Air duct for medical use. Algorithm for inserting an oropharyngeal airway

Rice. 2 "Chain of Survival"

1. 
   Early activation of emergency medical services.
2. 
   Early onset of basic life support (stages A-B-C).
3. 
   Early defibrillation using Automated external defibrillators (AED).
4. 
   Early initiation of further life support, including intubation and use of medications.

1. 
   ^ CARDIOPULMONARY AND CEREBRAL STAGES

P. Safar divided the entire SLCR complex into 3 stages, each of which has its own purpose and successive stages:

I. Stage: Elementary d holding life

Target- emergency oxygenation.

Stages:

1. 
   Control and restoration of airway patency.
2. 
   Artificial maintenance of respiration.
3. 
   Artificial maintenance of blood circulation.

The goal is to restore spontaneous circulation

1. 
   Drug therapy.
2. 
   Electrocardiography or electrocardioscopy.
3. 
   Defibrillation.

The goal is cerebral resuscitation and post-resuscitation intensive

therapy

1. 
   Assessment of the condition (establishing the cause of circulatory arrest and its elimination) and the possibility of fully saving the patient, taking into account the degree of damage to the central nervous system.
2. 
   Restoring normal thinking.
3. 
   Intensive therapy aimed at correcting impaired functions of other organs and systems.

Rice. 3 Methods for restoring airway patency

A. Control and restoration of airway patency

The “gold standard” for ensuring airway patency is the “triple maneuver” according to P. Safar and tracheal intubation.

The first thing you need to do near the victim is to make sure that there is no consciousness - call out (ask loudly: What happened? Open your eyes!), pat him on the cheeks, gently shake him by the shoulders.

The main problem that arises in unconscious persons is obstruction of the airways by the root of the tongue and the epiglottis in the laryngopharyngeal region due to muscle atony (Fig. 3 A). These phenomena occur in any position of the patient (even on the stomach), and when the head is tilted (chin to chest), obstruction of the airways occurs in almost 100% of cases. Therefore, after it is established that the victim is unconscious, it is necessary to ensure the airway is open.

P. Safar developed a “triple technique” on the respiratory tract, including: throwing back the head, opening the mouth and pushing the lower jaw forward(Fig. 3 D, C). Alternative methods for establishing airway patency are shown in Fig. 3 B and 3 D.

When performing manipulations on the respiratory tract, it is necessary to remember about possible damage to the spine in the cervical region. ^ Highest risk of cervical spine injury can be observed in two groups of victims:

1. 
   For road traffic injuries(a person was hit by a car or was in a car during the collision);

1. 
   ^ When falling from a height (including among “divers”).

Throwing back the head alone does not guarantee restoration of airway patency. Thus, in 1/3 of patients who are unconscious due to muscle atony, the nasal passages during exhalation are closed by the soft palate, which moves like a valve. In addition, there may be a need to remove foreign substances contained in the oral cavity (blood clots, vomit, tooth fragments, etc.). Therefore, first of all, in people with injuries, it is necessary to inspect the oral cavity and, if necessary, clean it of foreign contents. To open the mouth, use one of the following techniques (Fig. 4).

1. Reception using crossed fingers with a moderately relaxed lower jaw. The resuscitator stands at the head end or on the side of the patient’s head (Fig. 4 A). The index finger is inserted into the corner of the victim’s mouth and pressure is applied to the upper teeth, then the thumb is placed opposite the index finger on the lower teeth (Fig. 4 B) and the mouth is forced to open. In this way, a significant opening force can be achieved, allowing the mouth to be opened and the oral cavity to be examined. If foreign bodies are present, they should be removed immediately. To do this, turn the head to the right without changing the position of the fingers of the left hand (Fig. 4 B). With the right index finger, the right corner of the mouth is pulled down, which facilitates independent drainage of the oral cavity from liquid contents (Fig. 4 D). With one or two fingers wrapped in a scarf or other material, clean the mouth and throat (Fig. 4 E). Hard foreign bodies are removed using the index and middle fingers like tweezers or the index finger bent into a hook.

The “finger behind the teeth” technique is used in cases of tightly clenched jaws. The index finger of the left hand is inserted behind the molars and the mouth is opened while supporting the victim’s head with the right hand placed on the forehead (Fig. 5 A).

In the case of a completely relaxed lower jaw, insert the thumb of the left hand into the victim’s mouth and lift the root of the tongue with its tip. Other fingers grab the lower jaw in the chin area and push it forward (Fig. 5 B).

^ Rice. 4 Forced opening of the mouth using the crossed fingers method.

Rice. 5 Forced mouth opening

Restoration of airway patency can also be achieved using the Guedel airway (Fig. 6) and Safar (S-shaped airway) (Fig. 7).

Rice. 6 Technique for introducing the Guedel air duct

1. 
   Select the required size of the air duct - distance from the shield
   air duct to the earlobe (Fig. 6.1);
2. 
   After a forced opening of the mouth, the air duct is inserted convexly downward, sliding along the hard palate to the level of the shield;

^ Rice. 7 Technique for introducing the Safar air duct

The Safar air duct is used for mechanical ventilation using the mouth-to-air duct method.

