Terminal states and clinical death. clinical death

clinical death(CS) - the extinction of the body's activity, when chemical reactions, physical and electrical processes are so changed that they are not able to provide manifestations of the function. This is a period of functional inactivity, however, all tissues and cells of the body are viable. This period is reversible. The most vulnerable is the central nervous system, because. irreversible changes in the cerebral cortex in conditions of normothermia occur within 3-5 minutes after the cessation of blood circulation.

The main causes of clinical death:

1. Primary respiratory arrest(in children observed in 60-80%)

Central genesis (PPCNS, cerebral edema, IVC and PVC, etc.),

Violation of the patency of the upper respiratory tract (retraction of the tongue, epiglottitis, viral croup, foreign body, aspiration syndrome),

Paresis of the intestine.

2. Primary cardiac arrest

Various forms of rhythm disturbance,

Drowning,

Defeat electric shock,

Anaphylactic shock,

Injury chest and hearts.

3. Primary lesion of the central nervous system

Clinical signs of circulatory arrest:

I. Main:

1. Lack of breath.

2. No carotid pulse or no heart sounds on auscultation.

3. Wide pupils without reaction to light.

II. Additional:

1. Absence of consciousness.

2. Cyanosis or pallor of the skin.

3. Immobility.

4. Complete areflexia.

Circulatory arrest and cessation of the pumping function of the heart can be due to several pathological processes:

1. Asystole- cardiac arrest due to impaired conduction between its departments. A typical type of circulatory arrest in children. The main cause of asystole is progressive hypoxia with vagotonia.

2. Ventricular fibrillation, which develops as a result of impaired conduction of excitation along the conduction system of the myocardium with additional ectopic foci of excitation. The most common causes of ventricular fibrillation are: asphyxia of various origins, true drowning, electrical injury, overdose of cardiac glycosides. In infants, fibrillation develops extremely rarely.

3. Electromechanical dissociation(electrical activity without a pulse) - circulatory arrest against the background of the correct heart rhythm. The main causes are mechanical factors: cessation of venous return, cardiac tamponade, mediastinal displacement.

Cardiopulmonary resuscitation- a set of measures aimed at replacing the lost functions of respiration and blood circulation.

Critical to the success of resuscitation efforts are:

Time factor,

Technically correct and consistent performance of CPR.

The main tasks of CPR:

1. Restoration and maintenance of airway patency.

2. Ensuring breathing.

3. Ensuring the minimum necessary blood circulation.

4. Elimination of metabolic disorders.

5. Prevention of irreversible damage to the central nervous system.

The sequence of CPR activities is divided into 3 phases:

1. Basic life support activities (Primary CPR).

2. Further life support measures.

3. Measures for long-term maintenance of life.

First phase (primary) CPR:

It should be started directly at the scene by any person familiar with the elements of CPR;

The logical sequence of its three most important techniques is formulated in the “Safar alphabet” - in the volume A B C:

A - ensuring the patency of the respiratory tract.

B - providing breathing - mechanical ventilation by the expiratory method (from mouth to mouth), mechanical ventilation with an Ambu bag, a respirator.

C - restoration of blood circulation - indirect heart massage (NMS).

In the second phase it is necessary to carry out the following activities:

Diagnosis and therapy of ventricular fibrillation.

Provide vascular access.

This phase is formulated in the "ABC of P. Safar" in volume (D, E, F).

D - drug therapy.

E - ECG control.

F - defibrillation.

Complications of CPR:

dislocation of the lower jaw,

Regurgitation with possible aspiration of stomach contents

Rupture of the alveoli with the development of pneumothorax,

Fractured ribs and sternum

fat embolism,

cardiac tamponade,

Damage internal organs(liver rupture).

CPR may not start:

More than 25 minutes have passed since the stop,

If there are signs of biological death.

An extreme condition that occurs as a result of an impact that is extraordinary in strength or duration and is expressed by critical pathological changes in the activity of all physiological systems organism.

Clinical death is a reversible stage of dying, a transitional period between life and biological death. At this stage, the activity of the heart and the process of breathing cease, all external signs of the vital activity of the organism completely disappear. At the same time, hypoxia (oxygen starvation) does not cause irreversible changes in the organs and systems most sensitive to it.

This period terminal state, with the exception of rare and casuistic cases, on average lasts no more than 3-4 minutes, a maximum of 5-6 minutes (with an initially low or normal body temperature).

Third stage of death

Clinical death is a state of the human body when there are no primary signs life - breathing stops, the work of the heart stops, no visible signs activity of the central nervous system (unconscious person). This condition may seem inexplicable, but only at first glance, if considered in isolation, by itself.

In fact, clinical death is the third, penultimate stage of the dying process, naturally associated with the previous and subsequent stages. The first stage is the pre-agonal state, when a person feels general weakness, his consciousness is confused, the general behavior is lethargic, the blue of the skin (cyanosis) or their pallor, the difficulty of determining blood pressure, weakness or absence of a pulse in the peripheral arteries.

The second stage is the agonal stage, better known as the agony. This is a period of sharp activation of the activity of almost all parts of the body, which indicate its decisive attempt to return to normal condition. Most often characteristic outward sign agony is deep short breath often accompanied by wheezing. Usually consciousness is already absent, since the work of the central nervous system is seriously disrupted, however, periods of returning to a conscious state are possible.

Clinical death is the third stage, when the body actually gives up and turns off its "life support system". During this period, which on average does not exceed five minutes, doctors have the opportunity to bring a person back to life - during this time, the accumulated reserve is spent in the cells of the human body. essential substances and, most importantly, oxygen.

After these five minutes, the most “hungry” cells for oxygen, the cells of the brain, begin to collapse, after which the restoration of a person is almost impossible. This means the onset of the fourth stage of dying, biological death when there are no options for returning to life.

How is clinical death different from coma?

Often one can observe the identification of clinical death with another state of the human body, known as coma. These are close in their content, but still not identical concepts. Coma is, first of all, difficult pathological condition, in which the main negative point is the progressive inhibition of the functions of the central nervous system, that is, a violation of a person's response to external stimuli and loss of consciousness. In the future, the coma can turn into a deep coma, resulting in brain damage.

Coma in its initial form can be one of the signs of clinical death. However, clinical death, unlike coma, is not only a loss of consciousness, but also the cessation of heart contractions and respiratory arrest.

In a coma, a person is unconscious, but retains the instinctive ability to breathe and his heart works, which is determined by the presence of a pulse on the main arteries. Often in cases of recovery from clinical death after resuscitation the person goes into a coma varying degrees depths. After that, it remains to wait for signs by which it is possible to determine whether the doctors managed to bring the patient out of the state of clinical death before he received brain damage or not. In the latter case, the person falls into a deep coma.

Non-material aspects of clinical death

But in our time, clinical death is no longer known because of its physiological significance, oddly enough, but in connection with psychological and ideological aspects. The fact is that the mental sensations experienced by a certain part of people who have undergone a state of clinical death have become widely known, and which in the near-scientific press are called near-death experiences.

Most often, they come down to a standard set: a feeling of euphoria, lightness, getting rid of physical suffering, observing a visual image of light at the end of a dark tunnel, seeing previously deceased relatives or religious characters, observing a picture of one’s body from the outside, and the like. For religious or mystical people, near-death experiences during near-death experiences are evidence of the existence of the other world and the immortality of the soul.

Official science explains such experiences exclusively by physical causes.

