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Ascertainment of death and rules for handling a corpse. Biological death is confirmed

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Ministry of Health of the Republic of Belarus

EE "Vitebsk State Order of Peoples' Friendship Medical University"

Department of Propaedeutics of Internal Diseases

Abstract on the topic:

“Statement of clinical and biological death»

Prepared by:

2nd year student

Samokhvalova E.N.

Teacher:

Arbatskaya I. V.

Vitebsk 2015

4. Ascertainment of death

Literature

1. Problems of defining the concept of “death”

As paradoxical as it may sound, there is not as clear a transition between life and death as is sometimes imagined. What can serve as a criterion for death?

So, the cessation of the three beats of life (the work of the heart, breathing and blood circulation) for a long time was considered death. But the development of resuscitation since the second half of the 20th century has forced us to finally reassess these phenomena. Today, the heart can work with the help of an electrical stimulator, the lungs can breathe due to the movements of a mechanical respirator, and blood can be circulated through a heart-lung machine. Thus the old definition of death is no longer valid. It retained the name “clinical death,” that is, a condition that can be reversible thanks to the efforts of doctors to restore breathing, heartbeat, and circulation.

In the arsenal modern medicine Now there are dozens of techniques to bring a person out of a state of clinical death: closed (through the chest) and open cardiac massage, electrical stimulation of the heart, methods of artificial respiration (mouth-to-mouth breathing, etc.), artificial ventilation of the lungs using special devices . Every day, resuscitators bring back to life thousands of people whose condition would previously have been regarded as death.

In addition to clinical death, there is also biological death, that is, an irreversible state of the body that is accompanied by cadaveric phenomena.

A person is considered dead if his brain does not function and his brain cells do not emit waves detected by an encephalograph. But it may also happen that as a result of the action of the resuscitation team, it was possible to restore the activity of the heart, restore blood circulation, and maintain respiratory function with the help of an artificial lung ventilation device, but the brain died, and died irreversibly.

How then to evaluate the human condition? Is he alive or dead?

From the point of view of the old definition of death, he is alive because his heart beats, blood circulates through the vessels, is maintained constant temperature bodies.

From a new point of view, modern definition who interprets the onset of death as brain death - such a person is dead.

This is a new definition of death - not quite medical and not quite biological. It is not traditionally medical, because certain vital functions are preserved, and some organs continue to live. Not completely biological, because the metabolism in cells does not stop. It is rather from the realm of metaphysics: the death of a person is different from the death of all other living beings. If a person exists only biologically and lacks consciousness, he is considered dead, because he is dead as a person.

As a result of brain death, all its functions irreversibly disappear, including even spontaneous breathing. The activity of the heart is now supported only by artificial ventilation. One has only to turn off the artificial respiration apparatus, and the heart will stop, biological death will occur.

But does the doctor have the right to take this step even knowing for sure that the brain is irretrievably lost? Wouldn't this be murder? Who will take responsibility and turn off the device?

As a result of discussion of this issue by the medical community at a number of international forums, as well as by the legislative bodies of many countries, it was considered correct to clarify the concept of death, linking it with irreversible brain damage as a substrate of a person’s personality, determining his social and biological essence.

Irreversible brain damage has been given the name brain death. The existence of two mechanisms for the development of human biological death has been recognized: the usual one, with the primary cessation of cardiac activity and respiration for a period that excludes the possibility of brain recovery, and a new one, determined by brain death.

The new definition of death, as the death of the brain even while the activity of the heart is preserved, gained recognition among doctors abroad in the 70s. In the former USSR, doctors were able to be guided by this definition only since 1985, when the “Instructions for ascertaining death as a result of complete irreversible cessation of brain functions”, approved by the USSR Ministry of Health and agreed with the legislative bodies of the country, was issued.

The redefinition of death as brain death has raised a number of complex ethical issues. First of all, it turned out to be difficult to change the ideas about the essence of death that have developed over thousands of years among people far from medicine, and especially in connection with the possibility of taking organs from dead people with a beating heart to transplant them to another person.

The generally accepted legal definition of death based on the cessation of breathing and heartbeat has become outdated due to the new concept of brain death.

For this reason, many casuistic court cases arose.

In 1971, in Portland, Oregon, a court was deciding the cause of death of a man with a gunshot wound who was in unconscious, with signs of electrical silence of the brain on the electroencephalogram, who underwent artificial ventilation. The patient's kidneys were removed for transplantation. The question was what was the cause of death: organ harvesting or injury caused by a bullet? The jury concluded that the direct cause of death was a gunshot wound, but the actions of the doctors were still assessed as murder under mitigating circumstances. Messages about similar court cases, as well as others, even more confusing, reflect the difficulties that could be avoided if the state of brain death as a manifestation of human death acquired legal status.

It is in connection with these difficulties that in our country the use of the “Instructions for ascertaining death as a result of complete irreversible cessation of brain function” is so far permitted only to a limited number of sufficiently prepared medical institutions, the number of which can only be expanded gradually. In the meantime, from the point of view of the law, three options for the doctor’s behavior are legal.

Firstly, he can continue resuscitation measures and artificial ventilation until natural cardiac arrest, which lasts for many days, and sometimes even for several weeks.

This involves a senseless waste of expensive medications and time, as well as maintaining unjustified hopes for the patient’s relatives, but it frees the doctor from heavy psychological responsibility when turning off the artificial ventilation device.

The doctor can also turn off the respirator and inform the family of the patient's death, which seems legitimate from both an ethical and economic point of view, but turns out to be psychologically difficult for the doctor. Finally, the doctor, having determined death, can transfer the patient with a beating heart to transplant specialists for the use of organs, especially the heart, for the purpose of transplantation to other patients. In this case, termination resuscitation measures performed by a transplantologist. The choice of any of these options is determined both by the doctor’s psychology and by the entire complex of circumstances associated with a specific clinical case.

In recent years, publications have increasingly appeared condemning the resuscitation of brain-dead patients, calling such resuscitation senseless therapeutic stubbornness. Moreover, voices are heard demanding that the patient be given the right to decide his own destiny.

2. Signs of clinical death

clinical biological death electrical stimulation

Signs:

1) absence of pulse in the carotid or femoral artery;

2) lack of breathing;

3) loss of consciousness;

4) wide pupils and their lack of reaction to light;

5) pallor, cyanosis of the skin.

Therefore, first of all, it is necessary to determine the presence of blood circulation and breathing in the patient or victim.

Determination of signs of clinical death:

1. The absence of a pulse in the carotid artery is the main sign of circulatory arrest.

2. Lack of breathing can be checked by visible movements chest when inhaling and exhaling, or by placing your ear to your chest, hear the sound of breathing, feel (the movement of air when exhaling is felt by your cheek), and also by bringing a mirror, glass or watch glass, as well as cotton wool or thread to your lips, holding them with tweezers. But it is precisely on the determination of this characteristic that one should not waste time, since the methods are not perfect and unreliable, and, most importantly, they require a lot of precious time for their determination.

3. Signs of loss of consciousness are a lack of reaction to what is happening, to sound and pain stimuli.

4. The victim’s upper eyelid is raised and the size of the pupil is determined visually, the eyelid lowers and immediately rises again. If the pupil remains wide and does not narrow after lifting the eyelid again, then we can assume that there is no reaction to light.

If one of the first two of the 4 signs of clinical death is determined, then you need to immediately begin resuscitation. Since only timely resuscitation (within 3-4 minutes after cardiac arrest) can bring the victim back to life.

Resuscitation is not performed only in the case of biological (irreversible) death, when irreversible changes occur in the tissues of the brain and many organs.

3. Signs of biological death

Signs:

1) drying of the cornea;

2) the “cat’s pupil” phenomenon;

3) decrease in temperature;

4) bodies cadaveric spots;

5) rigor mortis.

Determination of signs of biological death:

1. Signs of drying out of the cornea are the loss of the iris of its original color, the eye appears to be covered with a whitish film - a “herring shine”, and the pupil becomes cloudy.

2. Use your thumb and forefinger to squeeze eyeball, if a person is dead, then his pupil will change shape and turn into a narrow slit - a “cat’s pupil”. This cannot be done in a living person. If these 2 signs appear, this means that the person died at least an hour ago.

3. Body temperature drops gradually, by about 1 degree Celsius every hour after death. Therefore, based on these signs, death can only be confirmed after 2-4 hours or later.

4. Purple cadaveric spots appear on the underlying parts of the corpse. If he lies on his back, then they are identified on the head behind the ears, on the back of the shoulders and hips, on the back and buttocks.

5. Rigor mortis - post-mortem contraction skeletal muscles“top to bottom”, i.e. face - neck - upper limbs - torso - lower limbs.

Full development of signs occurs within 24 hours after death.

4. Ascertainment of death

Direct confirmation of death is made upon discovery of a corpse on the basis of the above listed signs ambulance doctors.

In the event of death in a medical institution, death is certified by a council of doctors consisting of at least 3 doctors whose work experience exceeds 5 years. The consultation should not include doctors directly related to organ transplantation (transplantologist). It is advisable that the consultation include an anesthesiologist and a neurologist.

Literature

1) S.A. MUKHINA, I.I. TARNOHIN "GENERAL PATIENT CARE", MOSCOW, "MEDICINE", 1989.

2) T. P. OBUKHOVETS, T. A. SKLYAROVA, O. V. CHERNOV “FUNDAMENTALS OF NURSING”, ROSTOV-ON-DON, “PHOENIX”, 2003.

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Ascertainment of biological death

The fact of biological death is determined by a doctor or paramedic based on the presence reliable signs, and before their appearance - according to the combination of the following symptoms:

Absence of cardiac activity (no pulse in large arteries, heart sounds cannot be heard, no bioelectrical activity of the heart);

The time of absence of cardiac activity is reliably more than 25 minutes (at normal ambient temperature);

Absence spontaneous breathing;

Maximum dilation of the pupils and their lack of reaction to light;

Absence of corneal reflex;

The presence of postmortem hypostasis in sloping parts of the body.

Brain death

With some intracerebral pathology, as well as after resuscitation measures, a situation sometimes arises when the functions of the central nervous system, primarily the cerebral cortex, are completely and irreversibly lost, while cardiac activity is preserved, blood pressure is preserved or maintained by vasopressors, and breathing is provided by mechanical ventilation. This condition is called brain death (“brain death”). The diagnosis of brain death is very difficult to make. There are the following criteria:

Complete and persistent lack of consciousness;

Persistent lack of spontaneous breathing;

Disappearance of reactions to external irritations and any types of reflexes;

Atony of all muscles;

Disappearance of thermoregulation;

Complete and persistent absence of spontaneous and evoked electrical activity of the brain (according to electroencephalogram data).

The diagnosis of brain death has implications for organ transplantation. After it has been identified, organs can be removed for transplantation into recipients. In such cases, when making a diagnosis, it is additionally necessary to:

Angiography of cerebral vessels, which indicates the absence of blood flow or its level below critical;

Conclusions of specialists (neurologist, resuscitator, forensic medical expert, as well as an official representative of the hospital) confirming brain death.

According to the legislation existing in most countries, “brain death” is equated to biological death.

Biological death- the final stage that ends life - the irreversible cessation of all processes of vital metabolism in cells and tissues, the breakdown of protein substances and structures.

Biological death occurs immediately after clinical death. Biological death is determined by a doctor based on the combination of the following signs.

1. Lack of spontaneous movements.

2. Stopping breathing and heartbeat.

3. Maximum dilation of the pupils, lack of their reaction to light.

4. Decrease in body temperature (to the level of ambient temperature).

5. Appearance of cadaveric spots.

6. The appearance of muscle rigor.

The first three signs are actually early signs of clinical death. The next three are actually signs of biological death, which, however, appear relatively late. In this case, the temperature of the corpse can remain quite high (at high temperature environment); in some cases, rigor mortis may not occur. Therefore, in real practice, when providing resuscitation measures, the onset of biological death is determined on the basis of consensus (i.e., agreement) currently established by resuscitators.

The most important guideline when declaring biological death is the time factor: 5-6 minutes from circulatory arrest plus 30 minutes of ineffective resuscitation measures.

Cadaveric spots on the skin of a corpse (blue-violet color) are formed as a result of post-mortem blood flowing into the underlying sections, overflow and dilation of skin vessels and blood saturation of the tissues surrounding the vessels.

Muscular rigor (or rigor mortis) is a process of post-mortem hardening of skeletal muscles and smooth muscles of internal organs, developing 2-6 hours after death, starting with the masticatory muscles. Rigor rigor persists for 3-9 days. Rigor of the heart muscle occurs 30 minutes after death.

The final (decisive) signs of biological death are a decrease in body temperature to ambient temperature, the appearance of cadaver spots and muscle rigor.

The fact of the patient's death, the exact time and date of death, the doctor records in the medical history.

If the death of a patient occurs in the ward, the remaining patients are asked to leave. If patients are on strict bed rest, they should be asked to turn away or close their eyes. Clothes are removed from the corpse, placed on a gurney specially designed for this purpose on the back with the knees bent, the eyelids are closed, the lower jaw is tied up, covered with a sheet and taken to the sanitary room of the department for 2 hours (until cadaveric spots appear). Only after that nurse writes down his last name, initials, and medical history number on the deceased’s thigh. All bedding from the bed of the deceased is sent for disinfection. During the day, it is not customary to place newly admitted patients on a bed where the patient recently died.

The death of a patient must be reported to emergency department hospitals, relatives of the deceased, and in the absence of relatives - to the police station.