These air ducts can be an adequate replacement for the two components of the “triple maneuver” - opening the mouth and protruding the lower jaw, but even with the use of air ducts, the third component - throwing back the head - is required. The most reliable method for sealing the airway is tracheal intubation.

As an alternative to endotracheal intubation, the use of a double-lumen Combitube airway (Fig. 8) or a laryngeal mask airway (Fig. 9) is recommended, as technically simpler compared to intubation, but at the same time reliable methods of airway protection, in contrast to the use of a face mask and airways.

Rice.8 Technique for introducing a double-lumen air duct Combitube. Patency of the airway is guaranteed regardless of the location of the airway tube - both in the esophagus and in the trachea.

A. After selecting the laryngomamask in accordance with the patient’s body weight and lubricating the cuff with one hand, the patient’s head is extended and the patient’s neck is flexed. The laryngomamask is taken like a pen for writing (with the aperture up), the tip of the mask is placed in the center of the front incisors on the inner surface of the oral cavity, pressing it against the hard palate. Using the middle finger, lower the lower jaw and inspect the oral cavity. Pressing the tip of the cuff, move the laryngomamask down (if the laryngomamask begins to turn outward, it should be removed and reinstalled);

B. Continue to move the laryngomamask down, while simultaneously pressing with the index finger in the area of ​​​​the connection between the tube and the mask, constantly maintaining pressure on the structures of the pharynx.
The index finger remains in this position until the mask passes next to the tongue and
do not go down the throat;

B. Using the index finger, resting on the junction of the tube and the mask, move the laryngomamask further down, while simultaneously performing a slight pronation with the hand. This allows you to quickly install it completely. The resistance that occurs means that the tip of the laryngomamask is located opposite the upper esophageal sphincter

D. Holding the laryngomamask tube with one hand, the index finger is removed from the pharynx. With the other hand, carefully pressing the laryngomask, check its installation.

D-e. The cuff is inflated and the laryngomamask is secured.

^ Rice. 8 Technique for introducing a laryngeal mask.

Stable side position

If the victim is unconscious, but has a pulse and maintains adequate spontaneous breathing, it is necessary to give a stable position on his side in order to prevent aspiration of gastric contents due to vomiting or regurgitation and perform a maneuver on the respiratory tract (Fig. 9).

^ Rice. 9 Stable position on the side of the unconscious victim

To do this, it is necessary to bend the victim’s leg on the side on which the person providing assistance is located (Fig. 9.1), put the victim’s hand under the buttock on the same side (Fig. 9.2). Then carefully turn the victim to the same side (Fig. 9.3), at the same time tilt the victim’s head back and hold him face down. Place his upper hand under his cheek to support his head position and avoid turning face down (Fig. 9.4). In this case, the victim’s hand behind his back will not allow him to assume a supine position.

Algorithm for providing assistance with obstruction of the respiratory tract by a foreign body

In case of partial obstruction of the airways (preservation of normal skin color, the patient's ability to speak and cough efficiency), immediate intervention is not indicated. In the event of complete airway obstruction (if the patient is unable to speak, cough is ineffective, there is increasing difficulty breathing, cyanosis), the following amount of assistance is recommended, depending on whether the patient is conscious or not:

^ Rice. 10 Technique for eliminating obstruction of the respiratory tract by a foreign substance in conscious persons

A) Conscious - 5 palm pats in the interscapular area (Fig. 10 A) or 5 abdominal compressions - Heimlich maneuver (Fig. 10 B). In the latter case, the resuscitator stands behind the victim, clenches one of his hands into a fist and applies it (with the side where the thumb is) to the stomach in the midline between the navel and the xiphoid process. Holding the fist tightly with the other hand, presses the fist into the stomach with quick upward pressure. The Heimlich maneuver is not performed in pregnant and obese persons, replacing it with chest compression, the technique of which is similar to that used for the Heimlich maneuver.

6) Unconscious:

1. 
   Open your mouth and try to remove the foreign body with your fingers.
2. 
   Diagnose the absence of spontaneous breathing (look, listen, feel).
3. 
   Give 2 artificial breaths using the mouth-to-mouth method. If it was possible to achieve restoration of airway patency within 5 attempts, following steps 1-3, proceed to point 6.1.
4. 
   In the event that attempts at mechanical ventilation (ALV) are unsuccessful even after changing the position of the head, chest compressions should be started immediately to relieve airway obstruction (as it creates a higher pressure in the airways, facilitating the removal of foreign material than patting in the interscapular area and the Heimlich maneuver, which are not recommended in unconscious persons).
5. 
   After 15 compressions, open your mouth and try to remove the foreign body, give 2 artificial breaths.
6. 
   Evaluate effectiveness.

1. 
   If there is an effect- determine the presence of signs of spontaneous circulation and, if necessary, continue chest compressions and/or artificial respiration.
2. 
   If there is no effect- repeat the cycle - steps 5-6.

