidation occurs in the mitochondria, is inaccessible to sugars. If an animal has high blood glucose levels, it is more resistant to cyanide poisoning, such as birds. The same is observed in patients with diabetes. When small portions of cyanide enter the body, the body can neutralize it on its own with the help of glucose contained in the blood. And in case of poisoning, 5% or 40% glucose solutions administered intravenously are used as an antidote. But this remedy works slowly.

For both Rasputin and the elephant Yambo, cakes containing sugar were stuffed with potassium cyanide. They were not eaten immediately, but in the meantime, potassium cyanide released hydrocyanic acid, and it joined the glucose. Some of the cyanide had definitely managed to be neutralized. Let us add that cyanide poisoning occurs more slowly on a full stomach.

There are other antidotes to cyanide. Firstly, these are compounds that easily split off sulfur. The body contains such substances as the amino acids cysteine and glutathione. They, like glucose, help the body cope with small doses of cyanide. If the dose is large, a 30% solution of sodium thiosulfate Na 2 S 2 O 3 (or Na 2 SO 3 S) can be specially injected into the blood or muscle. It reacts in the presence of oxygen and the enzyme rhodanase with hydrocyanic acid and cyanides according to the following scheme:

2HCN + 2Na2S2O3 + O2 = 2НNCS + 2Na2SO4

In this case, thiocyanates (rhodanides) are formed, which are much less harmful to the body than cyanides. If cyanides and hydrocyanic acid belong to the first class of danger, then thiocyanates are substances of the second class. They negatively affect the liver, kidneys, cause gastritis, and also suppress the thyroid gland. People systematically exposed to small doses of cyanide develop thyroid diseases caused by the constant formation of thiocyanates from cyanide. Thiosulfate reacts with cyanides more actively than glucose, but also acts slowly. It is usually used in combination with other anticyanides.

The second type of antidotes against cyanide are the so-called methemoglobin formers. The name suggests that these substances form methemoglobin from hemoglobin (see “Chemistry and Life”, 2010, No. 10). The hemoglobin molecule contains four Fe 2+ ions, and in methemoglobin they are oxidized to Fe 3+. Therefore, it is not able to reversibly bind Fe 3+ oxygen and does not transport it throughout the body. This can occur under the influence of oxidizing substances (including nitrogen oxides, nitrates and nitrites, nitroglycerin and many others). It is clear that these are poisons that “disable” hemoglobin and cause hypoxia (oxygen deficiency). Hemoglobin “spoiled” by these poisons does not carry oxygen, but is capable of binding cyanide ions, which experience an irresistible attraction to the Fe 3+ ion. Cyanide that enters the blood is bound by methemoglobin and does not have time to enter the mitochondria of cell nuclei, where it will inevitably “spoil” all cytochrome oxidase. And this is much worse than “spoiled” hemoglobin.

American writer, biochemist and popularizer of science Isaac Asimov explains it this way: “The fact is that the body has a very large amount of hemoglobin... Hemin enzymes are present in very small quantities. Just a few drops of cyanide are enough to destroy most of these enzymes. If this happens, the conveyor belt that oxidizes the body's flammable substances stops. Within a few minutes, the cells of the body die from lack of oxygen as inevitably as if someone grabbed a person by the throat and simply strangled him.”

In this case, we observe an instructive picture: some poisons that cause hemic (blood) hypoxia inhibit the action of other poisons that also cause hypoxia, but of a different type. A direct illustration of the Russian idiomatic expression: “knock out a wedge with a wedge.” The main thing is not to overdo it with the methemoglobin-forming agent, so as not to exchange the awl for soap. The content of methemoglobin in the blood should not exceed 25–30% of the total hemoglobin mass. Unlike glucose or thiosulfate, methemoglobin not only binds cyanide ions circulating in the blood, but also helps the respiratory enzyme “spoiled” by cyanide to free itself from cyanide ions. This occurs due to the fact that the process of combining cyanide ions with cytochrome oxidase is reversible. Under the influence of methemoglobin, the concentration of these ions in the blood plasma decreases - and as a result, new cyanide ions are split off from the complex compound with cytochrome oxidase.