Things and valuables are handed over to the relatives or loved ones of the deceased against signature.

S.A. Sumin, M.V. Rudenko, N.N. Bogoslovskaya

20.1. QUESTIONS OF TERMINOLOGY

Terminal state is defined as a borderline state between life and death, when, due to various reasons, such a pronounced disruption of the functioning of the basic life systems occurs that the body of an injured or sick person is not able to cope with these disturbances and, without outside intervention, inevitably ends in death. The reasons leading to the development of a terminal condition are diverse and can be both acute and sudden in nature (drowning, electric shock, etc.) and relatively gradual (severe, long-term illnesses in the final stage).

Reanimatology - science of revival (re - again, attache- revive), studying the issues of etiology, pathogenesis and treatment of terminal conditions, as well as post-resuscitation illness.

Resuscitation - this is directly the process of revitalizing the body during special resuscitation measures (Negovsky V.A., 1975). Currently, most countries have adopted the term "cardiopulmonary resuscitation" (cardiopulmonary resuscitation - CPR), or "cardiopulmonary and cerebral resuscitation" Safar P., 1984).

Any terminal condition, regardless of the underlying cause, is characterized by critical level disorders of the fundamental functions of the body: breathing, cardiovascular system, metabolism, etc., up to complete cardiac arrest. The following stages are distinguished in its development: preagonal state, terminal pause (not always noted), agony and clinical death. Biological death, which follows clinical death, is an irreversible state when revival of the organism as a whole is no longer possible.

Preagonal state. Consciousness is sharply depressed or absent. The skin is pale or cyanotic. Blood pressure progressively decreases to zero, there is no pulse in the peripheral arteries, but it is still preserved in the carotid and femoral arteries. At the initial stages, tachycardia is noted, followed by a transition to bradycardia. Breathing quickly changes from tachy to bradyform. Stem reflexes are disrupted and pathological ones may appear. The severity of the condition is quickly aggravated by increasing oxygen starvation and severe metabolic disorders. The central genesis of the above disorders should be especially emphasized.

Terminal pause doesn't always happen. Clinically manifested by respiratory arrest and transient periods of asystole from 1-2 to 10-15 s.

Agony. This stage is a precursor to death and is characterized by the last manifestations of the body’s vital activity. During this period of dying, the regulatory function of the higher parts of the brain and the control of vital processes ceases and begins to be carried out at a primitive level under the control of the bulbar centers. This can cause short-term activation of vital activity: a slight increase in blood pressure, a short-term appearance of sinus rhythm, and sometimes glimpses of consciousness are observed, but these processes cannot ensure the fullness of breathing and heart function, and the next stage very quickly occurs - the stage of clinical death.

Clinical death - reversible stage of dying, transition period between life and death. At this stage, the activity of the heart and breathing stops, all external signs of the body’s vital activity completely disappear, but hypoxia has not yet caused irreversible changes in the organs and systems that are most sensitive to it. This period, with the exception of rare and occasional cases, lasts on average no more than 3-4 minutes, maximum 5-6 minutes (at initially low or normal body temperature).

Biological death occurs after the clinical one and is characterized by the fact that against the background of ischemic damage, irreversible changes in organs and systems occur. Its diagnosis is carried out on the basis of the presence of signs of clinical death, followed by the addition of early and then late signs of biological death. Early signs of biological death include drying and clouding of the cornea and the cat's eye sign (to detect this symptom, you need to squeeze the eyeball; the symptom is considered positive if the pupil is deformed and elongated in length). TO late signs biological death includes rigor spots and rigor mortis.

"Brain (social) death" - This diagnosis appeared in medicine with the development of resuscitation. Sometimes in the practice of resuscitation doctors there are cases when, during resuscitation measures, it is possible to restore activity of cardio-vascular system(CVS) in patients who were in a state of clinical death for more than 5-6 minutes, but in these patients irreversible changes had already occurred in the cerebral cortex. The respiratory function in these situations can only be supported by mechanical ventilation. All functional and objective research methods confirm brain death. In essence, the patient becomes a “cardiopulmonary” drug. The so-called “persistent vegetative state” develops (Zilber A.P., 1995, 1998), in which the patient may be in the department intensive care for a long time (several years) and exist only at the level of vegetative functions.

20.2. CARDIOPULMONARY RESUSCITATION

Indications for CPR

The main indications for CPR are circulatory and respiratory arrest.

Stopping blood circulation

There are three types of circulatory arrest: asystole (cardiac arrest), ventricular fibrillation and myocardial atony (Fig. 20-1). After cardiac arrest, blood circulation stops and vital organs do not receive oxygen.

Rice. 20-1. Types of circulatory arrest

Asystole characterized by cessation of contractions of the atria and ventricles. It can be conditionally divided into sudden and occurring after previous rhythm disturbances. Sudden asystole against the background of complete well-being and without any previous rhythm disturbances indicates a sudden cessation of the electrical excitability of the heart in the form of a “short circuit”, most often as a result of acute ischemia associated with coronary heart disease (CHD). Asystole, which occurs after a long period (2-3 minutes) of ventricular fibrillation (VF), occurs due to depletion of high-energy phosphates (adenosine triphosphoric acid - ATP; creatine phosphate) in the myocardium. The occurrence of asystole is possible against the background of development complete blockade conductivity between the sinus node and the atria, in the absence of the formation of impulses in other foci of automatism.

This complication can occur reflexively as a result of irritation vagus nerves with initially increased tone, especially against the background of diseases accompanied by the development of hypoxia or hypercapnia.

Predispose to the occurrence of labile asystole nervous system, endocrine diseases, exhaustion, severe intoxication, etc. Unfortunately, in surgical practice there are sometimes cases of sudden death of patients from asystole during such relatively painless procedures.

and manipulations performed according to all the rules, such as bronchoscopy, tooth extraction, etc.

Asystole can occur suddenly in children due to the increased physiological sensitivity of their heart to vagal impulses and in healthy people, especially vagotonic people, during physical or mental stress. On the ECG, ventricular complexes disappear during asystole.

Ventricular fibrillation characterized sudden appearance discoordination in myocardial contractions, quickly leading to cardiac and circulatory arrest. The cause of its occurrence is the appearance of disturbances in the conduction of excitation within the conduction system of the ventricles or atria. Clinical harbingers of ventricular fibrillation may be the appearance of ventricular flutter or an attack paroxysmal tachycardia, and although in the latter type of disorder the coordination of myocardial contractions is preserved, a high frequency of contractions can cause ineffectiveness of the pumping function of the heart, followed by rapid death.

Risk factors for ventricular fibrillation include various unfavorable exo- and endogenous effects on the myocardium: hypoxia, disturbances in water-electrolyte and acid-base status, general cooling of the body, endogenous intoxication, the presence of ischemic heart disease, mechanical irritations of the heart during various diagnostic and therapeutic procedures, etc.

There are 4 stages in the development of ventricular fibrillation:

A - ventricular flutter, lasting 2 s, during which coordinated contractions occur, and high-amplitude rhythmic waves with a frequency of 250-300 per minute are recorded on the ECG;

B - convulsive stage(1 min), in which chaotic uncoordinated contractions of individual sections of the myocardium occur with the appearance of high-amplitude waves on the ECG with a frequency of up to 600 per minute;

B - stage of ventricular fibrillation(shallow wave VF) lasting about 3 minutes. Random excitation of individual groups of cardiomyocytes appears on the ECG as chaotic low-amplitude waves with a frequency of more than 1000 per minute;

G - atonic stage - damped excitation of individual areas of the myocardium; on the ECG, the duration increases and the amplitude of the waves decreases when their frequency is less than 400 per minute.

Myocardial atony(“inefficient heart”) is characterized by loss of muscle tone. It is the final stage of any type of cardiac arrest. The reason for its occurrence may be the depletion of the compensatory capabilities of the heart (primarily ATP, see above) against the background of such dangerous conditions as massive blood loss, prolonged hypoxia, shock states of any etiology, endogenous intoxication, etc. A harbinger of myocardial atony is the appearance on the ECG of signs of electromechanical dissociation - modified ventricular complexes.

Stopping breathing

Functional disorders external respiration cause gas exchange disorders in the lungs, which are clinically manifested by three main syndromes: hypok-

sia, hypercapnia and hypocapnia and may result in the development of apnea (stopping breathing movements).

The main causes of respiratory failure can be divided into pulmonary and extrapulmonary.

TO extrapulmonary causes include:

Violation of central regulation of breathing: a) acute vascular disorders (thromboembolism in cerebral vessels, strokes, cerebral edema); b) brain injury; c) intoxication with drugs acting on the respiratory center (narcotics, barbiturates, etc.); d) infectious, inflammatory and tumor processes leading to damage to the brain stem; e) comatose states leading to brain hypoxia;

Damage to the musculoskeletal framework of the chest and pleura: a) peripheral and central paralysis of the respiratory muscles; b) spontaneous pneumothorax; c) degenerative-dystrophic changes in the respiratory muscles; d) polio, tetanus; e) injuries spinal cord; f) consequences of exposure to FOS and muscle relaxants;

Impaired oxygen transport during large blood losses, acute circulatory failure and poisoning with “blood poisons” (carbon monoxide, methemoglobin formers).

Pulmonary causes:

Obstructive disorders: a) blockage of the airways with foreign bodies and sputum, vomit, amniotic fluid; b) mechanical obstruction to air access due to external compression (hanging, suffocation); c) allergic broncho- and laryngospasm; d) tumor processes of the respiratory tract; e) violation of the act of swallowing, paralysis of the tongue with its retraction; f) edematous-inflammatory diseases of the bronchial tree; g) increased tone of the smooth muscles of the bronchioles, disruption of the supporting structures of the small bronchi, decreased tone of the large bronchi;

Damage to respiratory structures: a) infiltration, destruction, dystrophy of lung tissue, b) pneumosclerosis;

Reduction of functioning pulmonary parenchyma: a) underdevelopment of the lungs; b) compression and atelectasis of the lung; c) a large amount of fluid in the pleural cavity; d) pulmonary embolism.

When initial respiratory arrest occurs, the heart and lungs continue to oxygenate the blood for several minutes, and oxygen continues to flow to the brain and other organs. Such patients retain signs of circulation for some time. If breathing stops or is inadequate, respiratory resuscitation is a life-saving measure and can prevent cardiac arrest.

Signs of clinical death

Signs of clinical death include: coma, apnea, asystole. It should be especially emphasized that this triad of signs concerns early period clinical death (when several minutes have passed since asystole), and does not apply to those cases where there are already clearly expressed signs of biological death (see above). The shorter the period between the statement of clinical

death and the beginning of resuscitation measures, the greater the patient’s chances of life, therefore diagnosis and treatment should be carried out in parallel.

To whom Diagnosed based on lack of consciousness and dilated pupils that do not respond to light. To determine the level of impairment of consciousness, you can use the Glasgow scale (Table 20-1).

Table 20-1. Assessment of coma severity using the Glasgow scale

The state of consciousness is assessed by summing up points from each subgroup. 15 points correspond to a state of clear consciousness, 13-14 - stupor, 9-12 - stupor, 4-8 - coma, 3 - brain death.

Apnea recorded visually by the absence of respiratory movements of the chest; there is no need to waste time applying a mirror or cotton wool or thread to the mouth and nose, because the resuscitator quite often does not know the true duration of clinical death in the patient. It is very important to immediately determine whether the victim has obstruction of the upper respiratory tract or not. This is quite easily diagnosed during the first attempt at mechanical ventilation. If it is carried out according to all the rules (see below), but air does not enter the lungs, this indicates the presence of obstruction.

Asystole is registered by the absence of a pulse in the carotid arteries. There is no need to waste time determining the pulse in the radial arteries. It is advisable to give the victim several artificial breaths before determining the pulse.

20.3. METHODS OF RESTORING THE AIRWAY PASSABILITY

Since 1960, many countries around the world have begun to intensively study and develop methods for revitalizing the body. In subsequent decades, various schemes (algorithms) for providing resuscitation care for terminal conditions were created. In 2000, the first World Scientific Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care was held, at which unified international recommendations in the field of resuscitation were first developed (Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care).

From a practical point of view, cardiopulmonary resuscitation (CPR) can be divided into two stages.

1. Basic Life Support - basic resuscitation measures (basic CPR, or primary resuscitation complex), which can carried out by non-professional rescuers (trained volunteers, firefighters, etc.), as well as must carried out by medical professionals.

2. Advanced Cardiovascular Life Support - specialized resuscitation measures (specialized or advanced CPR), which must be performed by medical personnel trained and equipped with appropriate equipment and medications (emergency medical services, doctors in intensive care units).

Basic CPR - this is to ensure airway patency (A irway), performing artificial respiration (B reathing) and indirect cardiac massage (C irculation) (techniques ABC). Essentially, basic CPR is the initial stage of resuscitation, when the rescuer often finds himself alone with the victim and is forced to carry out resuscitation measures “empty-handed.”

Specialized CPR involves the sequential implementation of the same techniques, but with the use of resuscitation equipment and medications, which makes it significantly more effective.

The effectiveness of resuscitation measures is largely determined by the clear sequence of ABC techniques; deviation from which is fraught with the transition of clinical death to biological death. If possible, time should be noted before resuscitation begins.

The survival of victims in a terminal condition depends on the earliest possible implementation of actions in a certain sequence - the “chain of survival” (Chain of Survival) consisting of the following units:

Early recognition of circulatory (respiratory) arrest and calling an ambulance or resuscitation team for specialized CPR;

Early implementation of basic CPR;

Early electrical defibrillation;

Early implementation of specialized CPR.