First of all, doctors pay attention to the fact that an insignificant part of those who survived clinical death recall some sensations in this state - about one person out of five hundred. However, given that several million people experience near-death experiences every year in the United States alone, the number of near-death experiences is significant. This leads to the fact that in the public mind the set of what a person “should” see at clinical death is already well known, which leads to self-hypnosis and memories that did not really exist. Finally, doctors say that near-death experiences are hallucinations caused by changes in the functioning of the brain during clinical death: for example, famous image a dark tunnel with light at its end is explained by a decrease in blood flow to the eyes and a state of "narrowing" of visual perception.

Introduction

Resuscitation is the science of revitalizing the body. And since I am a resuscitator, I will talk about life and death from the point of view of a resuscitator who has quite a lot of experience in monitoring, managing and preventing the dying-death process.

All information about the various sensations experienced by patients who have experienced clinical death is most often based on subjective data (a survey of these patients, often directed by the interviewee in the direction he needs). In this article, I will sequentially go through the stages of dying, describe the objective processes that occur with the body and consciousness of the dying, and touch on the possibility and conditions for complete social recovery of those who have experienced clinical death.

Terminal States

By definition, terminal states include pre-agony, agony, and clinical death. A qualitative transition from life to death seems to be a consistent natural violation of the functions and systems of the body, ending with their shutdown. It is this circumstance - the sequence and gradual deactivation of functions - that gives time and opportunity for intervention in order to restore life.

Preagonal state

Characteristics:

disruption of the central nervous system (stupor or coma),

low blood pressure,

centralization of blood circulation,

breathing disorders.

All this contributes to the development of oxygen starvation of tissues and a decrease in pH (tissue acidosis). Nevertheless, in the preagonal state, the main type of metabolism is oxidative. This period has no fixed duration. It may even be absent, for example, in the sudden development of cardiac arrest as a result of electric shock. In cases where the body has the ability to turn on various compensatory mechanisms (for example, blood loss), the preagonal state can continue for several hours, even if medical care was not carried out.

Agony

The onset of agony is often very clearly characterized clinically and in 100% of cases - on the ECG and EEG, tk. the transition between preagony and agony is the so-called terminal pause. Clinically, it is characterized by the fact that after a sharp increase in breathing, it suddenly stops, corneal reflexes disappear, and on the ECG, the regular rhythm is replaced by rare single impulses. The terminal pause lasts from a few seconds to 2...4 minutes.

The dynamics of agony is given by: agony begins with a short series of breaths or a single breath. The amplitude of breathing increases, its structure is disturbed - the muscles that carry out both inhalation and exhalation are simultaneously excited, which leads to an almost complete cessation of lung ventilation. Having reached a certain maximum, the respiratory movements decrease and quickly stop. This is due to the fact that the higher parts of the central nervous system are turned off at this stage, which was experimentally confirmed in , and the role of regulators of vital functions passes to the medulla oblongata and spinal cord. Regulation is aimed at mobilizing all the last possibilities of the body to save life. In this case, not only the respiratory movements described above are restored, but also a pulsation of large arteries appears, the correct rhythm and blood flow, which can lead to the restoration of the pupillary reflex and even consciousness. However, this struggle with death is ineffective, because. the energy of the body at this stage is replenished already due to anaerobic (oxygen-free) metabolism and not only becomes insufficient in quantitative terms, but also leads to qualitative changes - the rapid accumulation of under-oxidized metabolic products.

It is during the agony that the body loses those notorious 60...80 grams of weight (due to the complete burning of ATP and the depletion of cellular reserves), which in some scientific articles is called the weight of the soul that left the body after the agony.

The duration of agony is short, its severity depends on the nature of the pathological changes in the body, against which it arose. After that, breathing and heart contractions stop, and clinical death occurs.

clinical death

A peculiar transitional state between life and death, begins with the cessation of the activity of the central nervous system, blood circulation and respiration and continues for short span time until irreversible changes in the brain develop. From the moment they occur, death is regarded as biological (in the context of this article, I equate the concepts of social and biological death due to the irreversibility of the processes that have occurred in the body). Thus, the main dynamic characteristic of clinical death is the possible reversibility of this condition.

During clinical death, respiration, circulation and reflexes are absent, but cellular metabolism continues anaerobically. Gradually, the reserves of energy drinks in the brain are depleted, and nervous tissue dies.

It is generally accepted that under normal conditions, the term of clinical death in a person is 3 ... 6 minutes. It should be taken into account that irreversible changes in historically young formations of the brain (cortex) occur much faster than in older ones (stem, medulla oblongata). In the complete absence of oxygen in the cortex and cerebellum, necrosis foci appear in 2–2.5 minutes, and in the medulla oblongata, even after 10–15 minutes, only single cells die.

brain death

Brain death is the irreversible cessation of all brain functions. Its main diagnostic features are: lack of activity of the hemispheres (lack of reactions to stimuli), absence of brain reflexes, EEG - silence (even with artificial stimulation).

A sufficient sign of brain death is the absence of signs of intracranial circulation (Max Wertheimer, 1880-1943).

Life after death

After considering the dynamics of dying, let's move on to an analysis of the arguments and provisions that are used by almost all adherents of "life after death" and "immaterial soul".

Contingent

The vast majority of books are based on a survey of people who "suffered clinical death." Moreover, there is no data on when, by whom and how the fact of the onset of clinical death in these people was recorded. As mentioned above, in order to ascertain the onset of clinical death, it is necessary to fix three components:

lack of breathing;

lack of circulation;

complete absence of reflexes.

Thus, the data obtained when working with such groups of patients is simply incorrect to associate with the concept of actual clinical death - the general group of subjects could include patients who had been poisoned (for example, by inhibitory or hypnotic drugs), deep coma, epileptic seizure (pti mal ), shock, etc. Yes, and the researchers themselves sometimes do not hide the fact that certain strange symptoms are not associated with clinical death, but for some reason they do not evaluate this objectively.

So, one of the main adherents of "life after death" R. Moodycriticizing the physiological explanation of the symptoms he cites (tunnel, separation from the body, etc.), he writes:

“The main error in this view is this: as can be easily seen from the review of near-death experiences given above, in a large number of cases the experience of near-death experiences took place even before (!!! - Note by the author) any physiological damage suggested by the mentioned hypothesis."

What kind of near-death experience can we talk about in the absence of any physiological damage? The absence of physiological damage is studied by normal physiology - the physiology of a healthy organism. And then Moody writes:

Indeed, on several occasions during the entire NDE there were no bodily injury, while every single element that appeared in the case of severe injuries was also observed in other examples in which any injuries were completely absent.

And where are the elementary conclusions - in one case “there were no bodily injuries”, in another a person died from “severe injuries”, and in most cases (not described by the author) there were no symptoms at all - so, perhaps, what the author described fits into some other series and not a near-death experience?

Conclusion: if the respondent did not have a clear medical record of clinical death, he cannot be included in the general sample of patients demonstrating "life after death". No observable source proving the existence of "life after death" provides such data. This means that the material is initially based on incorrect samples and cannot be evaluated as scientific data.

Subjectivity

Suppose for the time being that the majority of the respondents conscientiously and completely recalled what they suffered during the “dying”. The question arises, how many people who have experienced clinical death can subsequently tell more or less in detail about this?

Here is what proponents of "life after death" say: "Only 10 percent of people who were on the verge of death or experienced clinical death could clearly remember what they experienced at the same time." Other researchers call big numbers - from 15 to 35%.

Now I will give the statistics of the Collaborative Study program, a collaborative program organized by the National Institute of Neurological and Communicative Disorders and Stroke (NINDS), in which 9 large clinics took part (see Table 1).