The reaction of cyanmethemoglobin formation is also reversible, so over time, cyanide ions return to the blood. To bind them, a thiosulfate solution is injected into the blood simultaneously with an antidote (usually nitrite). The most effective is a mixture of sodium nitrite and sodium thiosulfate. It can help even in the last stages of cyanide poisoning - convulsive and paralytic.

Where can I meet him?

Does an ordinary person, not the hero of a detective novel, have a chance to be poisoned by potassium cyanide or hydrocyanic acid? Like any substances of the first class of danger, cyanides are stored with special precautions and are inaccessible to the average attacker, unless he is an employee of a specialized laboratory or workshop. Yes, and there such substances are strictly registered. However, cyanide poisoning can occur without the involvement of a villain.

First, cyanide occurs naturally. Cyanide ions are part of vitamin B 12 (cyanocobolamine). Even in the blood plasma of a healthy person there are 140 mcg of cyanide ions per 1 liter. The cyanide content in the blood of smokers is more than twice as high. But the body tolerates such concentrations painlessly. It’s another matter if cyanide contained in some plants comes in with food. Serious poisoning is possible here. Among the sources of hydrocyanic acid available to everyone are the seeds of apricots, peaches, cherries, and bitter almonds. They contain the glycoside amygdalin.

Amygdalin belongs to the group of cyanogenic glycosides that form hydrocyanic acid upon hydrolysis. This glycoside was isolated from the seeds of bitter almonds, which is why it got its name (Greek μ - “almond”). The amygdalin molecule, as befits a glycoside, consists of a sugary part, or glycone (in this case, it is a gencibiose disaccharide residue), and a non-sugary part, or aglycone. In the gencibiose residue, in turn, two β-glucose residues are linked by a glycosidic bond. The role of the aglycone is the cyanohydrin of benzaldehyde - mandelonitrile, or rather its residue connected to the glycone by a glycosidic bond.

During hydrolysis, the amygdalin molecule breaks down into two glucose molecules, a benzaldehyde molecule and a hydrocyanic acid molecule. This occurs in an acidic environment or under the action of the emulsin enzyme contained in the stone. Due to the formation of hydrocyanic acid, one gram of amygdalin is a lethal dose. This corresponds to 100 g of apricot kernels. There are known cases of poisoning of children who ate 10–12 apricot kernels.

The content of amygdalin in bitter almonds is three to five times higher, but you hardly want to eat its seeds. As a last resort, they should be heated. This will destroy the emulsin enzyme, without which hydrolysis will not proceed. It is thanks to amygdalin that bitter almond seeds have their bitter taste and almond smell. More precisely, it is not amygdalin itself that has an almond smell, but the products of its hydrolysis - benzaldehyde and hydrocyanic acid (we have already discussed the smell of hydrocyanic acid, but the smell of benzaldehyde is, without a doubt, almond).

Secondly, cyanide poisoning can occur in industries where cyanide is used to create plating or to extract precious metals from ores. Gold and platinum ions form strong complex compounds with cyanide ions. Noble metals are not able to be oxidized by oxygen because their oxides are fragile. But if oxygen acts on these metals in a solution of sodium or potassium cyanide, then the metal ions formed during oxidation are bound by cyanide ions into a strong complex ion and the metal is completely oxidized. Sodium cyanide itself does not oxidize noble metals, but helps the oxidizer to fulfill its mission:

4Au + 8NaCN + 2H 2 O = 4Na + 4NaOH.

Workers engaged in such industries experience chronic exposure to cyanide. Cyanides are poisonous both if they enter the stomach, and if they inhale dust and splashes when servicing galvanic baths, and even if they come into contact with the skin, especially if there are wounds on it. No wonder Doctor Lazovert wore rubber gloves. There was a case of fatal poisoning from a hot mixture containing 80% which got on the worker’s skin.

Even people not employed in mining or plating production can be harmed by cyanide. There are known cases where wastewater from such industries ended up in rivers. In 2000, 2001 and 2004, Europe was alarmed by the release of cyanide into the Danube in Romania and Hungary. This led to dire consequences for river inhabitants and residents of coastal villages. There have been cases of poisoning from fish caught in the Danube. Therefore, it is useful to know the precautions when handling cyanide. And it will be more interesting to read about potassium cyanide in detective stories.