In adults, sudden death of non-traumatic origin is mainly of cardiac origin, with the main terminal cardiac

The main rhythm is ventricular fibrillation (in 80% of cases). For this reason, the most significant and determining factor for survival in adults is the time interval that elapses from the moment blood pressure falls until effective blood pressure is restored. heart rate and pressure, in accordance with international recommendations - until electrical defibrillation is performed as the leading link in the “chain of survival”. In addition, early initiation of CPR by others increases the victim's chances.

Sequence of basic resuscitation measures

Statement of lack of consciousness in the victim. Persistent loss of consciousness in the victim is a fairly universal clinical manifestation of severe pathology of various etiologies. It is necessary to make sure that the victim has permanently lost consciousness (with the help of loud verbal appeal, lightly shaking the victim by the shoulders). If consciousness does not return, it is necessary, if possible, to call an ambulance (in many countries this step is carried out when it is determined that the victim is not breathing).

Restoring and ensuring airway patency. If the victim is unconscious, the rescuer needs to assess the patency of his airway and the effectiveness of breathing. To do this, the victim must be in a supine position.

The position of the victim. To carry out resuscitation measures and increase their effectiveness, the victim must be in a supine position on a hard, flat surface. If the victim is lying face down, he must be carefully and carefully turned onto his back so that when turning, the head, shoulders and torso form a single whole, without twisting (to prevent additional injury from possible existing injuries).

Rescuer position. The rescuer must position himself in relation to the victim in such a way that he can carry out and artificial respiration, and indirect cardiac massage (preferably on the right side of the victim).

Restoration of airway patency. If the victim is unconscious, the muscle tone is reduced and both the tongue and the epiglottis can cause laryngeal obstruction. Retraction of the root of the tongue is the most common cause of airway obstruction in unconscious victims (Fig. 20-2 a). When the victim tries to inhale, the tongue and epiglottis can cause obstruction when a vacuum is created, a valve type of obstruction is created. Since the tongue is anatomically connected to the lower jaw, the movement of the latter forward is accompanied by a displacement of the tongue from back wall pharynx and opening of the airways (Fig. 20-2 b). If there is no evidence of a head or neck injury, the “throwing back the head - extending the lower jaw” technique is used. In this case, it is necessary to remove visible foreign bodies from the mouth (blood clots, vomit, dentures). You can remove fluid from your mouth fairly quickly using index finger, wrapped in any fabric (scarf, napkin). If deeper foreign bodies are suspected, forceps or the Heimlich maneuver can be used (see.

section 20.4.3. Foreign bodies of the upper respiratory tract). If it is impossible to restore the patency of the airways using all the described methods, it is possible to perform a conicotomy (cricothyroidotomy) (the technique for performing it is described in section 20.4.3).

Technique: “throwing back the head - protruding the lower jaw.” With one hand, located in the area of the victim’s forehead, the latter’s head is thrown back, at the same time with the second hand the victim’s chin is raised (the lower jaw extends), which completes this technique. In this case, the head is held in a tilted position with the chin raised and teeth almost closed. It is necessary to open the victim’s mouth slightly to facilitate his spontaneous breathing and prepare for mouth-to-mouth breathing. This maneuver (formerly described as the Peter-Safar "triple maneuver") is the method of choice for airway management in patients without suspected cervical spine injury.

Rice. 20-2. Restoration of airway patency (a, b)

Technique “only advancement of the lower jaw.” This limited technique, performed without throwing the head back, should be mastered by both lay and professional rescuers. The technique of extending the jaw without tilting the victim's head is the safest initial action in case of suspected injury to the cervical spine (divers, falls from a height, hanging people, some types of auto injuries), since it is performed without straightening the neck (Fig. 20-3). It is necessary to carefully fix the head without turning it to the sides or bending the cervical spine, since in such a situation there is a real threat of worsening spinal cord damage.

If the unconscious victim, after securing the airway, breathing is restored and there are signs of blood circulation (pulse,

Rice. 20-3. Technique of jaw extension without throwing back the head

normal breathing, coughing or movement), it can be given the so-called “recovery position” (recovery position) or a stable position on the right side (Fig. 20-4).

Rice. 20-4. Stable position on the right side

Recovery position (stable position on the right side).

The recovery position is used to keep victims unconscious (while waiting for emergency medical help to arrive), but still breathing and showing signs of circulation. Without suspected injuries to internal organs and damage to limbs. Positioning the victim on his or her back poses a risk of repeated respiratory distress and the risk of aspiration, such as gastric contents. The position of the victim on his stomach impairs his independent breathing, as it limits the mobility of the diaphragm and reduces the compliance of the lung tissue and chest.

Thus, the recovery position is a compromise, minimizing the risk of developing the complications described above and at the same time allowing for monitoring of the victim.

Assessing the victim's breathing efficiency. The presence and effectiveness of spontaneous breathing of the victim can be assessed by placing the ear near

the victim’s mouth and nose, while simultaneously observing the excursion of his chest, listening and feeling the movement of exhaled air (Fig. 20-5). Breathing assessment should be carried out quickly no more than 10 s!

Rice. 20-5. Assessing the victim's breathing efficiency

If the chest does not expand or collapse, and air is not exhaled, the victim is not breathing.

If the victim is not breathing or his breathing is inadequate (agonal type), or there is no confidence in the effectiveness of the victim’s breathing, it is necessary to begin artificial respiration.

Artificial respiration

Breathing "from mouth to mouth." This type of artificial respiration is a fast, effective way of delivering oxygen and replacing the victim's breathing. The air exhaled by the rescuer contains enough oxygen to maintain the minimum needs of the victim (approximately 16-17% of oxygen is supplied to the victim, while the partial tension of O 2 in the alveolar air can reach 80 mm Hg).

Immediately after the airway is restored, the rescuer must close his nasal passages with two fingers of the hand fixing the victim’s head in a tilted position, take a deep breath, then cover the victim’s mouth with his lips and perform a slow (duration at least 2 s) exhale into the victim (Fig. 20-6). The recommended reduced tidal volume for most adults is approximately 6-7 ml/kg (500-600 ml) at a rate of 10-12 breaths per minute (1 cycle every 4-5 seconds) and ensures effective oxygenation of the blood. From the started CPR it is recommended to perform from 2 to 5 breaths contract.

Rice. 20-6. Artificial respiration "mouth to mouth"

Large tidal volumes should be avoided, which lead, on the one hand, to distension of the stomach, and on the other, to an increase in intrathoracic pressure and a decrease in venous return to the heart.

The main criterion remains excursion of the chest, without swelling of the epigastric region (evidence of air entering the stomach). The latter can cause serious complications, such as regurgitation and aspiration of gastric contents, pneumonia. In addition, increasing pressure in the stomach leads to drooping of the diaphragm, restriction of lung excursion, and decreased compliance respiratory system. Air enters the stomach when the pressure in the esophagus exceeds the opening pressure of the lower esophageal sphincter. The likelihood of air entering the stomach increases during cardiac arrest when the lower esophageal sphincter relaxes. In addition, there are factors that contribute to the entry of air into the esophagus and stomach: short inspiratory period, large tidal volume, high peak inspiratory pressure.

Thus, the risk of air entering the stomach during mouth-to-mouth breathing can be reduced by inhaling slowly at the recommended tidal volume, guided by a visual assessment of the chest excursion with each breath.

The mouth-to-nose breathing method is less preferable, as it is even more labor-intensive and less effective due to the increased resistance when inhaling through the nasal passages. May be alternative method if it is impossible (injury) to breathe from mouth to mouth.

Significant disadvantages of the mouth-to-mouth breathing method include the risk of infection of the person performing respiratory resuscitation (HIV infection, hepatitis B and C viruses, cytomegalovirus, pathogenic bacteria).

However, the benefit of timely assistance in case of respiratory and circulatory arrest far outweighs the risk of secondary infection of the rescuer or patient; this risk will be even less if simple infection prevention measures are followed during CPR or training in its basic methods. You can protect yourself from possible contact infection with the help of devices that allow you to protect the rescuer from both direct contact with the victim’s tissues and from the air exhaled by him. These include various simple disposable face masks with a unidirectional (non-reversible type) air flow valve (“Key of Life”, etc.), recommended mainly for non-professional rescuers, an S-shaped air duct, an oronasal mask with a facial obturator, an esophageal-tracheal obturator and other professional equipment. On household level The air duct can always be found in a car first aid kit.

Additional and effective ways to restore and maintain airway patency are the use of a laryngeal mask airway, a combined tracheal-esophageal tube (combitube) and tracheal intubation. In particular, the design of the laryngeal mask (Fig. 20-7) allows it to be installed “blindly” (Fig. 20-8), and to be quite reliably disconnected Airways from the pharynx and esophagus (Fig. 20-9), perform artificial respiration, and also toilet the tracheobronchial tree through its lumen.

Tracheal intubation involves restoring the patency of the airway by introducing an endotracheal tube into the lumen of the trachea. This technique can be performed through the mouth or nose under direct laryngoscopy or blindly. Tracheal intubation is the most effective method of maintaining patency of the upper respiratory tract and a reliable method of preventing aspiration. Most often, orotracheal tracheal intubation is used under the control of direct laryngoscopy; other methods are used if the first one is not possible. Performing direct laryngoscopy with the left hand, the rescuer inserts the laryngoscope blade along the midline, pushing the tongue to the left and up. Moving the curved blade forward, its end is brought to the base of the epiglottis, and then the laryngoscope is moved forward and upward (Fig. 20-10 a). When performing these manipulations, the glottis and the entrance to the trachea open. Under visual control with the right hand, the rescuer inserts the endotracheal tube into the glottis and advances it until the gasp disappears.

Rice. 20-7. Laryngeal mask

Rice. 20-8.

Rice. 20-9. Installation and position of the laryngeal mask

It is necessary to ensure that the endotracheal tube is in the correct position.

This is evidenced by: uniform excursion of the chest and auscultation of respiratory sounds evenly over the entire surface of the chest (in the upper and lower parts of the lungs, right and left). After the rescuer is convinced of the correct position of the endotracheal tube, the latter is securely fixed to prevent its dislocation during resuscitation measures and/or transporting the victim to the hospital.

Rice. 20-10. Installation and position of the laryngeal mask (a, b)

Typical mistakes and complications when performing artificial respiration

The most common mistake is the lack of tightness in the “circuit” between the rescuer (resuscitator) and the victim. A novice doctor, who finds himself as a resuscitator for the first time, sometimes, when breathing from mouth to mouth, forgets to tightly pinch the victim’s nose. This will be indicated by the absence of chest excursions. The second most common mistake is the unresolved retraction of the root of the tongue in the victim, which may make it impossible to carry out further treatment, and instead of the lungs, air will begin to enter the stomach, which will be indicated by the appearance and growth of a protrusion in the epigastric region.

The most common complication when performing artificial respiration is the simultaneous entry of air into the respiratory tract and stomach. This is usually associated with either excessive tidal volume or too rapid (less than 1.5-2 s) inhalation. Stomach distension can cause regurgitation with subsequent leakage of gastric contents into the upper respiratory tract. An attempt to empty the stomach of air using manual compression in the epigastric region with the victim in the supine position only provokes regurgitation with a full stomach. If gastric distension does occur, it is necessary to quickly turn the patient onto either side and gently, but with sufficient force, press on the epigastric region. The above procedure should only be carried out with the patient in the lateral position and with suction at the ready.

Assessment of blood circulation. Since the first resuscitation guidelines in 1968, the “gold standard” for determining cardiac function has been the determination of pulses in the large arteries. According to the CPR standard, the absence of a pulse in the carotid artery indicates cardiac arrest (spending no more than 10-15 s!) and requires the start of cardiac massage (Fig. 20-11).

There are two methods of cardiac massage: open and closed (indirect, external). We do not consider the technique of open cardiac massage here, since it is only possible with an open chest, in particular, during cardio-thoracic operations.

Rice. 20-11. Landmarks for determining the carotid pulse

Method of indirect chest massage:

The victim must be in a horizontal position on his back, on a solid and level base; his head should not be higher than chest level, as this will worsen cerebral circulation during chest compressions; before starting chest compressions, in order to increase the central blood volume, the victim’s legs should be raised; Unfasten the waist belt to prevent liver injury, remove tight clothing;

The rescuer can be on either side of the victim; position of the hands on the sternum - two transversely located fingers of the hand upward from the base of the xiphoid process (Fig. 20-12 a), then both hands are parallel to each other, one on top of the other (“locked”) located in the lower third of the sternum; fingers are raised and do not touch the chest;

The depth of chest compressions is on average 4-5 cm, with a frequency of approximately 100 per minute; to maintain the desired rhythm, the rescuer is recommended to count out loud: “one and two and three and four...” up to 10, then up to 15 without the connecting conjunction “and”;

Effective cerebral and coronary blood flow, in addition to the recommended frequency, is ensured by the duration of the compression phase and the chest relaxation phase in a 1:1 ratio; must be adhered to correct position hands during the entire cycle of 30 compressions, without lifting or changing their position during pauses for artificial respiration;

The sequential ratio of compressions to respiratory cycles is 30:2 (regardless of the number of rescuers); after tracheal intubation and cuff inflation, the ratio remains unchanged.