After circulatory arrest and during CPR, the compliance of the lungs decreases. This in turn leads to an increase in the pressure required to inflate the optimal tidal volume into the patient's lungs, which, coupled with a decrease in pressure causing the gastroesophageal sphincter to open, allows air to enter the stomach, thereby increasing the risk of regurgitation and aspiration of gastric contents. Therefore, when performing mechanical ventilation using the mouth-to-mouth method, each artificial breath should not be forced, but should be carried out within 2 seconds to achieve the optimal tidal volume. In this case, the resuscitator must take a deep breath before each artificial breath in order to optimize the concentration of O 2 in the exhaled air, since the latter contains only 16-17 % O 2 and 3.5-4 % CO2. After carrying out the “triple maneuver” on the respiratory tract, one hand is placed on the victim’s forehead, ensuring that the head is thrown back and at the same time pinching the victim’s nose with his fingers, after which, tightly pressing his lips around the victim’s mouth, he blows air, following the excursion of the chest (Fig. 11 A ). If you see that the victim’s chest has risen, release his mouth, giving the victim the opportunity to make a full passive exhalation (Fig. 11 B).

^ Rice. 10 Technique for performing artificial respiration using the “mouth to mouth” method

The tidal volume should be 500-600 ml (6-7 ml/kg), respiratory rate - 10/min., in order to prevent hyperventilation. Studies have shown that hyperventilation during CPR, by increasing intrathoracic pressure, reduces venous return to the heart and reduces cardiac output, being associated with poor survival in these patients.

In the case of mechanical ventilation without airway protection, with a tidal volume equal to 1000 ml, the risk of air entering the stomach and, accordingly, regurgitation and aspiration of gastric contents is significantly higher than with a tidal volume equal to 500 ml. It has been shown that the use of low minute ventilation during mechanical ventilation can provide effective oxygenation during CPR. If air enters the stomach (protrusion in the epigastric region), it is necessary to remove the air. To do this, in order to avoid aspiration of gastric contents, the patient’s head and shoulders are turned to the side and the stomach area between the sternum and dome is pressed with a hand. Then, if necessary, the oral cavity and pharynx are cleaned, after which a “triple reception” is carried out on the respiratory tract and breathing continues “from mouth to mouth”.

Complications and errors during mechanical ventilation.

• 
  Clear airway is not ensured
• 
  Air tightness is not ensured

• 
  Underestimation (late start) or overestimation (start of CPR with intubation) of the value of mechanical ventilation

• 
  Lack of control over chest excursions
• 
  Lack of control over air entering the stomach
• 
  Attempts at drug stimulation of breathing

Precordial beat is performed when the resuscitator directly observes on the monitor the onset of ventricular fibrillation or pulseless ventricular tachycardia (VF/pulseless VT) and a defibrillator is not currently available. Only makes sense in the first 10 seconds of circulatory arrest. According to K. Groer and D. Cavallaro, a precordial blow sometimes eliminates VF/VT without a pulse (mainly VT), but most often it is not effective and, on the contrary, can transform the rhythm into a less favorable mechanism of circulatory arrest - asystole. Therefore, if the doctor has a defibrillator ready for use, it is better to refrain from precordial shock.

^ Chest compression. Two theories have been proposed to explain the mechanisms that maintain blood flow during chest compressions. The earliest was the heart pump theory(Fig. 11A), according to which blood flow is caused by compression of the heart between the sternum and the spine, as a result of which increased intrathoracic pressure pushes blood from the ventricles into the systemic and pulmonary beds. In this case, a prerequisite is the normal functioning of the atrioventricular valves, which prevent retrograde flow of blood into the atria. During the artificial diastole phase, the resulting negative intrathoracic and intracardiac pressure ensures venous return and filling of the ventricles of the heart. However, in 1980 J.T. Niemann, C.F. Babbs et al. discovered that cough, by increasing intrathoracic pressure, briefly maintains adequate cerebral blood flow. The authors called this phenomenon cough autoresuscitation. A deep, rhythmic, intense cough, with a frequency of 30-60 per minute, is capable of maintaining consciousness in trained patients (during cardiac catheterization) during the first 30-60 seconds from the moment of circulatory arrest, which is enough to connect and use a defibrillator.

^ Rice. 11 Theories explaining the mechanisms of chest compression

A. Heart pump theory; B. Breast pump theory

Subsequently, J. Ducas et al. (1983) showed that positive intrathoracic pressure is involved in the generation of systemic blood pressure. The authors measured blood pressure directly (in the radial artery) in a patient in a state of clinical death with refractory asystole during mechanical ventilation with an Ambu bag without chest compression. It was found that the pressure peaks in the curves were due to the rhythmic inflation of the lungs (Fig. 19).

Chest compression technique

1. 
   Correctly position the patient on a flat, hard surface.
2. 
   Determining the point of compression is palpation of the xiphoid process and retreating two transverse fingers upward, after which the hand is placed with the palmar surface on the border of the middle and lower third of the sternum, fingers parallel to the ribs, and the other on it (Fig. 20 A).