Bibliography:
Azimov A. Chemical agents of life. M.: Foreign Literature Publishing House, 1958.
Harmful chemicals. Directory. L.: Chemistry, 1988.
Kataev V. Broken Life, or Oberon's Magic Horn. M.: Soviet writer, 1983.
Oxengendler G.I. Poisons and antidotes. L.: Nauka, 1982.
Rose S. Chemistry of life. M.: Mir, 1969.
Encyclopedia for children "Avanta+". T.17. Chemistry. M.: Avanta+, 2001.
Yusupov F. Memoirs. M.: Zakharov, 2004.

INJURIES BY POISONIC SUBSTANCES WITH GENERAL TOXIC EFFECT: PYROCYCAL ACID AND POTASSIUM CYANIDE

Hydrocyanic acid and potassium cyanide are generally toxic substances, as are sodium, cyanogen chloride, cyanogen bromide, and carbon monoxide.
Hydrocyanic acid was first synthesized by the Swedish scientist Karl Scheele in 1782. History knows of cases of the use of cyanide for mass destruction of people. During the First World War (1916 on the Somme River), the French army used hydrocyanic acid as a poisonous substance; in Hitler’s extermination camps, the Nazis (1943-1945) used poisonous gases, cyclones (esters of cyanacetic acid), and American troops in South Vietnam. (1963) used toxic organic cyanides (CS type gases) against civilians. It is also known that in the United States the death penalty is used by poisoning convicts with hydrocyanic acid fumes in a special chamber.
Due to their high chemical activity 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 intoxication.
Thus, hydrocyanic acid and a large number of its derivatives are used in the extraction of precious metals from ores, in electroplating gilding and silvering, in the production of aromatic substances, chemical fibers, plastics, rubber, organic glass, plant growth stimulants, and herbicides. Cyanides are also used as insecticides, fertilizers and defoliants. Hydrocyanic acid is released in gaseous form during many industrial processes. There may also be cyanide poisoning due to eating large quantities of almond, peach, apricot, cherry, plum and other plants of the Rosaceae family or infusions from their fruits. It turned out that they all contain the glycoside amygdalin, 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 (up to 3%) and apricot seeds (up to 2%).
Physicochemical properties and toxicity of hydrocyanic acid
Hydrocyanic acid - HCN - is a colorless, easily boiling (at 26 ° C) liquid, with the smell of bitter almonds, with a specific gravity of 0.7, freezes at - 13.4 ° C. Cyanide poisoning develops when inhaling vapors of a toxic substance when entering through the skin and through the mouth. In wartime, the most likely route of entry into the body is inhalation. According to WHO, Lt50 of hydrocyanic acid is 2 g/min/m3. In case of poisoning by mouth, lethal doses for humans are: HCN - 1 mg/kg, KCN - 2.5 mg/kg; NaСN - 1.8 mg/kg.
Mechanism of toxic action
The mechanism of action of hydrocyanic acid has been studied in some detail. It is a substance that causes oxygen starvation of tissue type. In this case, a high oxygen content is observed in both arterial and venous blood and thus a decrease in the arteriovenous difference, a sharp decrease in oxygen consumption by tissues with a decrease in the formation of carbon dioxide in them.
It has been established that cyanide interferes with redox processes in tissues, disrupting the activation of oxygen by cytochrome oxidase. (The lecturer can dwell in more detail on modern concepts of cellular respiration).
Hydrocyanic acid and its salts, dissolved in the blood, reach the tissues, where they interact with the trivalent form of iron, cytochrome oxidase. 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 is delivered to the tissues in sufficient quantities with arterial blood, but is not absorbed by them and passes unchanged into the venous bed. At the same time, the processes of formation of macroergs necessary for the normal functioning of various organs and systems are disrupted. Glycolysis is activated, that is, the metabolism is rearranged from aerobic to anaerobic. The activity of other enzymes - catalase, peroxidase, lactate dehydrogenase - is also suppressed.
The effect of cyanide on various organs and systems
Effect on the nervous system. As a result of tissue hypoxia, which develops under the influence of hydrocyanic acid, the functions of the central nervous system are primarily disrupted. Cyanides in toxic doses initially cause excitation of the central nervous system, and then its depression. In particular, at the beginning of intoxication, excitation of the respiratory and vasomotor centers is observed. This is manifested by a rise in blood pressure and the development of severe shortness of breath. An extreme form of excitation of the central nervous system is clonic-tonic convulsions. Severe excitation of the nervous system is replaced by paralysis (of the respiratory and vasomotor centers).