For the most effective indirect massage and to reduce the possibility of possible injury to the chest, the first pressure on the chest should be applied smoothly, trying to determine its elasticity. Do not make jerking movements - this is a sure way to cause chest injury! The rescuer must position himself relative to the victim in such a way that there is a right angle between his arms, fully straightened at the elbow joints, and the victim’s chest (Fig. 20-12 b). When performing a massage, it is not the strength of the hands that should be used, but the weight of the rescuer’s torso. This will provide significant savings in energy and increase the effectiveness of the massage. If everything is done correctly, in time with chest compression, a synchronous pulse should appear in the carotid and femoral arteries.

Rice. 20-12. Method of indirect chest massage (a, b)

Monitoring the effectiveness of chest compressions and artificial respiration (every 1-3 minutes for 5 seconds) is determined by the following criteria:

The appearance of a pulse impulse on the carotid or femoral artery;

Constriction of the pupils with the appearance of a reaction to light;

Change in skin color (becomes less pale and cyanotic);

Spontaneous breathing may occur.

To ensure and maintain a higher level of coronary and cerebral blood flow in the victim, according to the new amendments and proposals of the International Consensus Conference on Cardiopulmonary Resuscitation of 2005, it is recommended to increase the number of chest compressions per cycle to 30 and adhere to the massage-breathing ratio as 30:2 regardless of the number of rescuers.

If the airway is protected by a tracheal tube with an inflated cuff to ensure a tight airway (qualified

CPR), chest compressions can be constant and independent of respiratory cycles, without pauses for artificial breaths, with a respiratory rate of 10-12 per minute in adults, 12-20 in children. In this case, the effectiveness of CPR increases.

Typical mistakes and complications when performing chest compressions

The most common mistake is insufficient intensity of chest compressions. Its cause may be the conduct of resuscitation on a soft surface, or the weak intensity of chest compressions itself. An objective indicator is the absence of synchronous pulsation in large arteries. Breaks during cardiac massage for more than 5-10 seconds (for example, for therapeutic or diagnostic measures) are also extremely undesirable.

The most common complication during chest compressions is fractures of the bone frame of the chest. Emergence this complication most typical in elderly people and uncharacteristic in pediatric patients. Rib fractures themselves can cause various mechanical damage to the lungs, but this, fortunately, is quite rare. More often, damage to the chest frame is accompanied by a violation of its suction properties for venous return from the systemic circle to the right atrium, which introduces additional difficulties into the resuscitation process. To avoid this complication, use the recommendations outlined above. If chest injury does occur, continue full CPR.

Medicines used in specialized (advanced) CPR

Medicines during resuscitation are used for the following purposes:

Optimizations cardiac output and vascular tone;

Normalization of rhythm disturbances and electrical instability of the heart. Adrenalin. Indicated for VF, asystole, symptomatic bradycardia.

The adrenergic effect of adrenaline is mainly used during circulatory arrest to increase myocardial and cerebral blood flow during CPR. In addition, it increases the excitability and contractility of the myocardium, however, this positive effect on the heart has a downside - with an overdose of adrenaline, the work of the heart and its need for oxygen sharply increase, which in itself can cause subendocardial ischemia and provoke fibrillation. The recommended dose is 1 ml of 0.1% solution (1 mg). The frequency of administration is every 3-5 minutes of CPR, until a clinical effect is obtained.

For faster delivery of the drug into the central bloodstream when administered (without prior dilution) into a peripheral vein (preferably cubital veins), each dose of adrenaline must be accompanied by the introduction of 20 ml of saline.

Norepinephrine. Adrenergic agonist with a more pronounced vasoconstrictor effect than adrenaline and a lesser stimulating effect on the myocardium. Indicated for severe arterial hypotension (without hypovolemia) and low peripheral

Vasopressin. As a natural antidiuretic hormone, in large doses, significantly exceeding the antidiuretic effect, vasopressin acts as a non-adrenergic peripheral vasoconstrictor. Today, vasopressin is considered as a possible alternative to epinephrine in the treatment of VF refractory to electrical defibrillation in adults. In addition, it may be effective in patients with asystole or pulseless ventricular tachycardia.

Atropine. Indicated in the treatment of symptomatic sinus bradycardia, with asystole in combination with adrenaline. Atropine has “confirmed” its effectiveness in the treatment of hemodynamically significant bradyarrhythmias. As recommended International conference 2000, with the development of circulatory arrest through asystole or electromechanical dissociation, it is proposed to administer atropine to adults every 3-5 minutes, 1 mg intravenously to a total dose of no more than 0.4 mg/kg.

Amiodarone (cordarone). It is considered the drug of choice in patients with VF and VT refractory to three initial defibrillator shocks. The starting dose is 300 mg, diluted in 20 ml of 5% glucose, administered intravenously as a bolus. An additional dose of 150 mg (in the same dilution) is possible if VF/VT is repeated, up to the maximum daily dose of 2 g of amiodarone.

Lidocaine. It is most effective for preventing or stopping frequent ventricular extrasystoles - a formidable harbinger of the occurrence of VF, as well as with developed VF. The recommended initial dose is 1-1.5 mg/kg (80-120 mg). For refractory VF or ventricular tachycardia After 3-5 minutes, you can administer half the dose.

Lidocaine may now be considered as an alternative to amiodarone only if it is unavailable, But should not (!) be introduced along with it. With the combined administration of the mentioned antiarrhythmics, there is a real threat of both potentiation of cardiac weakness and manifestation of arrhythmogenic effects.

Magnesium sulfate. Hypomagnesemia causes refractory ventricular fibrillation and interferes with intracellular potassium replenishment. Magnesium sulfate is recommended for refractory VF, especially if hypomagnesemia is suspected in patients receiving long-term thiazide and loop (non-potassium-sparing) diuretics. When carrying out resuscitation measures, 1-2 g of magnesium sulfate, diluted in 100 ml of 5% glucose, is administered intravenously over 1-2 minutes.

Sodium bicarbonate. Metabolic acidosis in conditions of circulatory arrest is an inevitable consequence of hypoxia. Properly performed artificial ventilation has a more effective effect on acid-base balance than the use of buffer solutions. The second circumstance limiting the use of sodium bicarbonate in conditions of circulatory arrest is the lack of adequate perfusion of the lungs during CPR and, therefore, impaired elimination of carbon dioxide. Under these conditions, soda will only contribute to the increase in intracellular acidosis. Sodium bicarbonate is indicated either after restoration of cardiac activity, or after 10-15 minutes of resuscitation measures. Initial dose - 1 mmol/kg

(2 ml of 4% soda solution per 1 kg), then half the calculated dose is administered every 10 minutes under the control of blood gases.

Calcium chloride. Previously, it was believed that this drug during CPR increases the amplitude of heart contractions and has a stimulating effect on the heart, but research in recent years has not confirmed this. The use of calcium chloride is limited to rare exceptions (initial hypocalcemia, hyperkalemia, overdose of calcium antagonists).

Routes of administration medicines during CPR

The common belief that the optimal method of administering drugs during CPR is through the intracardiac route has changed in recent years. Intracardiac punctures always carry the risk of damage to the conduction system of the heart and coronary vessels or intramural administration of drugs. In such a situation, preference is given to the intravenous route of administration. medicines when blood circulation stops. The most efficient and fastest delivery medicinal substances provides central venous access into the bloodstream, however, catheterization of the central veins requires time and considerable experience from the doctor; In addition, this approach is associated with quite severe complications. Peripheral access is usually easier, but the drug enters the central bloodstream relatively slowly. To speed up the flow of the drug into the central channel, it is recommended, firstly, to catheterize one of the cubital veins, and secondly, to administer the drug as a bolus without dilution, followed by “advancing” it with 20 ml of physiological solution.

Recent studies have shown that endotracheal administration of drugs through an endotracheal tube has an effectiveness similar to intravenous access. Moreover, if tracheal intubation is performed earlier than established venous catheter, then adrenaline, lidocaine and atropine can be administered endotracheally, with the dose for adults increased by 2-2.5 times (compared to the initial dose for intravenous administration), and for children - 10 times. In addition, endotracheal administration of drugs requires their dilution (up to 10 ml of saline solution each administration).

Electrical defibrillation

The founders of electrical defibrillation can rightfully be considered the Swiss scientists Prevost and Betelli, who in the late XIX centuries discovered this effect when studying arrhythmogenesis caused by an electrical stimulus.

The main goal of defibrillation shock is to restore the synchronization of contractions of cardiac fibers that are disrupted as a result of ventricular tachycardia or fibrillation. Experimental and clinical researches recent years have shown that the most significant determinant determining the survival of patients after sudden death is the time elapsed from the moment of circulatory arrest to electrical defibrillation.

Possible early defibrillation is essential to save victims after circulatory arrest due to ventricular fibrillation (VF), which is the most common initial rhythm (80%)

with a sudden stop of blood circulation. The likelihood of successful defibrillation decreases over time, as VF tends to transition to asystole within a few minutes. Many adults with VF can be saved without neurological consequences if defibrillation is performed within the first 6-10 minutes after sudden cardiac arrest, especially if CPR is performed.

If at the prehospital stage the ambulance team does not register fibrillation from the very beginning, then first it is necessary to preliminarily for approximately Perform basic CPR for 2 minutes(5 cycles of massage: breathing 30:2) and only then, if a defibrillator is available, perform defibrillation;

It has been shown that performing a single defibrillator shock followed without a pause by performing basic CPR for 2 minutes (until the rhythm is assessed) is more effective than the previously recommended 3-fold series of defibrillations;

Recommended shock value for defibrillation in adults using a device with monophasic pulse shape - 360 J., two-phase - 150-200 J. If there is no effect after the first shock, subsequent defibrillation attempts (after mandatory 2-minute cycles of CPR - massage: breathing) are carried out with shocks of similar magnitude;

When carrying out defibrillation in children aged 1 to 8 years, it is recommended, firstly, to use children's electrodes, and secondly, to select the value of the first shock - 2 J/kg, for subsequent attempts - 4 J/kg. Defibrillation is not recommended for children under 1 year of age.

Defibrillation technique

The external defibrillator electrodes should be placed on the anterior surface of the chest: one electrode on the right in the second intercostal space under the collarbone, the other in the projection of the apex of the heart. To avoid skin burns and improve electrical conductivity, it is necessary, firstly, to lubricate the electrodes with a special conductive gel (if it is not available, with saline solution or water), and secondly, to press the electrodes tightly against the chest (with a force of approximately 10 kg). Recommended defibrillation parameters for adults: first attempt - 200 J, if unsuccessful - 300 J, then 360 J.

Assistants should suspend resuscitation efforts and avoid touching the patient or metal objects that come into contact with the patient.

The time interval between attempts should be minimal and is required only to assess the effect of defibrillation and set, if necessary, the next shock.

In a patient with an implanted pacemaker, during defibrillation, one of the electrodes is located at least 10 cm from the pacemaker, and the other in the projection of the apex of the heart.

Typical mistakes when performing defibrillation:

Late electrical defibrillation;

Lack of CPR in preparation for defibrillation;

Poor contact between electrodes and tissues;

Incorrectly selected discharge energy value.

Precordial beat

A single precordial blow (a punch is delivered from a distance of 30 cm in the area of the lower third of the sternum) can be performed only by professionals in the absence of a defibrillator, if VF is established (recorded on the monitor or the clinical situation assessed by a professional corresponds to the classic description of VF). When this method is effective, a pulse appears in the carotid artery. In case of sudden cessation of blood circulation lasting more than 30 seconds, a precordial stroke is ineffective!

Universal algorithm for action in case of sudden death in adults (according to Guidelines 2000 for CPR and ECc)

Basic resuscitation measures (basic CPR):

Make sure that the victim is unconscious;

Ask for help;

Restore airway patency;

Check breathing;

Perform 2-5 breaths of mechanical ventilation (if necessary);

Check for blood circulation;

Start chest compressions (if there are no signs of blood circulation).

Apply a precordial blow (according to indications and if defibrillation is impossible) or(see below).

Connect defibrillator/monitor. Assess heart rhythm.

In case of VF or pulseless ventricular tachycardia:

Perform 3 defibrillation attempts (if necessary);

Resume CPR for 1 minute and re-assess the heart rhythm;

Try defibrillation again.

If there is no effect, start specialized (advanced) CPR(tracheal intubation, venous access, medications).

If there is no effect, analyze and eliminate possible reasons.

Hypovolemia.

Hypoxia.

Hyper/hypokalemia.

Hypothermia.

Acidosis.

“Pills” (drugs, poisoning).

Cardiac tamponade.

Coronary thrombosis.

Pulmonary embolism.

Tension pneumothorax.

Features of CPR in children

In children, the causes of sudden cessation of breathing and circulation are very diverse, including sudden infant death syndrome, asphyxia, drowning, trauma, foreign bodies in the respiratory tract, electrical shock.

electric shock, sepsis, etc. Therefore, unlike adults, it is difficult to determine the leading factor (“gold standard”) on which survival would depend upon the development of a terminal condition.

Resuscitation measures for infants and children differ from those for adults. Although there are many similarities in the methodology for performing CPR in children and adults, life support in children, as a rule, begins from a different starting point. As noted above, in adults the sequence of actions is based on symptoms, most of which are cardiac in nature. As a result, a clinical situation is created that usually requires emergency defibrillation to achieve effect. In children, the primary cause is usually respiratory in nature, which, if not recognized promptly, quickly leads to fatal cardiac arrest. Primary cardiac arrest in children is rare.