3. Proper compression: with your arms straightened at the elbow joints, using part of your body weight (Fig. 20 C).

During periods of cessation of mechanical ventilation, phasic pressure disappeared, indicating the ability of positive intrathoracic pressure to participate in the generation of systemic blood pressure.

These were the first works that made it possible to substantiate breast pump theory according to which, blood flow during chest compression is caused by an increase in intrathoracic pressure, creating an arteriovenous pressure gradient, and the pulmonary vessels act as a blood reservoir. The atrioventricular valves remain open during compression, and the heart acts as a passive reservoir rather than a pump. The thoracic pump theory was confirmed by transesophageal echocardiography data, according to which the valves remained open. On the contrary, in other studies using echocardiography, it was shown that at the time of compression systole the atrioventricular valves remain closed, but open during the artificial diastole phase.

Thus, it appears that both mechanisms are involved to varying degrees in the generation of blood circulation during CPR.

It should be noted that prolonged compression of the chest is accompanied by a progressive decrease in the mobility of the mitral valve, diastolic and systolic volumes of the left ventricle, as well as stroke volume, indicating a decrease in left ventricular compliance (compliance), up to the development of contracture of the heart muscle, i.e. the phenomenon of the so-called “heart of stone”.

^ The ratio of the number of compressions and the number of artificial breaths for both one and two resuscitators should be 30:2 .

Chest compression must be performed with frequency of 100 compressions/min., to a depth of 4-5 cm, synchronized with artificial respiration- pausing to perform it (it is unacceptable for non-intubated patients to inflate air at the time of chest compression - there is a danger of air getting into the stomach).

^ Signs of the correctness and effectiveness of chest compression are the presence of a pulse wave in the main and peripheral arteries.

To determine the possible restoration of independent blood circulation, every 4 ventilation-compression cycles, a pause is made (for 5 seconds) to determine the pulse in the carotid arteries.

^ Chest compression.

The fundamental problem with artificial circulatory support is the very low level (less than 30% of normal) cardiac output (CO) created during chest compression. Properly performed compression ensures the maintenance of systolic blood pressure at a level of 60-80 mm Hg, while diastolic blood pressure rarely exceeds 40 mm Hg and, as a result, causes low levels of cerebral (30-60% of normal) and coronary (5-20% from normal) blood flow. When performing chest compressions, coronary perfusion pressure increases only gradually and therefore, with each subsequent pause required for mouth-to-mouth breathing, it decreases rapidly. However, several additional compressions restore the original level of cerebral and coronary perfusion. In this regard, significant changes have occurred in relation to the chest compression algorithm. A compression to respiratory rate ratio of 30:2 has been shown to be more effective than 15:2 in providing the best balance between blood flow and oxygen delivery, and the following changes have been made to the ERC2005 guidelines:

A) the ratio of the number of compressions to the respiratory rate without airway protection as for one or two resuscitators should be 30:2 and carried out synchronously;

B) with respiratory tract protection (tracheal intubation, use of a laryngomamask or combitube) chest compression should be carried out with a frequency of 100 / min., ventilation with a frequency of 10 / min, asynchronously(because chest compression with simultaneous lung inflation increases coronary perfusion pressure).

Direct cardiac massage remains a more recent alternative. Despite the fact that direct cardiac massage provides a higher level of coronary and cerebral perfusion pressure (50% and 63-94% of normal, respectively) than chest compression, there is no data on its ability to improve the outcome of cardiac arrest, in addition, its use associated with more frequent complications. However, there are a number of direct indications for its implementation:

1. 
   The presence of an open chest in the operating room.
2. 
   Suspicion of viutrithoracic bleeding.
3. 
   Suspicion of impaired abdominal circulation due to compression of the descending thoracic aorta.
4. 
   Massive pulmonary embolism.
5. 
   Circulatory arrest due to hypothermia (allows direct warming of the heart).
6. 
   Failure of chest compressions to generate a pulse in the carotid and femoral arteries due to the presence of deformity of the chest bones or spine.
7. 
   Suspicion of a long period of undetected clinical death.

^ II. Further life support stage

D. Drug therapy

Route of administration of drugs.

A) Intravenous, into central or peripheral veins. The optimal route of administration is central veins - subclavian and internal jugular, since delivery of the administered drug to the central circulation is ensured. To achieve the same effect when administered into peripheral veins , drugs should be diluted in 10-20 ml of saline or water for injection.

B) Endotracheal : the dose of drugs is doubled and administered in a dilution of 10 ml of water for injection. In this case, more effective delivery of the drug can be carried out using a catheter passed through the end of the endotracheal tube. At the time of drug administration, it is necessary to stop chest compression, and to improve absorption, quickly pump air into the endotracheal tube several times.

^ Pharmacological support of resuscitation.

A) Adrenalin -1 mg every 3-5 minutes IV, or 2-3 mg per 10 ml of saline endotracheally.