Effect on the respiratory system. In the picture of acute poisoning, there is a pronounced increase in the frequency and depth of breathing. Developing shortness of breath should apparently be considered as a compensatory reaction of the body to hypoxia. The stimulating effect of cyanide on respiration is due to the stimulation of the chemoreceptors of the carotid sinus and the direct effect of the poison on the cells of the respiratory center. The initial excitation of breathing as intoxication develops is replaced by its suppression until it stops completely. The causes of these disorders are tissue hypoxia and depletion of energy resources in the cells of the carotid sinus and in the centers of the medulla oblongata.
Effect on the cardiovascular system. In the initial period of intoxication, a slowdown in heart rate is observed. An increase in blood pressure and an increase in cardiac output occurs due to cyanide stimulation of the chemoreceptors of the carotid sinus and cells of the vasomotor center, on the one hand, the release of catecholamines from the adrenal glands and, as a result, vasospasm, on the other. As poisoning progresses, blood pressure drops, pulse quickens, acute cardiovascular failure develops, and cardiac arrest occurs.
Changes in the blood system. The content of red blood cells in the blood increases, which is explained by the reflex contraction of the spleen in response to developing hypoxia. The color of venous blood becomes bright scarlet due to excess oxygen not absorbed by the tissues. The arteriovenous difference in oxygen decreases sharply. When tissue respiration is suppressed, both the gas and biochemical composition of the blood changes. The CO2 content in the blood decreases due to less formation and increased release during hyperventilation. This leads at the beginning of the development of intoxication to gas alkalosis, which changes to metabolic acidosis, which is a consequence of the activation of glycolytic processes. Under-oxidized metabolic products accumulate in the blood. The content of lactic acid increases, the content of acetone bodies increases, and hyperglycemia is noted. The development of hypothermia is explained by disruption of redox processes in tissues. Thus, hydrocyanic acid and its salts cause the phenomenon of tissue hypoxia and associated disorders of respiration, blood circulation, metabolism, and the function of the central nervous system, the severity of which depends on the severity of intoxication.
CLINICAL PICTURE OF CYANIDE POISONING
Cyanide poisoning is characterized by the early appearance of signs of intoxication, the rapid development of oxygen starvation, primary damage to the central nervous system and probable death in a short time.
There are lightning-fast and delayed forms. When poison enters the body in large quantities, death can occur almost instantly. The affected person immediately loses consciousness, breathing becomes rapid and shallow, the pulse quickens, is arrhythmic, and convulsions occur. The convulsive period is short-lived, breathing stops and death occurs. In the delayed form, the development of poisoning can extend over time and occur in various ways.
Mild degree of poisoning characterized mainly by subjective disorders: irritation of the upper respiratory tract, conjunctiva of the eyes, an unpleasant burning-bitter taste in the mouth, the smell of bitter almonds, weakness, dizziness. Somewhat later, a feeling of numbness in the oral mucosa, drooling and nausea occurs. With the slightest physical effort, shortness of breath and severe muscle weakness, tinnitus, difficulty speaking, and possible vomiting appear. After the action of the poison ceases, all unpleasant sensations subside. However, headaches, muscle weakness, nausea and a general feeling of weakness may remain for several days. With a mild degree of intoxication, complete recovery occurs.
In case of intoxication medium degree First, the subjective disorders described above are noted, and then a state of excitement arises, and a feeling of fear of death appears. The mucous membranes and skin become scarlet in color, the pulse is slow and tense, blood pressure rises, breathing becomes shallow, and short clonic convulsions may occur. With timely assistance and removal from the contaminated atmosphere, the poisoned person quickly regains consciousness. Over the next 3-6 days, weakness, malaise, general weakness, headache, discomfort in the heart area, tachycardia, and restless sleep are noted.