Table 1

Final outcome of clinical death (total 503 patients)

Three months after inclusion in the program of this study, 41 patients were alive (8.15%). Of these, 18 (3.58%) had certain violations of the higher nervous activity and required outside care, and one of them died four months after the first clinical death. Thus, only 5.17% of patients who underwent clinical death subsequently had a complete recovery of impaired functions. Of these patients, 14 were initially diagnosed with drug poisoning and were in a coma for more than 30 minutes.

Let's try to draw conclusions from the above:

Since life after death advocates cite much higher numbers (between 10 and 30%) for the number of people who "could clearly recall what they experienced", it is likely that a significant proportion of these memories are simply not related to near-death or recollection. “artificial”, imposed on the respondents.

Psychiatrists have the concept of “pathological suggestibility”, when a patient with an unstable psyche (a state before psychosis, mental exhaustion, etc.) obediently “sees” and “hears” what the doctor tells him. This fully applies to the group of patients who have undergone clinical death and postresuscitation illness. Thus, if any article provides data that more than 4.4 ... 6.0% of patients who have undergone clinical death have some kind of detailed post-mortem memories, these data are simply biased (the group of subjects is incorrectly defined, the methods are incorrect survey, etc.).

Symptoms

Before proceeding to a discussion of the symptoms cited as evidence of "life after death", I want to note that when discussing this issue, the memories of two completely different groups of people are equated (R. Moody):

the experience of people who were thought or declared clinically dead by doctors and who were resuscitated;

experience of people who, as a result of an accident, either dangerous injury or diseases were very close to the state of physical death.

This alone should make the researcher exclude death from the logical chain of further reasoning.

So the symptoms are:

"failure to express in words";

the ability to hear;

"feeling of peace" or "fear" (at suicide);

noise, ringing of varying intensity;

dark tunnel, dark void;

"out of the body", "moving in space regardless of the dead body";

exacerbation of physical senses (hearing, sight, smell);

meetings with other persons, often those who died earlier, a special emphasis on a luminous “spirit”, “angel”;

pictures of a past life;

reaching some limit (a very vague concept);

reluctance to return.

And now I will try to give the same symptoms in a slightly different terminology:

difficulty in expressing the seen images in the symbols of the second signal system;

strengthening of the pathological dominant (center of excitation of the cortex) by an auditory stimulus;

inhibition of the parts of the brain that stimulate the work of the cortex;

stronger energy supply of central vision mechanisms;

various violations of the integral work of the central nervous system;

greater resistance of deep foci of excitation, which have pronounced connections with each other;

complete cessation of the integration (unifying) function of the cortex.

Doesn't this enumeration remind intensive care physicians of anything? The symptoms are almost verbatim taken from the description of the action of ketamine (ketalar, callipsol) on the central nervous system. A distinctive feature of this drug is the stimulation of changes in the processes of excitation, inhibition of the cerebral cortex - the so-called dissociative (separating) anesthesia. As a result, patients do not feel specific irritations (pain, a feeling of pressure and stretching), but they also hear, see (and, by the way, quite often a tunnel or “pipe”), “leave”, “ascend”, meet relatives, etc. .d. And after all, all this has been repeatedly described in the specialized literature. The ability of some authors "not to see what they do not need" is simply surprising. At best, a caveat follows - "the people I interviewed were not under anesthesia."

And this is a conscious or "protective" distortion. After all, this is not about anesthesia, but about violations of connections between areas of the cerebral cortex that cause specific symptoms. During dying, such processes are due to oxygen starvation of tissues and a decrease in pH, but they occur and manifest themselves at the first stage of dying (when the cortex has not yet turned off) and after revival (if the brain has not died).

In conclusion, I want to give some more conditions, accompanied by a violation of cortical connections and the above symptoms:

poisoning (often an overdose of some medicinal substances, accompanied by a deep coma, are mistaken for death, and if the patient is taken out of this state, he describes almost all of the above symptoms, and sometimes he is even sure that he has been to the other world);

the effect of certain drugs that affect the psyche (without an overdose) - the mentioned ketamine, LSD;

coma caused by low blood sugar.

There is enough description in the literature of the symptoms that accompany the development of this condition - you just need to want to read. In particular, violations caused by physical influences - for example, coma during freezing, by the way, most often gave the phenomenon of “miraculous resurrection” in the past when warmed in a coffin or in a mortuary. After the body temperature rises to 35°C and above, the patient, if he wakes up, talks about "angels", and about "unearthly warmth", and about "the light at the end of the tunnel".

I would like to emphasize one nuance - about 15 ... 17% of those who took LSD note that after that they communicated with aliens. So, after that, write a treatise - "LSD as a guide to other worlds"?

Conclusion

In conclusion, I will quote the words of Raymond Moody, Ph.D.: “I do not seek to 'prove' that there is life after death. And I don't think such a "proof" is really possible at all."

Sources of information:

Negovsky V. et al. Postresuscitation disease. Moscow: Medicine, 1979.

Bunyatyan A., Ryabov G., Manevich A. Anesthesiology and resuscitation. M.: Medicine, 1984.

Walker A. Brain death. M.: Medicine, 1988.

Usenko L. et al. Anesthesiology and resuscitation: Practical exercises. K., High school, 1983.

Ado A.D. pathological physiology. M.: Triada-X, 2000.

Elisabeth Kübler-Ross. About death and dying. Sofia, 1969.

Moody R. Life after life. 1976.

Elisabeth Kübler-Ross. Death does not exist. 1977.

Wikler D.R. Journey to the other side. 1977.

Rose S. Soul after death. 1982.

Moody R. Reflections on death after death. 1983.

Kalinovsky P. Transition. 1991.

An appraisal of the criteria of cerebral death. A summary statement. A collaborative study. JAMA 237:982-986.

Chekman I. Complications of pharmacotherapy. K .: Health, 1980.

Thienes C., Haley T.J. clinical toxicology. 5th ed. Philadelphia: Lea and Febiger, 1972.

During clinical death, being at the highest moment of physical dying, a person hears a doctor announcing his death. At this moment, he begins to hear an unpleasant noise, a loud ringing and even buzzing, and at the same time feels that he is moving unusually fast along a long dark tunnel. Then he notices that he is outside his own physical body. He sees own body from the side and is at a distance. He also sees how they are trying to revive him, sees the fuss around him and experiences a strong shock at the same time.

After some time, he more or less gets used to unusual conditions. And yet he notices that he has a body, but it is different from the one he left. Soon, some shadows or spirits begin to flicker in front of him, which come to meet him. Among the spirits, he meets his friends and relatives who have already died. He is overwhelmed with strong positive emotions. But at some point he feels that he must return to earth. At this point, he begins to resist, as he is overwhelmed by his discoveries about afterlife and does not want to return. But he is reunited with his physical body and continues to live on.

Testimonies of people who have experienced clinical death

When my health began to improve, the doctor told me that things were really bad for me. I replied that I knew everything. The doctor asked: "What do you know?" And I said, "I can tell anything - anything that's happened to me."

He did not believe me, and thus I had to tell him everything: from the moment my breathing stopped to the moment when I kind of walked around. He was shocked that I knew everything down to the smallest detail. He did not know what to say, but then several times in a row he visited me and asked about everything.

Clinical death, after, eyewitness accounts, stories that after

Since ancient times, people have been interested in the question of what is clinical death. She was invariably referred to as irrefutable evidence of existence, because even people far from religion involuntarily began to believe that life would not end after death.

In fact, clinical death is nothing more than between life and death, when a person can still be returned if held for three or four, and in some cases even five or six minutes. In this state, the human body almost completely stops working. The heart stops, breathing disappears, roughly speaking, the human body is dead, it does not show any signs of life. It is interesting that caused by clinical death does not lead to irreversible consequences, as it happens in other cases.