B) Atropine - 3 mg IV once (this is enough to eliminate the vagal effect on the heart) for asystole and pulseless electrical activity associated with bradycardia (HR
V) Amiodarone (cordarone) is a first-line antiarrhythmic drug for
ventricular fibrillation/pulseless ventricular tachycardia (VF/VT), refractory to electrical impulse therapy after 3 ineffective shocks at an initial dose of 300 mg (diluted in 20 ml of saline or 5% glucose), if necessary, re-introduce 150 mg. Subsequently, continue intravenous drip administration at a dose of 900 mg for more than 24 hours.

D) Lidocaine - initial dose of 100 mg (1-1.5 mg/kg), if necessary, an additional bolus of 50 mg (the total dose should not exceed 3 mg/kg over 1 hour) - as an alternative in the absence of amiodarone. However, it should not be used as an adjunct to amiodarone.

E) Bicarbonate of soda Routine use during CPR or after ROSC is not recommended (although most experts recommend administering at pH

• 
  circulatory arrest associated with hyperkalemia or overdose of tricyclic antidepressants;
• 
  if there is no effect of SLCR for 20 - 25 minutes. after circulatory arrest if it is ineffective to restore independent cardiac activity.

H) Magnesium sulfate - if hypomagnesemia is suspected (8 mmol = 4 ml
50% solution).

AND) Calcium chloride - in a dose of 10 ml of 10% solution for hyperkalemia, hypocalcemia, overdose of calcium channel blockers.

^ D. Electrocardiographic diagnosis of the mechanismcirculatory arrest

The success of resuscitation measures largely depends on early ECG diagnosis (electrocardiograph or defibrillator monitor) of the mechanism of circulatory arrest, since this determines further tactics of resuscitation measures.

In resuscitation practice, ECG is used to evaluate ^ II standard lead, allowing to differentiate small-wave ventricular fibrillation from asystole.

Often, when recording an ECG from the defibrillator electrodes, VF may appear as asystole. Therefore, in order to avoid a possible error, it is necessary to change the location of the electrodes, moving them 90" relative to the original location. It should also be noted that during cardiopulmonary resuscitation, various types of interference often appear on the monitor (electrical; associated with uncontrolled movements of the patient during transportation, etc. .d.), which can significantly distort the ECG.

There are 3 main mechanisms of circulatory arrest: pulseless electrical activity (PEA), ventricular fibrillation or pulseless ventricular tachycardia (VF/pulseless VT), and asystole.

^ Indications for electrical cardiac defibrillation:

1. 
   Electrical activity without pulse (PEA), includes electromechanical dissociation and severe bradyarrhythmia (clinically, bradyarrhythmia manifests itself at heart rate
2. 
   ^ Pulseless ventricular tachycardia (pulseless VT) characterized by depolarization of ventricular cardiomyocytes with high frequency. The ECG shows no P waves and wide QRS complexes (Fig. 22).

^ 3) Ventricular fibrillation. Ventricular fibrillation is characterized by chaotic, asynchronous contractions of cardiomyocytes with the presence on the ECG of irregular, low-, medium- or large-amplitude oscillations with a frequency of 400-600 / min (Fig. 23).

^ Rice. 23 Ventricular fibrillation a) shallow wave; 6) medium wave;

c) large wave.

1. 
   Asystole- absence of both mechanical and electrical activity of the heart, with an isoline on the ECG.

^ Fig. 24 Asystole

E. Defibrillation.

The modern ERC2005 defibrillation algorithm recommends 1 initial shock instead of the three consecutive shock strategy of the earlier ERC2000 recommendations. If spontaneous circulation is not restored, a basic CPR complex is performed for 2 minutes. After which a second shock is administered, and if it is not effective, the cycle is repeated.

The first shock energy, which is currently recommended by ERC2005, should be 360 ​​J for monopolar defibrillators, as well as all subsequent shocks of 360 J. This contributes to a greater likelihood of depolarization of the myocardial critical mass. The initial energy level for bipolar defibrillators should be 150-200 J, with subsequent escalation of energy to 360 J with repeated shocks. With a mandatory rhythm assessment after each shock.

^ SHOCK → CPR FOR 2 MIN → SHOCK → CPR FOR

2 MINUTES...

The meaning of defibrillation is to depolarize the critical mass of the myocardium, leading to the restoration of sinus rhythm by the natural pacemaker (since the pacemaker cells of the sinus node are the first myocardial cells capable of depolarizing spontaneously). The energy level of the first discharge is a compromise between its effectiveness and the damaging effect on the myocardium. Only 4% of the transthoracic current passes through the heart, and 96% through the remaining structures of the chest. It has been shown that defibrillation in patients with prolonged untreated VF converts the rhythm to EABP/asystole in almost 60%. Secondary post-conversion EALD/asystole, compared with primary one, has a more unfavorable prognosis and low survival rate (0 - 2%).

In addition, defibrillation with high-energy shocks causes myocardial damage and the development of post-resuscitation myocardial dysfunction.