In the clinical picture severe intoxication There are four stages: initial, dyspnoetic, convulsive and paralytic. The initial stage is characterized mainly by the subjective sensations outlined above when describing mild poisoning. It is short-lived and moves on to the next one. For the dyspnoetic stage, some signs of oxygen starvation of the tissue type are typical: scarlet color of the mucous membranes and skin, gradually increasing weakness, general anxiety, discomfort in the heart area. The poisoned person develops a feeling of fear of death, the pupils dilate, the pulse slows down, breathing becomes frequent and deep. In the convulsive stage, the condition of the affected person deteriorates sharply. Consciousness is lost, the corneal reflex is sluggish, the pupils do not respond to light. Exophthalmos appears, breathing becomes arrhythmic and rare, blood pressure rises, and the pulse rate decreases. Widespread clonic-tonic convulsions occur. The scarlet color of the skin and mucous membranes remains. The duration of this stage can vary from several minutes to several hours. With further deterioration of the affected person's condition, the paralytic stage develops. By this time, the convulsions have stopped, but the patient is in a deep comatose state with complete loss of sensitivity and reflexes, muscle adynamia, involuntary urination and defecation are possible. Breathing is rare, irregular. Then a complete cessation of breathing occurs, the pulse quickens, becomes arrhythmic, blood pressure drops and after a few minutes cardiac activity stops.
Consequences and complications characteristic of severe intoxication. For several weeks after the injury, persistent and profound changes in the neuropsychic sphere may persist. As a rule, asthenic syndrome persists for 10-15 days. Patients complain of increased fatigue, decreased performance, headache, and poor sleep. Impaired motor coordination, persistent cerebellar disorders, paresis and paralysis of various muscle groups, difficulty speaking, and mental disorders may be observed. From co-
Pneumonia ranks first among the most common complications. Its occurrence is facilitated by aspiration of mucus, vomit, and prolonged stay of patients in a supine position. Changes are also observed in the cardiovascular system. Within 1-2 weeks, unpleasant sensations in the heart area, single extrasystoles, tachycardia, lability of pulse and blood pressure are observed, ECG changes are observed (signs of coronary insufficiency).
DIAGNOSIS OF PYROCANIC ACID POISONING
The diagnosis of damage by hydrocyanic acid is based on the following signs: sudden onset of symptoms of damage, the sequence of development and transience of the clinical picture, the smell of bitter almonds in the exhaled air, scarlet coloring of the skin and mucous membranes, wide pupils and exophthalmos.
TREATMENT OF POISONING WITH PRYANIC ACID
The effect of helping those poisoned by cyanide depends on the speed of use of antidotes and agents that normalize the functions of vital organs and systems.
Methemoglobin-forming substances, substances containing sulfur and carbohydrates have antidote properties. Methemoglobin formers include anthicyanin, amyl nitrite, sodium nitrite, and methylene blue. They oxidize the iron in hemoglobin, converting it into methemoglobin. Methemoglobin, containing ferric iron, is able to compete with cytochrome oxidase for cyanide. It should be borne in mind that methemoglobin is not able to bind with oxygen, therefore it is necessary to use strictly defined doses of these agents, since when hemoglobin is inactivated by more than 25-30%, hemic hypoxia develops. Methemoglobin binds primarily to cyanide dissolved in the blood. When the concentration of cyanide in the blood decreases, conditions are created to restore the activity of cytochrome oxidase and normalize tissue respiration. This is due to the reverse flow of cyanide from the tissues into the blood - towards its lower concentration. The formed cyanogen-methemoglobin complex is an unstable compound. After 1-1.5 hours, this complex begins to gradually disintegrate with the formation of hemoglobin and cyanide. Therefore, relapse of intoxication is possible. However, the dissociation process is extended over time, which makes it possible to neutralize the poison with other antidotes.
The standard antidote from the group of methemoglobin formers is anticyan.