Clinical death is characterized by the following symptoms: asystole, apnea and coma. The symptoms listed are initial stage clinical death. These signs are very important for the successful provision of assistance, because the sooner clinical death is determined, the higher the chance of saving a person's life.

Signs of asystole can be determined by palpation of the pulse on (it will be absent). Apnea is characterized by a complete cessation of respiratory movements (the chest becomes motionless). And in a state of coma, a person is completely unconscious, the pupils dilate and do not react to light.

clinical death. Effects

The outcome of this most difficult condition directly depends on the speed of a person's return to life. Like any other clinical death has its own specific consequences. It all depends on the speed of resuscitation. If a person can be brought back to life in less than three minutes, then the degenerative processes in the brain will not have time to start, that is, we can say that serious consequences will not happen. But if resuscitation is delayed, then the hypoxic effect on the brain can be irreversible, up to the complete loss of mental functions by a person. In order for hypoxic changes to remain reversible for as long as possible, the body cooling method is used. This allows you to extend the "reversible" period by several minutes.

Causes of clinical death

There are a large number of reasons due to which a person can be on the verge of life and death. Most often, clinical death is a consequence of an exacerbation of serious diseases, in which the lungs stop working. This causes a state of hypoxia, which, acting on the brain, leads to loss of consciousness. Often, signs of clinical death appear with massive blood loss, for example, after traffic accidents. The pathogenesis in this case is about the same - circulatory failure leads to hypoxia, cardiac and respiratory arrest.

dying visions

At the moment of clinical death, people often see certain visions and experience all sorts of sensations. Someone is rapidly moving through the tunnel towards a bright light, someone sees dead relatives, someone feels the effect of falling. There are still many discussions about visions during near-death experiences. Some people consider this a manifestation of the fact that the consciousness is not connected with the body. Some see it as a transition from ordinary life to the afterlife, and someone believes that such dying visions are nothing more than hallucinations that arose even before the onset of clinical death. Be that as it may, clinical death undoubtedly changes the people who survived it.

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The process of dying and the onset of death has been studied in detail in numerous studies [V. A. Negovsky, 1986;

P. Safar, 1997]. Usually there are three periods of dying - preagony, agony and clinical death.

Preagonal state characterized by the disintegration of all body functions, a critical level of blood pressure, impaired consciousness of varying severity, respiratory disorders. The preagonal state can last from several minutes to several hours. Then comes the terminal pause, the main manifestations of which are the cessation of breathing (from a few seconds to 3-4 minutes) and the presence of an idioventricular or ectopic heart rhythm. The terminal pause is due to a temporary increase in tone vagus nerve, after which agonal breathing occurs, indicating the onset of agony (the appearance of a short series of breaths or one shallow breath).

Duration agonal period is usually small. Heart contractions and breathing quickly stop. There are violations of the biomechanics of breathing - it is slow, superficial, auxiliary muscles are actively involved. Gas exchange is inefficient due to the simultaneous participation in the act of breathing of the muscles that provide inhalation and exhalation. There is a centralization of blood circulation (in favor of the brain, liver, kidneys, heart). The depletion of compensatory mechanisms quickly sets in and clinical death occurs.

clinical death - this is the period between life and death, when there are no visible signs of life, but life processes are still ongoing, making it possible to revive the body. The duration of this period at normal body temperature is 5-6 minutes, after which irreversible changes develop in the tissues of the body. Under special conditions (hypothermia, pharmacological protection), this period is extended to 15-16 minutes.

1. Circulatory arrest (absence of pulsation in the main arteries);
2. Lack of spontaneous breathing (no chest excursions);
3. Lack of consciousness;
4. Wide pupils;
5. Areflexia (no corneal reflex and pupillary reaction to light):
6. Type of corpse (pallor, acrocyanosis). The process of dying is characterized by the extinction of vital functions. important systems body (nervous, respiratory, circulatory, etc.).

Decay of the nervous system. The cerebral cortex and cerebellum are most sensitive to hypoxia. Under the influence of oxygen starvation of the brain, excitation and euphoria first arise, followed by deafening, stupor, coma. It takes 15 seconds from the moment the blood flow in the brain is turned off until the loss of consciousness.

Cessation of cardiac activity. Termination of the pumping function of the heart occurs as a result of asystole or myocardial fibrillation [P. E. Pele, 1994]. Asystole can occur suddenly (primary) or develop after ventricular fibrillation (secondary). After primary asystole, as a rule, there are reserve opportunities for successful revival of the body. After the secondary, there are no reserves, which significantly reduces the chances of a successful resuscitation.

Asystole should not be understood as an isoline on the electrocardiogram, firstly, in some cases this can disorient the doctor (electrocardiograph malfunction, accidental disconnection of electrodes, low-amplitude electrocardiogram, etc.), and secondly, the presence of cardiac electrical output does not indicate the preservation of blood flow - this the phenomenon is called electromechanical dissociation and occurs in 30-50% of cases of hemodynamic accidents. With this phenomenon, the heart muscle still generates bioelectric potentials that are recorded on the electrocardiogram, but are not accompanied by myocardial contractions.

Another mechanism for the development of circulatory arrest is ventricular fibrillation. With it, scattered, erratic, non-temporal and, most importantly, ineffective contractions of individual muscle bundles occur. Spontaneous cessation of ventricular fibrillation is extremely rare, although sometimes (usually in patients with myocardial infarction) short-term episodes of fibrillation (10-20 seconds) are recorded, which stop spontaneously.

The diagnosis of ventricular fibrillation is made by electrocardiogram, which shows irregular fluctuations of uneven amplitude with a frequency of 400-600 per minute (Fig. 2). Fibrillation leads to circulatory arrest (pulse and blood pressure are not determined, breathing stops, loss of consciousness occurs, pupils dilate). Gradually, with the depletion of energy reserves, fibrillation becomes mild (low-amplitude) and turns into a complete cessation of cardiac activity (secondary asystole). In this case, the compensatory reserves of the myocardium are largely depleted, which significantly reduces the chances of successful resuscitation of the victim.

vascular component. The development of terminal states and immediate circulatory arrest are accompanied by pronounced changes in various tissues and environments of the body. in the lumen blood vessels clots of various calibers are formed from blood cells. The deformability of erythrocytes is deteriorating, which cannot “squeeze” into the lumen of the capillaries, which leads to “blocking” of the vessels of the microvasculature (normally, the diameter of an erythrocyte slightly exceeds the lumen of the capillary; the ability to deform allows them to change their shape and pass through the capillaries).

Bonding of blood elements is noted due to the loss of their electrical charge. Due to changes in the lipid permeability of the vascular endothelium and lipid instability, the vascular bed is filled with large drops of fat and fat embolism occurs. There is a clogging of organ filters (primarily the lungs) with blood cells, exfoliating capillary endothelium. Since the capillary network is clogged, the blood flow is shunted.

The Meshalkin phenomenon. In a patient with cardiac arrest, the so-called Meshalkin phenomenon is observed - there is a pendulum movement of blood from arteries to veins, then from veins to arteries. With the restoration of blood flow, the development of reperfusion lesions is possible.

Metabolic disorders. The development of brain damage during circulatory arrest is extremely dangerous. Developing ischemia leads to damage to the structure of tissues and cells due to a decrease in the level of adenosine triphosphoric acid, the movement of calcium ions into the cell with the activation of phospholipase, and the accumulation free radicals About 2 .