If more than 4-5 minutes have passed before electrical defibrillation for VF/VT without a pulse, disturbances occur in the functional state of cardiomycytes due to a decrease in the ATP content in the myocardium, hyperproduction of lactate and extracellular accumulation of Na +, which leads to a decrease in the contractile function of the myocardium . Therefore, carrying out defibrillation in this case can adversely affect the myocardium and sharply reduce the effectiveness of defibrillation, since an additional defibrillation discharge to a patient in a state of hypoxia can cause additional electrical damage to myocardial structures.

In this regard, according to the latest recommendations, in case of prolongation ^ Pulseless VF/VT> 4-5 minutes, initial chest compressions for 2 minutes are recommended, followed by electrical defibrillation.

The effectiveness and safety of electrical defibrillation depends on a number of cardiac and extracardiac factors.

Among the extracardiac factors the following can be distinguished:

1. 
   The leading place belongs to the form of the electrical impulse - to carry out successful defibrillation with a bipolar impulse (compared to a monopolar one), approximately 2 times less energy is required (the maximum energy allocated to the patient is, respectively, 200 J for biphasic and 400 J of monophasic discharges). According to recent data, the success of defibrillation with a bipolar sinusoidal pulse
2. 
   The second important factor influencing the effectiveness of defibrillation is the correct placement of the electrodes on the chest. Since only 4% of the transthoracic current passes through the heart, and 96% through the remaining structures of the chest, therefore their adequate location is very important (Fig. 25).

^ Rice. 25 Technique for electrical defibrillation using chest electrodes

A. Incorrectly placed electrodes: too close together, the current does not completely pass through the heart.

B. Correctly placed electrodes: greater distance between electrodes - more current passes through the heart.

B. One electrode is placed below the right clavicle along the parasternal line, the other - at the apex of the heart (below the left nipple), along the mid-axillary line.

In the anterior-anterior position, one electrode is installed at the right edge of the sternum under the collarbone, the second lateral to the left nipple along the mid-axillary line (Fig. 26A). In an anteroposterior position, one electrode is installed medial to the left nipple, the other under the left scapula (Fig. 26B). If the patient has an implanted pacemaker, the defibrillator electrodes should be located at a distance of about 6-10 cm from it.

Rice. 26 Location of electrodes during defibrillation A. Anterior-anterior option. B. Anterior-posterior - one electrode is installed medial to the left nipple, the other under the left scapula.

3) The third factor influencing the effectiveness of defibrillation is chest resistance or transthoracic resistance. The phenomenon of transthoracic impedance (resistance) is of important clinical significance, since it is it that explains the difference in current energy between that accumulated on the apparatus scale and that released to the patient. If during resuscitation there are factors that significantly increase the transthoracic impedance, then it is likely that with the energy set on the defibrillator scale of 360 J, its real value on the myocardium can be, at best, 10% (i.e. 30-40) J.

Transthoracic resistance depends on body weight and averages 70-80 Ohms in an adult. To reduce transthoracic resistance, defibrillation must be carried out during the expiratory phase, because transthoracic resistance under these conditions is reduced by 16%; the optimal force applied to the electrodes is considered to be 8 kg for adults and 5 kg for children aged 1-8 years. However, 84% of the reduction in transthoracic resistance comes from ensuring good interface contact between the skin and the electrodes through the use of conductive solutions. It must be emphasized that the use of “dry” electrodes significantly reduces the effectiveness of defibrillation and causes burns. To reduce the electrical resistance of the chest, special self-adhesive pads for electrodes, electrically conductive gel or gauze moistened with a hypertonic solution are used. In extreme situations, the surface of the electrode can simply be moistened with any conductive solution (water).

Thick hair on the chest causes poor contact of the electrodes with the patient's skin, and increases impedance, reducing thus. the effectiveness of the applied discharge, and also increases the risk of burns. Therefore, it is advisable to shave the area where the electrodes are applied to the chest. However, in an urgent situation during defibrillation, this is not always possible.

Thus, the mandatory fulfillment in clinical practice of, first of all, three basic conditions: the correct location of the electrodes, the force of application of the electrodes within 8 kg and the mandatory use of pads moistened with a hypertonic solution are important conditions for ensuring the effectiveness of electrical defibrillation.

^ During defibrillation, none of the resuscitation participants should touch the skin of the patient (and/or his bed).

Most Frequent errors during defibrillation:

A) incorrect location of the electrodes (in particular in women on the left breast it is necessary directly under it);

B) poor skin-electrode contact;

C) the use of small diameter electrodes (8 cm).

Prevention of recurrence of VF is one of the primary tasks after restoration of effective cardiac activity. Preventive therapy for recurrent VF should be differentiated whenever possible. The number of shocks to eliminate refractory (especially rapidly relapsing) VF is not limited if resuscitation measures are started in a timely manner and there remains hope for restoration of cardiac activity.