In case of hydrocyanic acid poisoning, the first administration of anthicyanin 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 saline, the injection rate is 3 ml per minute. If necessary, after 30 minutes. the antidote can be repeated in a dose of 1.0 ml, but only intramuscularly. After another 30-40 minutes. You can carry out a third administration in the same dose, if there are indications for this.
Sodium nitrite is a powerful methemoglobin-forming agent. Aqueous solutions of the drug are prepared ex tempore, since they are unstable during storage. When providing assistance to poisoned people, sodium nitrite is administered intravenously slowly in the form of a 1-2% solution in a volume of 10-20 ml.
Amyl nitrite and propyl nitrite have a methemoglobin-forming effect. Methylene blue has a partial methemoglobin-forming effect.
Substances containing sulfur. When substances containing sulfur interact with cyanide, non-toxic rhodanium compounds are formed. Sodium thiosulfate turned out to be the most effective of the sulfur donors. 20-50 ml of a 30% solution is administered intravenously. It reliably neutralizes chemical agents. The disadvantage is the relatively slow action.
The next group of antidotes has the property of converting cyanogen into non-toxic cyanohydrins. This property is observed in carbohydrates. Glucose has a pronounced antitoxic effect, which is recommended to be administered in a dose of 30-50 ml of a 25% solution. In addition, glucose has a beneficial effect on respiration, cardiac function and increases diuresis.
An antidote effect is observed when using cobalt salts, which, when interacting with cyanides, lead to the formation of non-toxic cyanide-cobalt compounds.
The effect of antidotes is enhanced when used against the background of oxygen barotherapy. It has been shown that oxygen under pressure promotes a more rapid restoration of cytochrome oxidase activity.
There is information about the beneficial therapeutic effect of unithiol, which, without being a sulfur donor, activates the enzyme rhodonase, and thus accelerates the detoxification process. Therefore, it is advisable to introduce unithiol along with sulfur donors.
Antidote therapy for lesions with hydrocyanic acid is usually carried out in combination: first, methemoglobin formers are used, then sulfur donors and substances that promote the formation of cyanohydrins.
In addition to the use of antidotes, it is necessary to carry out all the general principles of treating poisoned people (removal of unabsorbed and absorbed poison, prevention of further entry of poison into the organs - by forced removal, symptomatic therapy, resuscitation measures).
STAGE TREATMENT
Poisoning develops quickly, so medical care is urgent.
First aid in an outbreak includes putting a gas mask on the poisoned person. Then evacuation outside the outbreak is carried out. Those affected in an unconscious state and in the convulsive stage of intoxication need to be evacuated while lying down.
First aid is carried out outside the outbreak, which allows you to remove the gas mask. Anticyan is administered - 1 ml intramuscularly, if necessary, cordiamine, mechanical ventilation.
First medical aid. The anticyant is reintroduced. If it was not prescribed at the stage of first aid, it is advisable to carry out the first administration intravenously with 10 ml of 25-40% glucose solution. Subsequently, 20-50 ml of 30% sodium thiosulfate solution is injected intravenously. According to indications, 2 ml of etimizol and cordiamine solution are used intramuscularly, mechanical ventilation.
Further evacuation is carried out only after the elimination of convulsions and normalization of breathing. Along the route, it is necessary to provide assistance for relapses of intoxication.
Qualified therapeutic care consists primarily of emergency measures: repeated administration of antidotes (anticyanin, sodium thiosulfate, glucose), injections of cordiamine, etimizol, mechanical ventilation (hardware method). Delayed measures of qualified therapeutic care include the administration of antibiotics, sulfonamides, desensitizing agents, and vitamins.
Those affected in a comatose and convulsive state are not transportable. Evacuation of the seriously injured is carried out in the VPTG, in the presence of neurological disorders - in the VPNG, those who have suffered mild intoxication remain in the medical hospital (OMO).
Specialized care is provided in the appropriate therapeutic hospitals (VPTG, VPNG) in full. At the end of treatment, convalescents are transferred to the VPGRL; in the presence of persistent changes in the nervous, cardiovascular, and respiratory systems, patients are subject to referral to VVC.