Due to the anatomical and physiological characteristics of pediatric patients, several age limits are identified to optimize the technique of resuscitation care. These are newborns, infants under 1 year of age, children from 1 to 8 years of age, children and adolescents over 8 years of age.

The most common cause of airway obstruction in unconscious children is the tongue. Simple tricks Extending the head and lifting the chin or moving the lower jaw ensures patency of the child's airway. If the cause of the child's serious condition is injury, it is recommended to maintain airway patency only by removing the lower jaw.

The peculiarity of artificial respiration in young children (under 1 year of age) is that, given anatomical features- a small space between the child’s nose and mouth - the rescuer breathes “from mouth to mouth and nose” of the child at the same time. However, recent research suggests that mouth-to-nose breathing is the preferred method for basic CPR in infants. For children aged 1 to 8 years, the mouth-to-mouth breathing method is recommended.

Severe bradycardia or asystole is the most common rhythm associated with cardiac arrest in children and infants. Assessing blood circulation in children traditionally begins with checking the pulse. In infants, the pulse is assessed on the brachial artery, in children - on the carotid artery. The pulse is checked for no longer than 10 s, and if it is not palpable or its frequency is in infants less than 60 beats per minute, you need to start immediately external massage hearts.

Features of indirect heart massage in children: for newborns, the massage is performed with the nail phalanges of the thumbs, after first covering the back with both hands, for infants - with one or two fingers, for children from 1 to 8 years old - with one hand. In children under 1 year of age, when performing CPR, it is recommended to maintain a frequency of compressions of more than 100 per minute (2 compressions per 1 s), for children aged 1 to 8 years - at least 100 per minute, with a ratio of 5:1 to respiratory cycles. For children over 8 years of age, adult recommendations should be followed.

The upper conventional age limit of 8 years for children was proposed due to the peculiarities of the method of performing indirect cardiac massage. However, children can have different body weights, so it is impossible to speak categorically about a certain upper age limit. The rescuer must independently determine the effectiveness of resuscitation measures and apply the most appropriate technique.

The recommended initial dose of epinephrine is 0.01 mg/kg or 0.1 ml/kg in saline, administered intravenously or intraosseously. Recent studies prove the advantage of using high doses of adrenaline in children for areactive asystole. If there is no response to the initial dose, it is recommended after 3-5 minutes to either repeat the same dose or administer adrenaline in a high dose - 0.1 mg/kg 0.1 ml/kg in saline solution.

Atropine is a parasympathetic blockade drug that has an antivagal effect. For the treatment of bradycardia, it is used at a dose of 0.02 mg/kg. Atropine is a mandatory drug used during cardiac arrest, especially if it occurs through vagal bradycardia.

INDICATIONS, CONTRAINDICATIONS AND DATES OF RESUSCITATION

The indication for resuscitation is the presence of preagonal, agonal states or clinical death in the patient.

Actions medical workers when providing resuscitation assistance to victims in our country are regulated by the order of the Ministry of Health of the Russian Federation dated March 4, 2003? 73 “ON APPROVAL OF INSTRUCTIONS FOR DETERMINING THE CRITERIA AND PROCEDURE FOR DETERMINING THE MOMENT OF DEATH OF A PERSON AND TERMINATION OF RESUSCITATION MEASURES.”

Appendix to the order of the Ministry of Health of the Russian Federation

from 03/04/03? 73.

INSTRUCTIONS FOR DETERMINING THE CRITERIA AND PROCEDURE FOR DETERMINING THE MOMENT OF DEATH OF A PERSON AND TERMINATION OF RESUSCITATION MEASURES.

I. General information.

The death of a person occurs as a result of the death of the organism as a whole. In the process of dying, stages are distinguished: agony, clinical death, brain death and biological death.

Agony is characterized by progressive extinction external signs vital functions of the body (consciousness, blood circulation, breathing, motor activity).

In clinical death, pathological changes in all organs and systems are completely reversible.

Brain death is manifested by the development of irreversible changes in the brain, and partially or completely reversible changes in other organs and systems.

Biological death is expressed by postmortem changes in all organs and systems that are permanent, irreversible, cadaveric in nature.

Post-mortem changes have functional, instrumental, biological and cadaveric signs.

Functional signs.

Lack of consciousness.

Lack of breathing, pulse, blood pressure.

Lack of reflex responses to all types of stimuli.

Instrumental signs.

Electroencephalographic.

Angiographic. Biological signs.

Maximum pupil dilation.

Paleness and/or cyanosis, and/or marbling (spotting) of the skin.

Decreased body temperature. Corpse changes.

Early signs.

Late signs.

II. Confirmation of a person's death.

The death of a person is declared when the brain or biological death of a person occurs (irreversible death of a person).

Biological death is established based on the presence of cadaveric changes ( early signs, late signs).

The diagnosis of “brain death” is established in health care institutions that have the necessary conditions to confirm brain death.

The death of a person on the basis of brain death is established in accordance with the Instructions for ascertaining the death of a person on the basis of a diagnosis of brain death, approved by order of the Ministry of Health of the Russian Federation dated December 20, 2001? 460 “On approval of the Instructions for ascertaining the death of a person based on the diagnosis of brain death” (order registered by the Ministry of Justice of the Russian Federation on January 17, 2002 No. 3170).

III. Termination of resuscitation measures.

Resuscitation measures are stopped only if these measures are recognized as absolutely futile or biological death is established, namely:

When a person is declared dead on the basis of brain death, including against the background of ineffective use of the full range of measures aimed at maintaining life;

If resuscitation measures aimed at restoring vital functions within 30 minutes are ineffective.

No resuscitation measures are carried out.

If there are signs of biological death.

When a state of clinical death occurs against the background of progression of reliably established incurable diseases or incurable consequences of acute injury incompatible with life.

Note. This instruction does not define the conditions for refusal to use resuscitation measures or their cessation in newborns and children under 5 years of age.

Prognosis after CPR.

The favorable outcome of CPR in a hospital setting currently ranges from 22 to 57%, the discharge rate of surviving patients is 5-29%, of which 50% leave with a neurological deficit. The outcome of prehospital CPR is an order of magnitude lower (G. Baltopoulos, 1999). The leading complication in people who have experienced clinical death is the development of post-resuscitation illness.

In conclusion of this chapter, it is necessary to note the following: successful revival of an injured person is possible only with the indispensable combination of three equally important conditions:

Want to help;

Know how to do it;

Be able to.

20.4. EMERGENCY MEDICAL CARE FOR PATIENTS WITH ACUTE BREATHING DISORDERS

20.4.1. Laryngospasm

Etiology. Mechanical or chemical irritation of the respiratory tract.

Pathogenesis. The syndrome is based on reflex spasm of striated muscles, regulating the functioning of the glottis.

Clinic. Against the background of relative well-being, the victim suddenly develops stridor breathing, signs of acute respiratory failure (ARF) of the 1st degree quickly appear, which within a few minutes turns into ARF of the 2nd-3rd degree; this is accompanied by loss of consciousness, disruption of the cardiovascular system and the development of a coma. Death occurs from asphyxia.

Urgent Care. In case of complete laryngospasm, a pathogenetically substantiated method of treatment is general curarization of the patient, followed by tracheal intubation and transfer to mechanical ventilation. Currently, apart from muscle relaxants, there are no other drugs that can quickly (within several tens of seconds - 1 minute) relieve spasms of striated muscles. Carrying out auxiliary ventilation using any breathing equipment against the background of complete laryngospasm is ineffective, however, with partial laryngospasm it must be carried out in any available way.

If it is not possible to immediately transfer the patient to mechanical ventilation using muscle relaxants, emergency conicotomy is indicated (see section 20.4.3. Foreign bodies of the upper respiratory tract). Tracheostomy in this situation is not indicated due to the complexity and duration of the surgical intervention (3-5 minutes). After eliminating laryngospasm and transferring the patient to mechanical ventilation, nonspecific antihypoxic therapy is carried out.

20.4.2. BRONCHIOLOSPASMS

Bronchiolospasm is synonymous with anaphylactic and anaphylactoid variants of status asthmaticus.

Asthmatic conditions

Asthmatic condition is defined as a syndrome characterized by an acute attack of suffocation. Suffocation defined as extreme

severity of shortness of breath, accompanied by a painful feeling of lack of air, fear of death.

Etiology. This condition can develop acutely with diseases of the upper respiratory tract (foreign bodies, tumors of the larynx, trachea, bronchi, attack bronchial asthma) and in diseases of the cardiovascular system (heart defects, AMI, pericarditis).

Pathogenesis caused by obstruction of the airways and impaired diffusion of oxygen into the blood.

The development of asthmatic conditions in diseases of the cardiovascular system mainly involves swelling of the bronchial mucosa as a result of the accumulation of interstitial fluid in it and compression of the small bronchi by edematous and interstitial tissue.

The following mechanisms take part in the development of bronchial obstruction: spasm of the smooth muscles of the bronchioles, discrinia and hypercrinia, inflammatory swelling of the bronchial mucosa, dyskinesia of the trachea and large bronchi, expiratory collapse of the small bronchi, sclerotic changes in the wall of the bronchi.

Depending on the reasons that caused the asthmatic condition, cardiac asthma, status asthmaticus against the background of bronchial asthma, and a mixed variant are distinguished.

Attack of bronchial asthma

Attack of bronchial asthma characterized by the development of severe expiratory shortness of breath, accompanied by a feeling of lack of air and disturbances in the gas composition of the blood (hypoxia and, in the case of a prolonged course, hypercapnia).

Clinical picture an attack of bronchial asthma consists of three periods: 1) the period of precursors; 2) peak period; 3) period of reverse development. The period of warning signs is individual for each patient and can manifest itself within a few minutes to several days in the form of headache, hay fever, urticaria, difficulty breathing, etc. During the peak period, the patient develops a cough with difficult-to-discharge viscous sputum, then the discharge of sputum stops; shortness of breath of an expiratory nature, accompanied by a feeling of lack of air; palpitations, interruptions in the functioning of the heart may occur. The patient is in a forced position with a fixed shoulder girdle, the inhalation is prolonged, “distant wheezing” may be observed, auxiliary muscles are involved in the act of breathing, the chest is emphysematous, a box sound is heard over the lungs by percussion, breathing is harsh, a large number of dry whistling and buzzing wheezing is heard, tachycardia , Blood pressure is normal or tends to increase. During the period of reverse development, sputum discharge improves, shortness of breath decreases, exhalation shortens, and the auscultatory picture in the lungs normalizes, although with exacerbation of bronchial asthma, hard breathing and wheezing may persist for a long time.

Urgent Care

Oxygen inhalation through a nasal catheter or mask - 2-6 l/min. The leading drugs for relieving an attack of suffocation are adrenergic agonists. Treatment should begin with subcutaneous injection of adrenaline.

Adrenaline is a stimulator of α 1 - β 1 - and β 2 - adrenergic receptors. It causes relaxation of the muscles of the bronchioles with their subsequent expansion, which is a positive effect against the background of bronchiolospasm, but, at the same time, acting on the β l -adrenergic receptors of the heart, causes tachycardia, increased cardiac output and a possible deterioration in the supply of oxygen to the myocardium. “Testing” doses are used, depending on the patient’s weight: for a weight less than 60 kg 0.3 ml, for a weight from 60 to 80 kg 0.4 ml, for a weight over 80 kg 0.5 ml of a 0.1% solution of adrenaline hydrochloride. If there is no effect, the subcutaneous injection at the initial dose can be repeated after 15-30 minutes (C.G. Scoggin, 1986; V.D. Malyshev, 1996). It is not recommended to exceed these doses, since excessive accumulation of adrenaline half-life products can cause paradoxical bronchiolconstriction. Administration of epinephrine is not recommended for elderly patients; persons suffering from ischemic heart disease, hypertension, parkinsonism, toxic goiter due to a possible increase in blood pressure, tachycardia, increased tremor, agitation, and sometimes worsening myocardial ischemia.

In addition to adrenaline, one of the β-agonists can be prescribed. Alupent(asthmopent, orciprenaline) - used in the form of a metered aerosol starting with one inhalation, if necessary, repeat after 5 minutes. The action begins in 1-2 minutes, complete relief of the attack occurs in 15-20 minutes, the duration of action is about 3 hours. It is possible to use subcutaneous or intramuscular injection of 1 ml of 0.05% alupent solution or intravenous drip ( 1 ml of 0.05% solution of alupenta in 300 ml of 5% glucose at a rate of 30 drops per minute). Alupent is a partially selective β 2 -adrenergic stimulator, so you can use Alupent 3-4 times during the day to avoid tachycardia and extrasystoles.

Salbutamol(ventolin, asmaline, aloprol) - a dosed aerosol is used, initially 1-2 breaths; If there is no effect, after 5 minutes you can take another 1-2 breaths. The permissible daily dose is 6-10 single inhalation doses (partially selective β 2 -adrenergic stimulant). The bronchial dilation effect of the drug begins after 1-5 minutes, the maximum effect occurs after 30 minutes, the duration of action is 3 hours.

Terbutaline(bricanil) - used in the form of a dosed aerosol: 1-2 breaths or 0.5 ml of a 0.05% solution intramuscularly up to 4 times a day. The bronchodilator effect is observed after 1-5 minutes, maximum after 45 minutes, duration of action is at least 5 hours. There is no significant change in heart rate and blood pressure after inhalation of terbutaline (selective β 2 -adrenergic stimulant).

Ipradol - applied in the form of a dosed aerosol: 1-2 breaths or 2 ml of 1% solution intravenously (selective β 2 -adrenergic stimulant).