Until recently, lidocaine was considered the drug of first choice for the prevention and treatment of VF. At present, there is insufficient evidence to suggest that lidocaine is a useful adjunct to electrical defibrillation. At the same time, evidence has been obtained that an alternative to lidocaine is amiodarone (cordarone), which is recommended to be administered during early defibrillation (1-2 min VF), if the first three shocks are not effective, at a dose of 300 mg IV in a bolus once after the first dose adrenaline (greater success of revival compared to lidocaine); cordarone is recommended to be administered for recurrent VF with periods of a hemodynamically effective rhythm (administration of amiodarone, if necessary, can be repeated at a dose of 150 mg) in patients with severe dysfunction of the left ventricular myocardium, amiodarone is preferable to other antiarrhythmics; in these cases it is either more effective or less arrhythmogenic.

It should be noted that after discharges (especially maximum values), an “isoelectric” line is often recorded on the monitor screen for several seconds. This is usually a consequence of a quickly transient “stunning” of the electrical activity of the heart by a high-voltage discharge. In this situation, the “isoelectric” line should not be regarded as asystole, because followed by a coordinated rhythm or VF continues. At the same time, if a “straight” line lasting more than 5 seconds appears on the monitor after defibrillation (visually this is greater than the width of the defibrillator monitor screen), it is necessary to perform CPR for 2 minutes and then evaluate the rhythm and pulse. If asystole continues or any other pulseless rhythm (but not VF/VT) is detected, administer another dose of epinephrine and perform CPR for an additional 2 minutes, then reassess the rhythm and pulse. Further resuscitation tactics will depend on the type of electromechanical activity of the heart: stable (persistent) asystole, its transformation into VF/VT, development of EMD or hemodynamically effective rhythm.

The likelihood of a favorable outcome of CPR for EALD/asystole (as well as for refractory VF/VT) can only be increased if there are potentially reversible causes of circulatory arrest that can be treated. They are presented in the form of a universal algorithm “four G - four T”.

Delay in starting CPR

• 
  Lack of a single leader
• 
  Lack of constant monitoring of the effectiveness of ongoing activities
• 
  Lack of clear accounting of treatment measures and control over their implementation
• 
  Reassessment of CBS violations, uncontrolled infusion of NaHCO 3
• 
  Premature termination of resuscitation measures
• 
  Weakening of control over the patient after restoration of blood circulation and breathing.

^ Criteria for stopping resuscitation

1. 
   Restoration of independent blood circulation by the appearance of a pulse in the main arteries (then chest compression is stopped) and/or breathing (ventilation is stopped).
2. 
   Ineffectiveness of resuscitation during 30 min.

• 
  Hypothermia (hypothermia);
• 
  Drowning in ice water;
• 
  Overdose of medications or drugs;
• 
  Electrical injury, lightning damage.

^ III. Long-term life support stage

F-assessment of the patient's condition

The first task after restoration of spontaneous circulation is to assess the patient's condition. It can be conditionally divided into two subtasks: 1) determining the cause of clinical death (in order to prevent repeated episodes of circulatory arrest, each of which worsens the prognosis for the patient’s full recovery); 2) determination of the severity of disorders of homeostasis in general and brain functions in particular (in order to determine the volume and nature of intensive care). As a rule, the cause of clinical death is clarified even during the first two stages of cardiopulmonary and cerebral resuscitation, since it is often impossible to restore spontaneous circulation without this. Assessing the severity of homeostasis disorders also helps prevent repeated episodes of circulatory arrest, since severe disturbances in systems such as the respiratory and cardiovascular systems, as well as in water-electrolyte balance and acid-base balance, can themselves be causes of clinical death.

^ Ascertaining the death of a person based on a diagnosis of brain death

1. General information

Decisive for declaring brain death is the combination of the fact that the functions of the entire brain have ceased with proof of the irreversibility of this termination.

The right to establish a diagnosis of brain death is provided by the availability of accurate information about the causes and mechanisms of development of this condition. Brain death can develop as a result of primary or secondary brain damage.

Brain death as a result of its primary damage develops due to a sharp increase in intracranial pressure and the resulting cessation of cerebral circulation (severe closed craniocerebral injury, spontaneous and other intracranial hemorrhages, cerebral infarction, brain tumors, closed acute hydrocephalus, etc.), as well as due to open craniocerebral injury, intracranial surgical interventions on the brain, etc.

Secondary brain damage occurs as a result of hypoxia of various origins, incl. in case of cardiac arrest and cessation or sharp deterioration of systemic circulation, due to long-term shock, etc.

2. Conditions for establishing a diagnosis of brain death

The diagnosis of brain death is not considered until the following effects have been excluded: intoxication, including drugs, primary hypothermia, hypovolemic shock, metabolic endocrine coma, as well as the use of narcotics and muscle relaxants.

3. A set of clinical criteria, the presence of which is mandatory to establish a diagnosis of brain death

1. 
   Complete and persistent lack of consciousness (coma).
2. 
   Atony of all muscles.
3. 
   Lack of response to strong painful stimuli in the area of ​​the trigeminal points and any other reflexes that close above the cervical spinal cord.
4. 
   Lack of pupil reaction to direct bright light. It should be known that no medications that dilate the pupils were used. The eyeballs are motionless.