Metabolic products, acids accumulate, the gas composition of the blood is disturbed, the affinity of hemoglobin to oxygen changes. There is a depletion of carbohydrate reserves of the body and inclusion in metabolic process fats with the development of ketonemia. The body accumulates up to 1.5 thousand metabolites, which are not normally present. The accumulation of acids leads to a decrease in blood pH to 7 and below (normal 7, 35-7, 45).

Stages and stages of cardiopulmonary and cerebral resuscitation

According to P. Safar, during resuscitation, 3 stages and 9 stages are distinguished.

Stage I- basic life support. Consists of three stages:

A (airway open) - restoration of airway patency;

B (breath for victim) - emergency artificial lung ventilation and oxygenation;

C (circulation his blood) - maintaining blood circulation.

Stage II- further maintenance of life. It consists in restoring independent blood circulation, normalizing and stabilizing blood circulation and respiration. Stage II includes three stages:

D (drug) - drugs and infusion therapy;

E (ECG) - electrocardioscopy and cardiography;

F (fibrillation) - defibrillation.

Stage III- long-term maintenance of life. It consists in post-resuscitation intensive care and includes the following steps:

G (gauging) - state assessment;

H (human mentation) restoration of consciousness;

I - correction of insufficiency of organ functions.

Resuscitation actions today can be divided into three complexes [A. P. Zilber, 1996]:

1) Primary resuscitation complex (PRC), used by both medical and non-medical workers who have undergone special training.

2) Specialized resuscitation complex (SRC), the mastery of which today is necessary for all medical workers and absolutely mandatory for workers in critical care medicine.

3) Post-resuscitation intensive care (PRIT), carried out by resuscitators in intensive care units.

The main principle of resuscitation for each of these complexes is the triad - “know”, “be able”, “have”.)

STAGE I. BASIC LIFE SUPPORT

Stage A. Restoration of airway patency

In emergencies, airway patency is often impaired due to retraction of the tongue, which covers the entrance to the larynx and air cannot enter the lungs. In addition, in an unconscious patient, there is always a risk of aspiration and blockage of the airways by foreign bodies and vomit [S. V. Vasiliev et al., 1987].

To restore airway patency, it is necessary to perform a “triple airway intake” [R. J. F. Baskett et al., 1996]. With this manipulation, the anterior muscles of the neck are stretched, due to which the root of the tongue rises above back wall throats.

The technique for performing a triple reception (Fig. H):

2) advancement of the lower jaw forward;

3) mouth opening.

II-V fingers of both hands capture the ascending branch of the patient's lower jaw about auricle and push it forward (upward) with force, shifting the lower jaw so that the lower teeth protrude in front of the upper teeth.

In case of obstruction of the respiratory tract by a foreign body, the victim should be placed in a lying position on his side and in the interscapular region, make 3-5 sharp blows with the lower part of the palm. Clean the oropharynx with a finger, trying to remove the foreign body, then make an attempt artificial respiration. If there is no effect, press on the abdomen. In this case, the palm of one hand is applied to the stomach along the midline between the navel and the xiphoid process. The second hand is placed on top of the first and pressure is applied to the abdomen with quick movements up the midline.

Due to the risk of infection of the resuscitator through direct contact with the mucous membrane of the mouth and nose of the victim, it is advisable to carry out artificial respiration using special devices. The simplest of them include air ducts, a device for artificial ventilation UDR, “life-key”, face masks, etc.

Intubation tubes and tracheal intubation

Every emergency physician should be proficient in tracheal intubation, as it remains the “gold standard” of care. reliable protection respiratory tract and ventilation control in resuscitation practice [I. P. Latto, M. Rosen, 1989]. Tracheal intubation allows you to isolate the airways, maintain their patency, prevent aspiration, carry out ventilation, oxygenation and sanitation of the tracheobronchial tree. It can be done through the mouth or nose. Orotracheal intubation is preferred in emergency situations as it can be performed more quickly.

The essence of the method is the introduction of an elastic air duct (endotracheal tube) into the trachea under the control of a laryngoscope. Tracheal intubation can be done blindly (on the finger). There is a large selection of endotracheal tubes of different lengths and diameters.

The technique of orotracheal intubation with a curved Mackintosh blade [according to A. A. Bunyatyan, 1984]:

1) open the patient's mouth right hand;

2) place the laryngoscope in the left hand and insert the blade into the right corner of the patient's mouth, moving his tongue to the left so that the patient's oral cavity can be examined;

3) hold the laryngoscope blade forward along the midline (making traction along the axis of the laryngoscope handle), examine the patient's mouth, uvula, pharynx and epiglottis;

4) examine the arytenoid cartilages, the entrance to the larynx and vocal cords, lifting the epiglottis with the blade of the laryngoscope;

5) insert the endotracheal tube with the conductor with the right hand through the right corner of the patient's mouth under visual control so that the cuff is located behind the vocal cords;

6) remove the conductor and start ventilation of the lungs;

7) remove the laryngoscope, inflate the cuff to achieve tightness, fix the tube with a tie or adhesive tape.

To prevent regurgitation of gastric contents, it is necessary to use the Sellick maneuver, which consists in compressing the esophagus by pressing on the cricoid cartilage.

Intubation, if necessary, can be successfully performed blindly (on the finger). At the same time, the epiglottis is raised with the ring finger, and the index finger is inserted into the esophagus. An endotracheal tube is passed between them into the glottis.

Conicotomy

Conicotomy (cricothyrotomy) consists in opening (puncture) of the cricothyroid membrane if tracheal intubation is impossible or there is an obstruction in the larynx. The main advantages of this method are the simplicity of technical implementation and the speed of execution (compared to tracheostomy).

The cricothyroid membrane is located between the lower edge of the thyroid and top edge cricoid cartilage of the larynx. There are no large vessels and nerves in this area. Conicotomy is performed in the position of maximum extension of the head back. It is better to put a small roller in the subscapular region. With the thumb and middle finger, it is necessary to fix the larynx behind side surfaces thyroid cartilage. A transverse skin incision is made above the cricothyroid membrane. The membrane itself is perforated along the nail of the index finger with a scalpel, after which a plastic or metal cannula is passed through the hole into the trachea.

To facilitate conicotomy, special devices have been created - conicotomes. Disposable “Partex” conicotomy kits consist of a skin incision knife, trocar and cannula.

Tracheostomy

Tracheostomy is called the creation of an anastomosis of the trachea with environment by introducing a cannula or endotracheal tube through the dissected tracheal rings (tracheotomy - dissection of the tracheal rings) [R. J. F. Baskett et al., 1996]. Tracheostomy is performed when the airway is obstructed upper divisions, the impossibility of tracheal intubation, the need for prolonged artificial ventilation of the lungs, etc. Depending on the level of dissection of the tracheal rings, there are upper, middle and lower tracheostomy (in relation to the isthmus thyroid gland). Adults usually produce an upper tracheostomy.

To facilitate the imposition of a tracheostomy, it is necessary to bring the larynx and trachea as close as possible to the anterior surface of the neck. The patient at the same time lies on his back, his head is thrown back, a small roller is placed under his shoulders. Usually, the manipulation is carried out under local anesthesia with novocaine or lidocaine. AT emergency conditions tracheostomy is performed without anesthesia. A skin incision is made along the midline subcutaneous tissue and superficial fascia from the lower edge of the thyroid cartilage to the jugular fossa. Muscles are pushed apart in a blunt way. A transverse incision is made to cut the fascia that attaches the capsule of the thyroid gland to the cricoid cartilage. Having exposed the tracheal rings above the isthmus, they are opened with a longitudinal incision (between the first-second or second-third). The edges of the incision are diluted with a dilator and a cannula or endotracheal tube is inserted.