Berotek(fenoterol) - used in the form of a dosed aerosol: 1-2 breaths. The onset of the bronchioldilating effect is after 1-5 minutes, the maximum effect is after 45 minutes, the duration of action is 5-6 hours (even up to 7-8 hours). Yu.B. Belousov, 2000 considers Berotec as the drug of choice due to its sufficient duration of action (partially selective β 2 -adrenergic stimulant).

Berodual - used in the form of a dosed aerosol: 1-2 breaths, if necessary, the drug can be inhaled up to 3-4 times a day (a combination of a β 2 -adrenergic stimulant and an anticholinergic ipratropium bromide, which is a derivative of atropine). The drug has a pronounced bronchioldilating effect.

Ditek - used to relieve a bronchial attack mild asthma and moderate severity (1-2 inhalations of the aerosol), if there is no effect, inhalation can be repeated after 5 minutes at the same dose (combined dosed aerosol consisting of fenoterol (Berotec) and mast cell stabilizer - Intal).

If there is no improvement after 15-30 minutes, then repeat the administration of β-adrenergic substances.

If after another 15-30 minutes there is no improvement, then intravenous drip infusion of aminophylline is established at a dose of 0.6 mg/kg per 1 hour for patients who have previously received theophylline; at a dose of 3-5 mg/kg over 20 minutes to persons who have not received theophylline, and then switch to maintenance doses (0.6 mg/kg per 1 hour).

Lack of improvement within 1-2 hours after the start of aminophylline administration requires additional administration of inhaled atropine (in patients with moderate cough) or intravenous corticosteroids (100 mg hydrocortisone or an equivalent amount of another drug).

20.4.3. FOREIGN BODIES OF THE UPPER RESPIRATORY TRACT

Foreign bodies of the upper respiratory tract cause ARF clinics of varying severity. Given pathological condition most common in children and mentally ill people.

The most common cause of airway obstruction in conscious adults is the entry of a foreign body while eating. A piece of food may cause partial or complete obstruction. At the same time, timely identification of the true cause of acute respiratory distress is a key point in determining the outcome of such an extreme situation. It is necessary to differentiate between a foreign body entering the respiratory tract and fainting, stroke, heart attack, or bronchial asthma attack. In the West, cases of aspiration in restaurants, mistakenly taken for a heart attack, have even been called “cafe coronary syndrome.”

The most common “internal” cause of upper airway obstruction in unconscious victims is retraction of the tongue root and closure of the epiglottis. “External” causes of obstruction can be foreign bodies, blood clots from head and face trauma, vomit, which are sometimes more difficult to diagnose, especially if the patient is unconscious.

The severity of the clinical picture depends on the size of the foreign body. The clinical symptoms that arise in this case will be characteristic features ADN: an attack of suffocation occurs, accompanied by severe cough, hoarseness, aphonia, pain in the throat or chest. The shortness of breath is inspiratory in nature. Partial obstruction can occur with satisfactory or impaired gas exchange. In the first case, the victim retains the ability to force a cough, without obvious signs of hypoxia; in the second, a weak, ineffective cough, noisy breathing, and the appearance of cyanosis are noted. Such partial obstruction in terms of assistance must be equated to complete obstruction.

With complete obstruction, a person is unable to speak, breathe, or cough. In this case, the victim’s posture is quite eloquent for those around him.

(Fig. 20-13). Failure to provide emergency assistance leads to a rapid drop in blood oxygenation, loss of consciousness followed by circulatory arrest and ends in death within a few minutes.

Urgent Care. Among the methods used today to provide resuscitation assistance when a foreign body enters the respiratory tract of a conscious patient, along with palm strikes in the back of the victim at the level of the shoulder blades (Fig. 20-14 a), chest compression, the Heimlich maneuver is considered the most popular (Heimlich maneuver), also known as “subdiaphragmatic abdominal compression” or “abdominal compression” (Fig. 20-14 b). The essence of the technique is as follows: abdominal compression is accompanied by an increase in intra-abdominal pressure and a rise in the diaphragm, leading to increased pressure in the respiratory tract and increased release of air from the lungs, creating a kind of artificial cough, which helps remove the foreign body.

Rice. 20-13. Posture of the victim with complete airway obstruction

The Heimlich maneuver is carried out as follows: the rescuer should be in relation to the sitting or standing victim from the back. Grab the victim under his arms and close your hands so that one hand, gathered into a fist, is located in the midline between the xiphoid process and the navel, and the hand of the second hand covers the first (see Fig. 20-14 b). Then begin to carry out rapid abdominal compressions (toward yourself and slightly upward) until either the foreign body is removed or until the victim loses consciousness.

In case of impaired consciousness or its absence, it is necessary to check for the presence of a foreign body in the oropharynx using the index finger (Fig. 20-15), perform techniques to restore patency of the airways (triple

Rice. 20-14. A blow to the back. Abdominal compression. A blow to the back with impaired consciousness

Peter Sachar's technique), attempt artificial respiration, and if unsuccessful, apply blows (up to 5 blows) to the back (see Fig. 20-14 c).

If it is not effective, perform the Heimlich maneuver (5-6 short pushes towards the spine and head) as shown in Fig. 20-16, you should again check for the presence of a foreign body in the oropharynx and perform artificial respiration. If the foreign body is removed, artificial respiration must be continued until spontaneous respiration is restored.

Even if this technique is carried out correctly, complications are possible, most often associated with regurgitation and aspiration of gastric contents, less often with damage to internal organs.

Rice. 20-15. Monitoring the presence of a foreign body in the oropharynx

Rice. 20-16. Variant of the Heimlich maneuver when the victim loses consciousness

If the Heimlich maneuver fails, emergency conicotomy is indicated, followed by removal of the foreign body by endoscopic or surgical method. Tracheostomy, even in experienced hands, requires a certain amount of time, while conicotomy can be performed within a few tens of seconds.

Technique of conicotomy (cricothyroidotomy)

The victim is placed on his back, a cushion (10-15 cm) is placed under his shoulder blades, and his head is tilted back. By palpation, the cricoid-thyroid ligament is determined, located between the lower edge of the thyroid and the upper edge of the cricoid cartilage (Fig. 20-17). A small one is made above the ligament (up to 1.5 cm) cross section skin (Fig. 20-18), insert the index finger into the incision, palpate the cricoid-thyroid ligament and dissect it with a scalpel inserted along the nail. Any hollow tube is inserted into the resulting hole in the trachea and fixed to the skin. Today, in the arsenal of doctors involved in providing emergency care, there is a special device - a conicotome, consisting of a trocar and a plastic cannula, which is inserted into the trachea along the trocar as a guide after puncturing the cricoid-thyroid ligament. The use of a conicotome significantly speeds up and simplifies the entire procedure.

In the absence of the possibility of performing conicotomy and obstruction of the airways at the level of the larynx, restoration of airway patency can be ensured by puncture of the cricothyroid ligament and leaving 2-3 needles of large (2-2.5 mm) internal diameter in the trachea (Chen G. et al. .,

1996) (Fig. 20-19).

Rice. 20-17. Anatomical features of the location of the cricoid ligament

Rice. 20-18. Place of incision of the cricoid ligament during conicotomy

Rice. 20-19. Cricothyroid ligament puncture site

20.4.4. DROWNING

Drowning - an acute pathological condition that develops during accidental or intentional immersion in liquid, with the subsequent development of signs of ARF and AHF, the cause of which is the entry of liquid into the respiratory tract.

There are three types of drowning in water.

True (wet).

Asphyxial (dry).

Death in the water ( syncopal type drowning).

Etiology. True drowning. It is based on the entry of water into the alveoli. Depending on the water in which drowning occurred (fresh or sea), there will be different pathogenesis. Fresh water, due to the similarity of the osmotic gradient with the blood, quickly leaves the alveoli and penetrates the vascular bed (Fig. 20-20 a). This leads to an increase in blood volume and hemodilution, pulmonary edema, hemolysis of erythrocytes, a decrease in the concentration of sodium, chlorine and calcium ions in the plasma, as well as plasma proteins. When drowning in sea water as a result of the difference in the osmotic gradient between blood and sea water, and here there is a clear predominance of the sea water gradient over blood, part of the plasma leaves vascular bed(see Fig. 20-20 b). In this regard, the mass of circulating blood decreases (up to 45 ml/kg), and the hematocrit increases (V.A. Negovsky, 1977).

Rice. 20-20. Pathogenesis of drowning in fresh (a) and sea (b) water

Asphyxial drowning occurs without aspiration of water. The basis of this pathology is reflex laryngospasm. The glottis does not allow water to pass through, but it also does not allow air to pass through. Death occurs from mechanical asphyxia.

Syncopal drowning (death in water) occurs as a result of a reflex arrest of cardiac activity and breathing. Most common option This type of drowning occurs when the victim is suddenly immersed in cold water.

Clinic. In case of true drowning, 3 periods are distinguished: initial, agonal and clinical death. The state of consciousness depends on the period of drowning and its type. Breathing disturbances range from noisy to agonal. Cyanosis, chills, and goose bumps are observed. When drowning in fresh water, symptoms of pulmonary edema, arterial and venous hypertension, tachycardia, and arrhythmia are observed. The upper respiratory tract may produce foam, sometimes with a pink tint, as a result of hemolysis of red blood cells. When drowning in sea water, arterial hypotension and bradycardia are more typical.

Urgent Care. Regardless of the water in which the drowning occurred, if breathing or cardiac activity stops, the victim needs

It is possible to carry out a complex of resuscitation measures. Before performing artificial respiration, the upper respiratory tract (URT) should be cleared of water and foreign bodies (river sand, algae, silt, etc.). The optimal way to release the VDP, especially in children, is to lift the victim by the legs. If it is impossible to carry out this manual, it is recommended to place the victim with his stomach on the bent knee of the person providing resuscitation care and wait for the fluid to flow out of the upper respiratory tract (Fig. 20-21). This procedure should take no more than 5-10 seconds, after which it is necessary to begin resuscitation (see section 20.3. Cardiopulmonary resuscitation).

Rice. 20-21. Position of the victim on a bent knee

In a hospital setting, treatment is syndromic in nature and consists of the following areas.

Carrying out a complex of resuscitation measures and transferring the patient to mechanical ventilation (according to indications).

Sanitation of the tracheobronchial tree, therapy of bronchiolospasm, pulmonary edema.

Relief of OSSN.

Correction of acid-base balance and electrolytes.

Prevention of pneumonia and kidney failure.

20.4.5. PULMONARY EMBOLISM

Pulmonary embolism(PE) - is defined as a syndrome of acute respiratory and heart failure that occurs when a blood clot or embolus enters the pulmonary artery system.

Etiology

Deep vein thrombosis of the leg- cause of pulmonary embolism in 5% of patients.

Thrombosis in the inferior vena cava system is the cause of pulmonary embolism, according to V.B. Yakovleva (1995), in 83.6% of patients.

Diseases of the cardiovascular system, extremely predisposing to the development of blood clots and embolisms in the pulmonary artery are:

Rheumatism, especially in the active phase, with the presence of mitral stenosis and atrial fibrillation;

Infective endocarditis;

Hypertonic disease;

Coronary heart disease (usually transmural or subendocardial myocardial infarction);

Severe forms of non-rheumatic myocarditis;

Cardiomyopathies.

Malignant neoplasms often lead to the development of recurrent thrombophlebitis of the upper and lower extremities (paraneoplastic syndrome), which can be a source of pulmonary embolism. This most often happens with cancer of the pancreas, lungs, and stomach.

Generalized septic process in some cases, it is complicated by thrombosis, which is usually a manifestation of the hypercoagulable phase of disseminated intravascular coagulation syndrome (DIC), which can cause pulmonary embolism (PE).

Thrombophilic conditions - This is an increased tendency of the body to intravascular thrombus formation, which is caused by a congenital or acquired violation of the regulatory mechanisms of the hemostasis system.

Antiphospholipid syndrome - a symptom complex based on the development of autoimmune reactions and the appearance of antibodies to phospholipids present on the membranes of platelets, endothelial cells, and nervous tissue, which can lead to thrombosis of various locations.

Risk factors(A. N. Okorokov, 2000):

Prolonged bed rest and heart failure (due to slowing blood flow and the development of venous stagnation);

Massive diuretic therapy (excessive diuresis leads to dehydration, an increase in hematocrit and blood viscosity);

Polycythemia and some types of hematological malignancies (due to the high content of red blood cells and platelets in the blood, which leads to hyperaggregation of these cells and the formation of blood clots);

Long-term use hormonal contraceptives(they increase blood clotting);

Systemic diseases connective tissue And systemic vasculitis(in these diseases there is an increase in blood clotting and platelet aggregation);

Diabetes;

Hyperlipidemia;

Varicose veins (conditions are created for stasis of venous blood and the formation of blood clots);

Nephrotic syndrome;

Indwelling catheter in the central vein;

Stroke and spinal cord injury;

Malignant neoplasms and chemotherapy for cancer.

Pathogenesis. Mechanical blockage of the common trunk of the pulmonary artery by a massive thrombus or embolus causes a cascade of pathological reflex reactions.

Instantly, generalized arteriolospasm occurs in the pulmonary circulation and collapse of the systemic vessels. Clinically, this is manifested by a drop in blood pressure and a rapid increase arterial hypertension small circle (central venous pressure increases).

Generalized arteriolospasm is accompanied by total bronchiolospasm, which causes the development of ARF.

Right ventricular failure quickly develops, resulting from the work of the right ventricle against high resistance in the pulmonary circle.

A small output of the left ventricle is formed due to a catastrophic decrease in the flow of blood into it from the lungs. A drop in stroke volume of the left ventricle causes the development of reflex arteriolospasm in the microcirculatory system and disruption of the blood supply to the heart itself, which can provoke the appearance of fatal rhythm disturbances or the development of AMI. These pathological changes quickly lead to the formation of acute total heart failure.

Massive entry from ischemic sites into the bloodstream of a large number of biologically active substances: histamine, serotonin, some prostaglandins increases permeability cell membranes and contributes to the occurrence of interoceptive pain.

As a result of complete blockage of the pulmonary artery, pulmonary infarction develops, which aggravates ARF.

Anatomical variants of pulmonary embolism by localization (V.S. Savelyev et al., 1990)

Proximal level of embolic occlusion:

Segmental arteries;

Lobar and intermediate arteries;

Main pulmonary arteries and pulmonary trunk. Affected side:

Left;

Right;

Two-way.

Clinical forms of pulmonary embolism

Lightning fast. Death occurs within a few minutes.

Acute (fast). Death can occur within 10-30 minutes.

Subacute. Death can occur within several hours or days.

Chronic. Characterized by progressive right ventricular failure.

Recurrent.

Erased.

Clinical picture

IN clinical picture the first place is occupied by sudden shortness of breath, both at rest and after minor physical exertion. The nature of the shortness of breath is “quiet”, the number of breaths is from 24 to 72 per minute. It may be accompanied by a painful, nonproductive cough. More often, cough complaints appear already at the stage of pulmonary infarction; at this time, the cough is accompanied by chest pain and the discharge of bloody sputum (hemoptysis is observed in no more than 25-30% of patients). The widespread belief that hemoptysis is an integral sign of the early stage of pulmonary embolism is not always true. EAT. Tareev (1951) noted hemoptysis in 10-12% in the first 3 days, P.M. Zlochevsky (1978) encountered this syndrome in 19% of patients. It should be emphasized that hemoptysis is more typical for days 6-9 of the disease, and not for days 1-2. Hemoptysis is caused by hemorrhage into the alveoli due to a gradient between low pressure in the pulmonary arteries distal to the embolus and normal pressure in the terminal branches of the bronchial arteries.

Almost immediately, compensatory tachycardia appears, the pulse becomes thread-like, and atrial fibrillation may occur in every fourth patient. There is a rapid drop in blood pressure. Circulatory shock develops in 20-58% of patients and is usually associated with massive pulmonary occlusion, which is considered one of common signs TELA.

Depending on the location of the thrombus, the pain syndrome may be angina-like, pulmonary-pleural, abdominal or mixed. With embolism of the main trunk of the pulmonary artery, recurrent chest pain occurs due to irritation of the nerve apparatus embedded in the wall of the pulmonary artery. In some cases of massive PE, sharp pain with widespread irradiation resembles that of a dissecting aortic aneurysm. The duration of pain can vary from a few minutes to several hours. Sometimes anginal pain is observed, accompanied by ECG signs of myocardial ischemia due to a decrease in coronary blood flow due to a decrease in stroke and minute volumes. An increase in blood pressure in the cavities of the right heart is also of some importance, which disrupts the outflow of blood through the coronary veins. Sharp pain in the right hypochondrium may be observed, combined with intestinal paresis, hiccups, symptoms of peritoneal irritation associated with acute congestive liver swelling with right ventricular failure or the development of massive infarctions of the right lung. When pulmonary infarction develops in subsequent days, sharp pains in the chest, aggravated by breathing and coughing, they are accompanied by pleural friction noise.

With massive or submassive pulmonary embolism, an acute cor pulmonale is formed in the first minutes, characterized by the following symptoms: swelling of the jugular veins, pathological pulsation in the epigastric region and in the second intercostal space to the left of the sternum; extension right border heart, accent and bifurcation of the second tone over the pulmonary artery, systolic murmur over the xiphoid process, increased central venous pressure, painful swelling of the liver and a positive Plesh sign (pressure on the painful liver causes swelling of the jugular veins). The skin becomes pale in color (possibly an ashen tint), feels moist and cold to the touch. Against the background of a small emission, syn-

symptoms of central nervous system damage: inappropriate behavior, psychomotor agitation. Cerebral disorders with pulmonary embolism can manifest themselves in two ways:

Syncopal (like deep fainting) with vomiting, convulsions, bradycardia;

Comatose.

In addition, psychomotor agitation, hemiparesis, polyneuritis, and meningeal symptoms may be observed.

A common symptom of pulmonary embolism is an increase in body temperature, which usually occurs from the first hours of the disease. Most patients have a low-grade fever without chills, while a minority of patients have a febrile temperature. The total duration of the febrile period ranges from 2 to 12 days.

Diagnosis of pulmonary embolism

If PE is suspected, the doctor must confirm the presence of embolism, determine its location, assess the state of hemodynamics of the small and large circles, eliminate the threat to life, and prescribe adequate treatment. Selective pulmonary angiography, spiral angiography can help in diagnosis. CT scan with vascular contrast, ventilation-perfusion scanning of the lungs, chest radiography, electrocardiography, determination of D-dimer in the blood and diagnosis of deep vein thrombosis. Convincing laboratory data confirming this pathology, not currently.

Selective angiopulmonography is the most informative method in diagnosing pulmonary embolism; The following angiopulmonographic signs are characteristic:

Increase in the diameter of the pulmonary artery;

Complete (with occlusion of the main right or left branch of the pulmonary artery) or partial (with occlusion of segmental arteries) lack of contrast of the pulmonary vessels on the affected side;

“blurred” or “spotty” nature of contrasting vessels with multiple, but not complete obstruction of the lobar and segmental arteries;

Filling defects in the lumen of blood vessels in the presence of single wall thrombi;

Deformation of the pulmonary pattern in the form of expansion and tortuosity of segmental and lobar vessels with multiple lesions of small branches.

Angiographic examination in mandatory should include both sounding of the right heart and retrograde iliocavography, which makes it possible to clarify the sources of embolism, which most often are floating thrombi in the iliac and inferior vena cava.

Spiral computed tomography with vascular contrast. Using this method, blood clots in the pulmonary artery can be visualized and other lung diseases such as tumors, vascular abnormalities, etc. can be detected.

Ventilation-perfusion scanning of the lungs. PE is characterized by the presence of a perfusion defect with preserved ventilation of the affected lung segments.

Depending on the severity of pulmonary tissue perfusion defects, high (> 80%), medium (20-79%) and low (< 19%) вероятность наличия ТЭЛА.

X-ray data. In the early stages of pulmonary embolism X-ray methods studies may not be sufficiently informative. The most characteristic signs of PE are: bulging of the pulmonary cone (manifested by flattening of the waist of the heart or protrusion of the second arch beyond the left contour) and expansion of the heart shadow to the right due to the right atrium; enlargement of the contours of the pulmonary artery branch with subsequent rupture of the vessel (with massive pulmonary embolism); sharp expansion of the root of the lung, its chopped off, deformation; local clearing of the pulmonary field in a limited area (Westermarck's symptom); high standing of the dome of the diaphragm (due to reflex shrinkage of the lung in response to embolism) on the affected side; expansion of the shadow of the superior vena cava and azygos veins; the superior vena cava is considered dilated when the distance between the line of the spinous processes and the right contour of the mediastinum increases by more than 3 cm. After the appearance of a pulmonary infarction, infiltration of the pulmonary tissue is detected (sometimes in the form of a triangular shadow), often located subpleurally. The typical picture of pulmonary infarction is detected no earlier than the second day and in only 10% of patients. In addition, you need to know the following: to obtain a high-quality image, it is necessary to examine the patient on a stationary X-ray machine with breath holding. Mobile devices, as a rule, make it difficult to obtain a high-quality image. Based on this, the doctor must clearly decide the question: does a patient in serious condition need an X-ray examination.

ECG. There are nonspecific signs of overload of the right heart: pattern S I, Q III, T III, which consists of a deep tooth S in standard lead I, deep wave Q and tooth inversion T in lead III. There is an increase in the tooth R in lead III and displacement of the transition zone to the left (in V 4 -V 6), splitting of the complex QRS in V 1 -V 2, as well as signs of blockade of the right bundle branch, however, this symptom may be absent.

Determination of D-dimer in blood. The basis of this research method is the presence of endogenous fibrinolysis, accompanied by the destruction of fibrin with the formation of D-dimers (normal D-dimer levels are less than 500 μg/l). The sensitivity of an increase in D-dimer in diagnosing PE reaches 99%, but the specificity is 53%, since this D-dimer also increases in many other diseases: AMI, bleeding, after surgical operations etc.

Laboratory data nonspecific. Neutrophilic leukocytosis with a band shift, lymphopenia, relative monocytosis, increased ESR may be observed; increased lactate dehydrogenase levels; moderate hyperbilirubinemia is possible; increased content of seromucoid, haptoglobin, fibrin; hypercoagulability.

Principles of intensive care for pulmonary embolism

Based on the pathogenesis, the principles of intensive care should contain the following directions.

Maintaining life in the first minutes.

Elimination of pathological reflex reactions.

Elimination of a blood clot.

Relieving collapse.

Reduced pressure in the pulmonary circulation.

Oxygen therapy.

Life support in the first minutes includes a complex of resuscitation measures (see section 20.3. Cardiopulmonary resuscitation).

Elimination of pathological reflex reactions includes the fight against fear and pain. For this purpose use:

Carrying out pain relief narcotic analgesics or by the method of neuroleptanalgesia (NLA), which reduce fear and pain, reduce hypercatecholaminemia, and improve the rheological properties of blood;

Heparin is used not only as an anticoagulant, but also as an antiserotonin drug;

To relieve arteriolo- and bronchiolospasm, drugs of the xanthine group, atropine, prednisolone or its analogues are used.

Relieving collapse. When systolic blood pressure is less than 90 mm Hg. and if there are signs of low cardiac output, intravenous bolus administration should be started until systolic blood pressure rises above 90 mmHg. The goal is to increase the filling of the heart by increasing the volume of blood volume and, therefore, normalize cardiac output.

If arterial hypotension does not stop after IV 500 ml of colloidal solution, dobutamine should be added to infusion therapy at a rate of 10 mcg/kg/min. If there is no rise in blood pressure within 5-10 minutes, the rate of dobutamine administration should be increased to 40 mcg/kg/min.

If after this systolic blood pressure remains less than 90 mm Hg, dobutamine should be replaced with dopamine or norepinephrine. If after 30-60 minutes systolic blood pressure remains less than 90 mm Hg. and the diagnosis of PE is clearly established, in the absence of contraindications, thrombolytic therapy should be started (Sprigings D., Chambers J., 2006).

Clot elimination can be carried out conservatively and operatively, however, the latter method (operative), despite repeated attempts to use it, has not become widespread due to great technical difficulties and high level postoperative mortality.

Conservative pathogenetic treatment has two directions.

Thrombolytic therapy.

Stopping further thrombus formation.

Thrombolytic therapy (TLT) is indicated in the presence of massive or submassive PE. Appropriate laboratory support is required. The criteria for thrombolysis are maintaining systolic blood pressure less than 90 mmHg. after therapy colloidal solutions(see above), the presence of characteristic clinical signs of pulmonary embolism, the presence of risk factors for thromboembolism and the absence of other probable illness. The optimal method of thrombolytic therapy is the administration of thrombolytics through a catheter inserted into the pulmonary artery and under the control of an electron-optical converter connected directly to the thrombus. It is possible to administer thrombolytics into a central or peripheral vein. Currently, streptokinase and alteplase are considered the drugs of choice for thrombolytic therapy.

When treating with streptokinase, 250,000 units dissolved in an isotonic solution of sodium chloride or glucose are administered intravenously during the first 30 minutes. Over the next 12-72 hours, this drug is continued to be administered at a rate of 100,000 units per hour. To stop possible allergic reactions With the first dose of streptokinase, it is recommended to administer 60-90 mg of prednisolone intravenously.

When treating with alteplase, 10 mg is administered intravenously during the first 1-2 minutes, then 90 mg in the next 2 hours (maximum total dose - 1.5 mg/kg in patients weighing less than 65 kg).

Thrombolytic therapy with streptokinase or alteplase should be carried out under constant monitoring of blood coagulation parameters. Thrombin time (TT) or activated partial thromboplastin time (APTT) should be determined 3-4 hours after stopping the administration of these drugs. If TT/APTT increases less than 2 times, heparin should be resumed.

Anticoagulant therapy. Direct anticoagulants are used: unfractionated heparin (UFH), low molecular weight heparins (LMWH) and indirect anticoagulants (primarily warfarin).

Direct anticoagulants (DFG). Heparin should be used if there is reasonable suspicion of the development of pulmonary embolism. Its use prevents the development of continued thrombosis in the pulmonary arterial bed; under its influence, the boundaries of thrombotic occlusion in the main veins are fixed and microcirculation improves (V.S. Savelyev et al., 2001).

Treatment UFH should be performed by long-term continuous intravenous infusion; the rate of administration is regulated by APTT, which is maintained at a level of 1.5-2.5 H control (Sprigings D., Chambers J., 2006).

Infusion of unfractionated sodium heparin

(Quoted in Drug and Therapeutics Bulletin 1992; 30: 77 - 80). Loading dose 5,000-10,000 units (100 units/kg) IV over 5 minutes. Infusion 25,000 units, diluted saline solution up to 50 ml (500 units/ml). Begin administration at a rate of 1,400 units/hour (2.8 ml/hour) using a pump. Determine the activated partial thromboplastin time (aPTT) at 6 hours.