Stage B. Artificial respiration

Artificial respiration is the blowing of air or an oxygen-enriched mixture into the lungs of a patient, performed without or with the use of special devices, that is, a temporary replacement of the function of external respiration. The air exhaled by a person contains from 16 to 18% oxygen, which allows it to be used for artificial respiration during resuscitation.

It should be noted that in patients with respiratory and cardiac arrest, lung tissue collapses, which is largely facilitated by chest compressions [P. E. Pele, 1994]. Therefore, it is necessary to carry out adequate ventilation of the lungs during heart massage. Each breath should take 1-2 seconds, because with a longer forced breath, air can enter the stomach. Blowing should be done abruptly and until the patient's chest begins to noticeably rise. The figures show the method of artificial ventilation mouth-to-mouth and mouth-to-nose.

In this case, the victim exhales passively, due to the increased pressure in the lungs, their elasticity and the mass of the chest. Passive exhalation should be complete. The frequency of respiratory movements should be 12-16 per minute. The adequacy of artificial respiration is assessed by periodic expansion of the chest and passive exhalation of air.

It should be noted that since 1988 these methods of expiratory artificial respiration are not recommended by the World Association of Anesthesiologists due to the risk of infection of the resuscitator through direct contact with the mucous membrane of the mouth and nose of the victim (the use of the “key of life”, UDR, face masks, air ducts, etc. is shown .) .

Assisted ventilation is used against the background of preserved independent, but inadequate breathing in a patient. Simultaneously with the patient's inhalation, additional air is blown in 1-3 respiratory movements. Inhalation should be smooth and in time correspond to the inhalation of the patient.

It should be noted that the restoration of spontaneous breathing quickly restores all other functions. This is due to the fact that the respiratory center is the pacemaker for the brain.

Stage C. Maintaining circulation

After circulatory arrest for 20-30 minutes, automatism and conduction functions are preserved in the heart, which allows it to “start”. Regardless of the mechanism of cardiac arrest, cardiopulmonary resuscitation should be started immediately to prevent the development of irreversible damage to body tissues (brain, liver, heart, etc.) and the onset of biological death [S. V. Vasiliev et al., 1987]. The main purpose of heart massage is to create artificial blood flow. However, cardiac output and blood flow created by external cardiac massage is no more than 30% of the norm [P. Safar, 1997] and only 5% of normal cerebral blood flow [P. Marino, 1996]. As a rule, this is sufficient to maintain the viability of the central nervous system during cardiopulmonary and cerebral resuscitation, provided that sufficient oxygenation of the body is achieved for several tens of minutes.

Biophysics of artificial blood flow during cardiac massage during cardiopulmonary resuscitation.

It is generally accepted that the basis of indirect heart massage is the compression of the heart in front of the sternum, behind - the spinal column, as a result of which blood from the heart cavities enters the vessels of the body. This is the so-called heart pump. But during an indirect heart massage, not only the heart is compressed, but also other intrathoracic structures (the most important is the compression of the lungs, which contain a significant amount of blood and are easily squeezed). This mechanism is called the breast pump.

Since the beginning of the eighties, the question has been considered, what moves the blood during a closed (indirect) heart massage - a heart or chest pump? Ultrasound scanning and other research methods in experiment and clinical conditions have shown that both mechanisms work with closed massage, but the chest pump predominates in a person, when, when the chest is compressed, the movement of blood into the aorta is ensured by the compression of all vascular capacities. The main capacity is the lungs with their pulmonary circulation [A. P. Zilber, 1997].

With an open heart massage, only the heart pump works. This understanding of the biophysics of artificial blood flow requires adjustments to cardiopulmonary resuscitation.

Stop bleeding

Stopping bleeding also applies to stage I, since against the background of ongoing and unreplenished blood loss, resuscitation will simply be ineffective.

To temporarily stop arterial external bleeding at the prehospital stage, pressing the artery above the injury site to the bone protrusion or maximum flexion of the limb, followed by the application of a hemostatic tourniquet, is used. Bleeding from the great vessels in traumatic limb amputations can be stopped by applying hemostatic clamps. Venous and capillary bleeding is stopped by applying a tight pressure bandage.

Bleeding in the pelvis and extremities can be successfully controlled by the use of pneumatic anti-shock clothing (“anti-shock trousers”, “anti-shock suit”, LOD device, “bracelet”). In this way, it is possible to carry out tamponade of bleeding vessels, pneumatic splinting of fractures and expel from the vessels lower extremities and pelvis up to 500-1000 ml of blood into the central circulation.

Step F. Electrical Defibrillation

Electrical defibrillation of the heart has taken a strong place in cardiopulmonary resuscitation. It should be remembered that even against the background of heart massage, the conditions for oxygenation of the fibrillating myocardium are unfavorable and myocardial hypoxia progresses, therefore, the earlier defibrillation is performed, the greater the chances for successful restoration of independent cardiac activity [N. L. Gurvich, 1975]. It is known that today electrical defibrillation is the only effective method of restoring cardiac activity in myocardial fibrillation. Considering that ventricular fibrillation occurs in most cases of circulatory arrest, and the application of an electrical shock from a defibrillator has little or no harm in asystole or terminal bradyarrhythmias, an attempt at electrical defibrillation can be made before specifying the type of hemodynamic catastrophe (asystole or fibrillation) [R. Martens, Y. Vandekerck-hove, 1996].

For electrical defibrillation, both direct and alternating current defibrillators are used. The former are more effective and safer.

When conducting external defibrillation, one of the electrodes is placed on the anterior surface of the chest below the collarbone at the right edge of the sternum, and the other - in the region of the apex of the heart. The electrodes must be lubricated special paste or wrapped with multiple layers of gauze soaked in physiological or hypertonic saline to reduce transthoracic resistance. The electrodes must be pressed tightly against the patient's body. It is very important to apply strong pressure to the chest with the electrodes before defibrillation to reduce chest resistance. For the same purpose, defibrillation should be carried out in the expiratory phase so that the size of the chest is minimal (this reduces transthoracic tension by 15-20%). The magnitude of the current must be of sufficient strength to suppress ectopic foci of excitation in the myocardium.

When conducting external defibrillation, the initial discharge is 3-3.5 thousand volts (about 200 J). If the first attempt failed, then it must be repeated, increasing the voltage each time by 0.5 thousand volts (limit 5-6 thousand volts or 360 J). When conducting open defibrillation, the initial value of the defibrillating voltage is 1.5-1.75 thousand volts, and the limiting voltage is 2.5-3 thousand volts.

After the rhythm is restored, repeated ventricular fibrillation may develop due to electrical instability of the myocardium due to acute coronary insufficiency and secondary metabolic disorders. To stabilize the effect, it is recommended to normalize the acid-base state, correct metabolic acidosis.

In some cases, repeated electrical defibrillation is ineffective, usually with low-amplitude ventricular fibrillation and unresolved oxygen debt. In this case, the introduction of adrenaline, sodium bicarbonate, additional efforts to oxygenate the body, and after a short period of heart massage, conduct electrical defibrillation again are indicated.

AT recent times some authors have revised the principles of resuscitation during the primary arrest of systemic blood flow in favor of stages C and D. So M. X. Weil believes that if the main cause of circulatory arrest is ectopic arrhythmias in occlusive diseases coronary arteries in the absence of asphyxia, then during cardiopulmonary resuscitation, priority is given to defibrillation, cardiac massage and drug therapy.