Adjust the dose as follows:

APTT ratio (target 1.5-2.5xcontrol) - Action.

7.0 - Suspend administration for 30-60 minutes, then reduce the rate of administration by 500 units/hour.

5.1-7.0 - Recheck APTT after 4 hours, then reduce the infusion rate by 500 U/hour.

4.1-5.0 - Recheck APTT after 4 hours, then reduce the infusion rate by 300 U/hour.

3.1-4.0 - Recheck APTT after 10 hours, then reduce the infusion rate by 100 U/hour.

2.6-3.0 - Recheck APTT after 10 hours, then reduce the infusion rate by 50 U/hour.

1.5-2.5 - Re-determine APTT after 10 hours, then do not change the rate of administration

1.2-2.4 - Re-determine APTT after 10 hours, then increase the infusion rate by 200 U/h

< 1,2 - Повторно определите АЧТВ через 10 ч, затем увеличьте скорость введения на 400 ЕД/ч и повторно определите АЧТВ через 4 ч

After each change in infusion rate, wait 10 hours before the next APTT assessment, except APTT >5 or<1,2, когда повторная оценка необходима через 4 ч.

If the infusion rate is stable, assess APTT daily.

Heparin sodium may cause immune-mediated thrombocytopenia, which is often complicated by thrombosis: assess platelet counts daily when using heparin for more than 5 days and immediately discontinue heparin if thrombocytopenia occurs.

In the absence of the possibility of continuous infusion of UFH, there are methods of fractional intravenous or subcutaneous administration of heparin.

The initial dose of regular UFH is determined as follows: the patient’s body weight is multiplied by 450 units, then the resulting number is divided by the number of injections of the drug. Thus, with fractional intravenous administration of heparin, the number of injections is 8 (with a frequency of 3 hours each), with subcutaneous administration - 3 (with a frequency of 12 hours).

To achieve the most rapid anticoagulant effect, it is necessary to first administer a bolus of 5,000 units of heparin.

The dose of heparin is selected individually based on laboratory determination of activated partial thromboplastin time (aPTT) and thrombin time (TT). The analysis is carried out immediately before each regular injection on the 1st day of therapy. When a therapeutic effect is achieved, hemostasis studies are carried out daily. The values of these indicators should be 1.5-2 times higher compared to the norm (cited from V.S. Savelyev et al., 2001).

Direct anticoagulants. Low molecular weight heparins (LMWH), such as nadroparin calcium (Fraxiparine), have a pronounced therapeutic effect. In comparison with UFH, they give a lower incidence of hemorrhagic complications, have a longer effect, and are easy to use (2 injections per day). LMWH is administered subcutaneously; APTT monitoring is not required.

Heparin sodium(UFG) - 450 IU/kg IV or SC per day.

Enoxaparin(clexane) (LMWH) - 1 mg/kg subcutaneously 2 times a day.

Dalteparin(Fragmin) (LMWH) - 100 IU/kg subcutaneously 2 times a day.

Nadroparin calcium(fraxiparine) (LMWH) - 85 IU subcutaneously 2 times a day.

A mandatory addition to heparin therapy, especially in the first days, is the use of low molecular weight dextrans (reopolyglucin, reomacrodex), at a dose of 10 ml/kg per day (cited by A.V. Pokrovsky, S.V. Sapelkin,

Indirect anticoagulants. During heparin therapy, warfarin is prescribed and they should be taken simultaneously for 3-4 days: during this period, the APTT and international normalized ratio (INR).

Warfarin is usually taken for 3-6 months after the first episode of PE (the INR should be maintained at 2.0-3.0). For recurrent thromboembolism, lifelong therapy may be indicated.

Heparin administration can be discontinued after 5 days if the INR reaches more than 2.0.

Reduced pressure in the pulmonary circulation. In the absence of clinical signs of shock due to pulmonary embolism, nitrovasodilators are effective means of reducing pressure in the pulmonary artery. With the development of acute or subacute cor pulmonale at the prehospital stage, it is recommended to prescribe nitroglycerin intravenously or orally in short-acting forms under blood pressure control.

In addition, aminophylline is administered intravenously - 10 ml of a 2.4% solution per 200 ml of isotonic sodium chloride solution. Eufillin reduces pressure in the pulmonary artery and causes a bronchodilator effect. Eufillin is administered under blood pressure control. When the systolic blood pressure level is below 100 mm Hg. You should refrain from administering nitrates and aminophylline.

With the development of myocardial infarction, antibiotic therapy: third generation parenteral cephalosporins [cefotaxime (claforan) 4-8 g/day, ceftriaxone (Longacef) 2-4 g/day] + parenteral macrolides (spiramycin 1.5-3 g/day, erythromycin 1-2 g/day) or macrolides orally [azithromycin (sumamed) 500 mg/day]. Alternative agents - parenteral fluoroquinolones [ciprofloxacin (ciprobay) 0.5-1.0 g/day, pefloxacin (abactal) 0.8-1.2 g/day]; ceftazidime (Fortum, Myrocef) 2-6 g/day) + aminoglycosides (amikacin 10-15 mg/kg/day, gentamicin 240 mg/day).

Inhalation of humidified oxygen carried out through nasal catheters at a rate of 2-7 l/minute.

Scope of emergency care for suspected pulmonary embolism

Provide resuscitation assistance if necessary.

Consistently, intravenously, inject 10-20 thousand units of heparin, 10 ml of 2.4% aminophylline solution, 90-120 mg of prednisolone.

If necessary, administer narcotics, analgesics, mesaton, norepinephrine.

Record an ECG, and if possible, if the patient’s condition allows, take a chest x-ray.

Once the diagnosis is confirmed, begin anticoagulant therapy.

Transfer and further treatment in the intensive care unit.

Prevention of pulmonary embolism consists of timely diagnosis and treatment of thrombophlebitis of the veins of the lower extremities, expansion of bed rest in the postoperative period and in patients with cardiac pathology.

In recent years, in order to prevent pulmonary embolism, an umbrella filter has been implanted into the infrarenal portion of the inferior vena cava. This operation is indicated: for embologenic thrombosis of the ileocaval segment, when it is impossible to perform embolectomy; with repeated embolism into the pulmonary artery system in patients with an unknown source of embolism; with massive pulmonary embolism.

20.4.6. ASPIRATION PNEUMONITIS

Aspiration pneumonitis(Mendelssohn's syndrome) is a pathological syndrome that occurs as a result of aspiration of gastric contents into the respiratory tract and is manifested by the development of signs of ARF followed by the addition of an infectious component.

Etiology. Most often, this syndrome occurs in anesthesiological practice, when the patient is given general anesthesia against the background of a full stomach. However, this pathological condition can also develop with incompetent cardiac sphincter (in pregnant women at 20-23 weeks), with severe alcohol intoxication, various comatose states in combination with vomiting or spontaneous aspiration of gastric contents. Aspiration pneumonitis most often causes E. coli, Fusobacterium, Peptostreptococcus, Pseudomonas aeruginosa, Enterobacteriae, Staphylococcus aureus.

Pathogenesis. There are two possible scenarios for the occurrence of this syndrome. In the first case, fairly large particles of undigested food enter the respiratory tract with gastric juice, usually of a neutral or slightly acidic reaction. Mechanical blockage of the respiratory tract occurs at the level of the middle bronchi and a clinical episode of acute respiratory failure occurs, stage I-III. In the second option, acidic gastric juice is aspirated into the respiratory tract, possibly even without admixture of food, this causes a chemical burn of the mucous membrane of the trachea and bronchi, followed by the rapid development of edema of the mucous membrane; Ultimately, bronchial obstruction forms, and then within 1-2 days symptoms of bronchopneumonia and severe intoxication appear. Aspiration pneumonitis is often complicated by lung abscess. In addition, pneumonia develops on the second day. Clinical manifestations correspond to other bacterial pneumonias, but are distinguished by a more pronounced intoxication syndrome and high mortality.

Clinical picture. Regardless of the variant of pathogenesis, patients experience three stages of this syndrome.

As a result of reflex bronchiolospasm, acute respiratory failure of degrees I-III occurs with possible death from suffocation.

If the patient does not die at the first stage, then after a few minutes, as a result of partial spontaneous relief of bronchiolospasm, some clinical improvement is noted.

The pathogenesis of the third stage is the rapid appearance and increase of edema and inflammation of the bronchi, which causes an increase in the signs of ARF.

One should remember about the frequent occurrence of respiratory distress syndrome in adults, which significantly worsens the prognosis in this category of patients.

Urgent Care

Urgent sanitation of the oral cavity and nasopharynx, tracheal intubation, transfer to mechanical ventilation, aspiration sanitation of the trachea and bronchi.

Carrying out mechanical ventilation using hyperventilation (minute breathing volume (MVR) - 15-20 l) with inhalation of 100% oxygen.

Aspiration of gastric contents. Administration of 0.5% sodium bicarbonate or 0.9% sodium chloride, 10-15 ml, followed by aspiration until the airways are completely cleared.

Sanitation bronchoscopy.

At the initial stage, it is advisable to prescribe glucocorticosteroids (GCS) (prednisolone 60-90 mg IV), aminophylline 2.4% - 15-20 ml to eliminate bronchial obstruction syndrome and reduce bronchial edema.

Heparin therapy: 5,000 units subcutaneously 4 times a day.

Antibacterial therapy should include third-generation cephalosporins [claforan - 2 g every 6 hours IV (maximum dose 12 g/day); longacef - 2 g intravenously per day (maximum dose 4 g/day); fortum - 2 g IV per day (maximum dose 4 g/day)] in combination with aminoglycosides of the third and fourth generations (amikacin 15 mg/kg IV, IM, every 12 hours; tobramycin 5 mg/kg IV , IM, every 8 hours).

Alternative drugs: fluoroquinolones [ciprobay - 200-400 mg IV every 12 hours; Tarivid - 400 mg IV every 12 hours; pefloxacin (abactal) - 400 mg IV every 12 hours] or carbapenems (thienam - 1-2 g IV, IM every 6-8 hours).

20.4.7. STRANGULATION ASPHIXIA

Strangulation asphyxia(hanging) is characterized as a syndrome of acute respiratory and cardiovascular failure resulting from mechanical compression of the neck.

Etiology. The most common causes are suicide attempts or accidents associated with mechanical compression of the neck.

Pathogenesis with consists of four main components.

Mechanical compression of the neck by a loop as a result of displacement and pressing of the tongue against the back wall of the pharynx blocks the patency of the upper respiratory tract, which causes the development of ARF, which sequentially occurs in four stages lasting from several seconds to several minutes. The first stage is characterized by attempts to take a deep forced breath with the participation of auxiliary muscles. Cyanosis of the skin, arterial and venous hypertension, and tachycardia quickly appear and increase. In the second stage, the patient loses consciousness, convulsions and involuntary urination appear. Blood pressure decreases, breathing becomes arrhythmic and slows down. In the third stage, breathing stops, in the fourth - death.

Compression of the neck veins against the background of preserved arterial patency is accompanied by rapid overflow of cerebral vessels with venous blood, resulting in increased intracranial pressure.

Mechanical injury to the carotid sinus leads to reflex disorders in the cardiovascular system.

Mechanical damage to the cervical spine and spinal cord is possible.

Clinical picture. Upon examination, attention is drawn to a violation of the vital functions of the body. State of consciousness - from confused to complete absence; pale skin, acrocyanosis. Characterized by convulsive syndrome with pronounced tension in the muscles of the back and limbs; involuntary urination and feces. Dilation of the pupils, lack of reaction to light, and nystagmus are also noted. Small punctate hemorrhages are often observed on the inner surface of the eyelids and sclera. Violations of the cardiovascular system are most often possible in two ways: tachycardia up to 160-180 per minute and arterial hypertension up to 200 mm Hg. and more or less severe hypotension in combination with bradycardia, which is an unfavorable diagnostic sign (mortality in this subgroup is 3 times higher).

Urgent Care. Long-term treatment results largely depend on the timeliness and correctness of medical care at the prehospital level. The ideal treatment option is the use of muscle relaxants followed by tracheal intubation and mechanical ventilation at the scene of the incident. If there is no opportunity to implement this benefit at the emergency stage, relief of convulsive syndrome comes to the fore.

The optimal remedy for this purpose is the intravenous administration of 2-4 ml of relanium per 10-20 ml of isotonic sodium chloride solution. This dose allows you to stop convulsive syndrome in 70-80% of cases. If necessary, the administration of Relanium can be repeated after 5-10 minutes. Otherwise, prehospital therapy is symptomatic. It is advisable to begin pathogenetic therapy (administration of antispasmodics, diuretics, soda solution) at the prehospital stage, if the time of evacuation of the victim exceeds 30-40 minutes.

Note. The administration of respiratory analeptics for this pathology is inappropriate, since they increase the need of brain cells for oxygen, which can deepen its ischemia and cause or intensify the existing convulsive syndrome.

Hospital Principles of treatment

Relief of convulsive syndrome.

Carrying out mechanical ventilation according to indications (presence of stage II-III ARF).

Relief of cerebral edema.

Correction of acid-base balance and electrolyte status.

Prevention of hypostatic complications.

Antibiotic therapy.

In the presence of hypoxic encephalopathy, hyperbaric oxygen therapy (HBO) is indicated.

Symptomatic therapy.