STAGE II. FURTHER LIFE SUPPORT

Stage D. Medications and fluid therapy

To restore spontaneous circulation, it is necessary to start the administration of medications and infusion therapy as soon as possible [V. V. Moroz, 1996]. The introduction of drugs should begin as early as possible and repeat every 5 minutes.

Drugs used in the primary resuscitation complex and their dosage

Adrenalin. Adrenomimetic, most commonly used in cardiopulmonary and cerebral resuscitation. Improves coronary and cerebral blood flow, increases the excitability and contractility of the myocardium. The initial dose of epinephrine is 1 mg [K. lender, 1991]. With inefficiency, adrenaline is administered at the same dose every 3-5 minutes [A. P. Zilber, 1995]. After the restoration of cardiac activity, there is a high risk of recurrence of ventricular fibrillation due to inadequate coronary perfusion [K. Under, 1991]. For this reason, “aggressive” doses of vasopressors are used [P. E. Pepe, 1994].

Currently, there is a tactic of using large doses of adrenaline (5 mg or more) during resuscitation [P. Basket, 1993]. The goal of this therapy is to achieve spontaneous and stable hemodynamics with a systolic pressure of at least 100-110 mm Hg. Art.

sodium bicarbonate. At present, the attitude towards the use of sodium bicarbonate during resuscitation is being reviewed [P. E. Pepe, 1992]. It is not recommended to use it until the restoration of independent work of the heart. This is due to the fact that acidosis with the introduction of sodium bicarbonate will be reduced only if the CO 2 formed during its dissociation is removed through the lungs. In the case of inadequate pulmonary blood flow and ventilation, CO 2 increases extra- and intracellular acidosis. However, the introduction of sodium bicarbonate at a dose of 0.5-1.0 mmol / kg is considered indicated if the resuscitation process is delayed for more than 15-20 minutes.

Calcium chloride. Currently, the use of calcium preparations in cardiopulmonary resuscitation is also limited due to possible development reperfusion injury and impaired energy production. The introduction of calcium preparations during resuscitation is indicated in the presence of hypocalcemia, hyperkalemia and an overdose of calcium antagonists [A.P. Zilber, 1995].

Atropine. The use of atropine is indicated for asystole and bradysystole. The initial dose should be 1 mg. In case of inefficiency, repeated administration after 3-5 minutes is permissible.

Lidocaine. A loading dose of lidocaine 80-100 mg (1.5 mg/kg) is administered intravenously by bolus. After achieving spontaneous circulation, a maintenance infusion of lidocaine is performed at a dose of 2-4 mg / min.

solutions of glucose. Currently, it is not recommended to use glucose infusion during resuscitation due to the fact that it enters the ischemic region of the brain, where, being included in anaerobic metabolism, it is broken down to lactic acid. Local accumulation in the brain tissue of lactate increases its damage [P. Marine, 1996]. More preferably, saline or Ringer's solution is used.

Already during the primary resuscitation complex, measures should be taken to prevent brain damage. Usually sodium oxybutyrate (2-4 g), seduxen (20-40 mg), barbiturates (2-5 mg/kg) are usually administered for this purpose. The use of blockers can get a certain value in this regard. calcium channels(verapamil at a dose of 0.1 mg/kg) and magnesium sulfate (at a dose of 100 mg/kg). In an animal experiment, evidence was obtained for the effective preservation of cerebral blood flow in the postresuscitation period.

STAGE III. FURTHER LIFE SUPPORT

The central place in carrying out resuscitation measures at stage III (restoration of consciousness, correction of insufficiency of organ functions) undoubtedly belongs to the stationary stage of treatment.

Stage G. Status assessment

To assess the condition of patients and conduct differentiated intensive care at the Research Institute of General Resuscitation of the Russian Academy of Medical Sciences, all patients in the postterminal period were proposed to be divided into three groups [G. V. Alekseeva, 1996; A. M. Gurvich, 1996].

1 group. Fast, uncomplicated dynamics of the restoration of the central nervous system. Patients regain consciousness in a few hours, they have no gross somatic pathology.

2 group. Complicated dynamics of restoration of the central nervous system. Unconsciousness within 3-4 hours with the development of upper-stem symptoms of a transient nature.

3rd group. Patients of this group are characterized by late restoration of the functions of the central nervous system (unconsciousness for more than 1 day, complicated by cerebral and polymorphic focal neurological symptoms.

STAGES H AND I. RESTORATION OF CONSCIOUSNESS AND CORRECTION OF INSUFFICIENT FUNCTIONS

When carrying out resuscitation measures, first of all, they strive to stabilize vital functions. But it is very important for the patient to be full-fledged, so that he retains his intellect, thinking, and emotional sphere [V. Teak. 1993]. The success of cerebral resuscitation largely depends on:

1. The severity and duration of the damaging effect (trauma, metabolic disorders, poisoning, hypoxia of any origin, etc.).

2. From the timeliness and quality of the primary resuscitation benefit.

3. On the level and quality of post-terminal intensive care. In this case, secondary disturbances of homeostasis, such as acid-base state, water-electrolyte state, osmolarity, etc., are of great importance. They have a direct impact on the state of the brain and on the prospects for its recovery [R. A. Steen, 1992].

All measures to maintain and restore brain functions can be divided into 2 large groups:

Measures to maintain extracerebral homeostasis;

Maintenance and restoration of intracerebral homeostasis.

Measures to maintain extracerebral homeostasis

Control over the level of systemic arterial pressure and its correction. In some cases, it is beneficial to create brain hyperperfusion for 5-7 minutes after a terminal state by artificial modeling of systemic hyperperfusion (to combat the “no reflow” phenomenon). Arterial pressure at the same time exceeds the norm by 20% The only exception is traumatic brain injury. Here, high systemic blood pressure is not beneficial to create. Optimal for patients with cranial brain injury is to maintain systolic blood pressure not higher than 110 mm Hg. Art.

Use of barbiturates in anesthetic and subnarcotic doses (to eliminate anxiety, tension, convulsions and to create hypometabolism in brain cells) [D. E. Cottrell, 1996]. Currently, a number of studies dispute the appropriateness of the use of barbiturates, but in Russia their use in the postterminal period is still popular.

Conducting controlled hyperventilation recommended to prevent the development of acidosis of the body (especially the brain) and reduce intracranial pressure(due to decreased intracranial blood volume). The oxygen tension in the arterial blood should be maintained at 100 mm Hg. Art. and higher voltage carbon dioxide- at the level of 25-35 mm Hg. The concentration of oxygen in the inhaled air should not exceed 50% for a long period of treatment.

Creation of medical relaxation with the help of small doses of muscle relaxants against the background of artificial ventilation of the lungs and tracheal intubation.

Medical improvement rheological properties blood. Using rheologically active drugs (rheopoluglyukin, chimes, trental, etc.), as well as normovolemic hemodilution, one should strive to make the blood more fluid and less viscous, change the pH value of the blood and maintain it within 7, 3-7, 6 (that is, from acidified state of the blood to go to normal values).

The optimal value of hematocrit in the correction of blood rheology is to maintain it at the level of 30-35. It is also necessary to provide other homeostatic characteristics: water balance, electrolytes, etc. The creation of a slight plasma hypermolarity at the level of 320-330 mosmol/l (the norm is 280-290 mosmol/l) is shown. This is achieved by using osmotically active drugs and by increasing colloidal pressure using plasma, protein, albumin, and the like. The creation of oncotic and osmotic pressure exceeding the norm allows the interstitium of the brain to be freed from excess water. Maintaining a normal blood glucose level is taken into account, since glucose is the main energy substrate for the brain.

Corticosteroids. Prednisolone and other corticosteroids are used during the first 2-3 days post-terminal. The effectiveness of the use of corticosteroids at this stage of resuscitation is questioned in a number of studies. In domestic practice, most resuscitators use corticosteroids to reduce intracranial pressure.

temperature balance. It is necessary to maintain the normothermia of the body. Patients who have undergone a terminal state are prone to the development of hyperthermia. Firstly, this is due to hypermetabolism, and secondly, with a large energy expenditure of the body. Therefore, one should strive to create normothermia, and in some cases moderate hypothermia. The reference point is the temperature in the esophagus, equal to 35 ° C. Lower cooling is fraught with the development of hypothermic pathology and various difficulties in the regulation of vital functions.

Food. It is necessary to provide parenteral and, in some cases, enteral nutrition. In the next few days from the moment of the transferred terminal state, we begin to restore the disturbed energy of the body. If enteral nutrition is not possible, then a balanced parenteral diet should be established. To reduce the intensity of catabolism, the appointment is shown anabolic drugs(nerabol, retabolil).

In some cases, they resort to a number of targeted methods of exposure: anticoagulant therapy, inhibition of proteolysis (introduction of protease inhibitors), the use of antioxidants (ionol, cyruloplasmin, olein, olfen, tocopherol), antihypoxants (GHB, phosphorylated glucose, gutimine).

Maintenance and restoration of intracerebral homeostasis

Before actively influencing intracranial homeostasis, it is necessary to exclude organic damage to the brain in order to timely conduct surgery for intracerebral hematomas, etc. This is achieved by collecting anamnesis data, assessing clinical picture, application of instrumental research methods (echolocation, tomography).

All measures to maintain intracranial homeostasis should be carried out against the background of monitoring the main characteristics of brain activity. An integral indicator of brain activity is electroenzolography. It is advisable to monitor this indicator of brain function.

It is very important to control intracranial pressure. For this purpose, it is possible to catheterize the spinal space in the lumbar region and, thus, measure the spinal pressure. The data obtained in this case are not always reliable, since the brain and lumbar region spinal cord may be separated. A more accurate, but technically complex technique is the measurement of intracranial pressure in the ventricles of the brain. Abroad, there are a number of devices that allow invasive and non-invasive control of intracranial pressure in dynamics (strain gauges, ultrahigh and infrared wave action sensors).

The value of intracranial pressure should not exceed the value of venous pressure. Such an excess is fraught with blocking of the venous outflow. Intracranial pressure at the level of 15 cm aq. Art. may already exceed venous. Blockade of the venous outflow will lead to a blockage of blood flow to the brain, so you need to keep these two indicators under control and not exceed intracranial pressure. For this purpose, hyperventilation mode and osmotic diuretics are used. Osmodiuretics allow, due to the difference in osmotic pressure, to extract excess fluid from the brain cavity and remove excess water through the kidneys [M. Hammer, 1991].

Mannitol. It is administered at a dose of 1-2 g/kg of body weight once. To create a difference in osmotic pressure and quickly free the brain from excess water, mannitol must be administered at a rate of 60 cal/min.

Glycerol. It can be administered orally (70-200 g as a 50% solution) or intravenously at a rate of 1-2 ml/kg body weight. FROM

using glycerin, you can achieve a decrease in intracranial pressure and improve blood flow in the brain for several hours.

As effective ways To maintain and restore intracerebral homeostasis, drug therapy, extracorporeal methods, quantum effects on cerebrospinal fluid, brain infusion are used.

Scheme of drug therapy for patients in the postterminal period [G. V. Alekseeva, 1996]

In the first 3 hours of the post-resuscitation period, all patients are given the following to prevent neurological disorders:

1) antioxidants - tocopherol 6 ml of a 30% solution intramuscularly;

2) drugs that reduce the energy needs of the brain

Relanium 0.5% solution 2 ml,

Sodium thiopental 200 mg

3) antiplatelet agents - eufillin 2, 4% solution 10 ml + nicotinic acid 1% solution 1 ml per physiological saline IV drip (or Complamin, Cavinton, Trental);

4) membrane stabilizers - corticosteroids; preferably methylprednisolone at the rate of 30 mg/kg of body weight, bolus administration - 1/4 of the calculated dose.

Depending on the dynamics of the restoration of the functions of the central nervous system, further therapy is carried out.

1 group. In order to block metabolic activity, the appointment of antiplatelet agents, antihypoxants and antioxidants is indicated. Decreased metabolism with sedatives carried out over 2-3 days. Within 5 days it is recommended to use drugs such as glutamic acid, lipostabil, from the fifth day - haloperidol and antidepressants. Treatment with nootropics, glutamic acid, lipocerebrin for this group of patients should be carried out for 1 month.

2 group. The introduction of the same drugs that were prescribed for group 1 is shown. Additionally, rheologically active substances are prescribed to improve microcirculation (cavinton, trental, chimes). The drugs are administered over a longer period (2 months). Vitamin therapy is carried out (10-14 days).

3rd group. They will have a very long medicinal work, physiotherapy procedures. In the acute period, as for the first two groups, the introduction of drugs that reduce the energy needs of the brain (opioids, enkephalins, barbiturates, propofol, neurovegetative stabilization) is indicated.

zation, etc.). AT subacute period it is necessary to cancel drugs that reduce the energy needs of the brain, continue treatment with drugs that enhance the metabolic processes of the brain (cerebrolysin, piracetam; creatine phosphate, instenon, nakom). Continue the introduction of antioxidants, antiplatelet agents, lipostabil, vitamin therapy, according to indications - membrane stabilizers and beta-blockers.

Extracorporeal treatments

When performing cerebral resuscitation, Extracorporeal methods of treatment are successfully used, such as blood ultrafiltration, filtration and sorption. cerebrospinal fluid. Their use can reduce mortality from resuscitation cerebral pathology by 10-18% [B. L. Radushkevich, I. E. Gorbachev, 1997].

Methods of quantum influence

A technique has been developed for blood irradiation using devices that generate a certain length of light flux - ultraviolet or laser light. Laser action on the blood makes it possible to achieve a universal, extensive therapeutic effect, because the blood carries the effect of the laser beam throughout the body. The wavelength during blood irradiation with a laser is 6328 angstroms, the power is 20-10 -3 W, the exposure is 20 minutes. The procedure is carried out daily for several days. The choice of the vessel used to introduce the wave probe is of secondary importance (because blood is a liquid crystal).

The combination of intracarotid infusion and laser blood irradiation is very effective.

brain infusion

For brain infusion, catheterization of the superficial temporal artery is performed. The catheter is passed towards the heart to get into the trunk of the common carotid artery (it carries about 70% of the blood flow to the brain).

Perfusion cooling of the brain with blood substitute fluid

At the hospital stage, a promising method is perfusion cooling of the brain [V. L. Radushkevich, 1985]. The technique consists in creating a model of an isolated open perfusion of the brain with blood-substituting fluids collected in the form of various mixtures. The arterial and venous main vessels are clamped, the perfusate is injected into the vascular network of the brain, where it passes through the capillary network, ensuring the viability of the brain, and, with the help of special catheters, is collected from the venous collectors and removed from the body.

The use of perfusion cooling of the brain with a blood-substituting fluid makes it possible to preserve the viability of brain cells during circulatory arrest, and thus gain time for surgical intervention or other life-saving measures.

LITERATURE

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stages "D" and "C" now dominate. //Materials of the International Symposium "Resuscitation at the turn of the 21st century". - Moscow, 1996.

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M., Practice, 1996.

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