1. 
   Absence of corneal reflexes.
2. 
   Absence of oculocephalic reflexes.

3.7 Absence of oculovestibular reflexes.

To study oculovestibular reflexes, a bilateral caloric test is performed. Before performing this procedure, it is necessary to ensure that there is no perforation of the eardrums. The patient's head is raised 30 degrees above the horizontal level. A small catheter is inserted into the external auditory canal, and the external auditory canal is slowly irrigated with cold water (t + 20°C, 100 ml) for 10 s. With preserved brain stem function, after 20-25 s. Nystagmus or deviation of the eyes towards the slow component of nystagmus appears. The absence of nystagmus and deviation of the main apples during a caloric test performed on both sides indicates the absence of peri-vestibular reflexes.

1. 
   Absence of pharyngeal and tracheal reflexes, which are determined by the movement of the endotracheal tube in the trachea and upper respiratory tract, as well as by advancing the catheter in the bronchi for aspiration of secretions.
2. 
   Lack of spontaneous breathing.

A) to monitor the blood gas composition (PaO 2 and PaC0 2), one of the arteries of the limb must be cannulated;

B) before disconnecting the respirator, it is necessary to carry out mechanical ventilation for 10-15 minutes in a mode that ensures the elimination of hypoxemia and hypercapnia - FiO 2 1.0 (i.e. 100% oxygen), optimal PEEP (positive end-expiratory pressure);

B) after completing paragraphs. “a” and “b” the ventilator is turned off and humidified 100% oxygen is supplied to the endotracheal or tracheostomy tube at a rate of 8-10 liters per minute. During this time, endogenous carbon dioxide accumulates and is monitored by taking arterial blood samples. The stages of blood gas monitoring are as follows: before the test under mechanical ventilation; 10-15 minutes after the start of mechanical ventilation with 100% oxygen, immediately after disconnection from mechanical ventilation; then every 10 minutes until PaCO 2 reaches 60 mm Hg. Art. If at these and (or) higher values ​​of PaCO 2 spontaneous respiratory movements are not restored, the disconnection test indicates the absence of functions of the respiratory center of the brain stem. When minimal respiratory movements appear, mechanical ventilation is immediately resumed.

4. Additional (confirmatory) tests to the set of clinical criteria when establishing a diagnosis of brain death

4.1. Establishing the absence of electrical activity of the brain is carried out in accordance with the international provisions of electroencephalographic research in conditions of brain death. At least 8 needle electrodes are used, located according to the “10-20%” system and 2 ear electrodes. The interelectrode resistance must be at least 100 Ohms and no more than 10 kOhms, the interelectrode distance must be at least 10 cm. It is necessary to determine the safety of switching and the absence of unintentional or intentional creation of electrode artifacts. Recording is carried out on channels with a time constant of at least 0.3 s with a gain of at least 2 µV/mm (the upper limit of the frequency bandwidth is not lower than 30 Hz). Devices with at least 8 channels are used. EEG is recorded with bi- and monopolar leads. The electrical silence of the cerebral cortex under these conditions should remain for at least 30 minutes of continuous recording. If there is doubt about the electrical silence of the brain, repeated EEG registration is necessary. Assessing EEG reactivity to light, loud sound and pain: total stimulation time with light flashes, sound stimuli and painful stimuli
niyami for at least 10 minutes. The source of flashes, fired at a frequency of 1 to 30 Hz, should be located at a distance of 20 cm from the eyes. The intensity of sound stimuli (clicks) is 100 dB. The speaker is located near the patient's ear. Stimuli of maximum intensity are generated by standard photo- and phonostimulators. For painful stimulation, strong injections of the skin with a needle are used. An EEG recorded by telephone cannot be used to determine the electrical silence of the brain.

4.2. Determination of absence of cerebral circulation.

Contrast double panangiography of the four main vessels of the head (common carotid and vertebral arteries) is performed with an interval of at least 30 minutes. Mean arterial pressure during angiography should be at least 80 mm Hg.

If angiography reveals that none of the intracerebral arteries are filled with a contrast agent, this indicates cessation of cerebral circulation.

5. Duration of observation

In case of primary brain damage, to establish the clinical picture of brain death, the duration of observation should be at least 12 hours from the moment of the first establishment of the signs described in paragraphs 3.1-3.9; in case of secondary damage, observation should continue for at least 24 hours. If intoxication is suspected, the duration of observation is increased to 72 hours.

During these periods, the results of neurological examinations are recorded every 2 hours, revealing loss of brain functions in accordance with paragraphs. 3.1-3.8. It should be taken into account that spinal reflexes and automatisms can be observed under conditions of ongoing mechanical ventilation.

In the absence of functions of the cerebral hemispheres and brain stem and cessation of cerebral circulation according to angiography (section 4.2). brain death is declared without further observation.

6. Brain death diagnosis and documentation

6.1 The diagnosis of brain death is established by a commission of doctors consisting of: a resuscitator (anesthesiologist) with at least 5 years of experience in the intensive care unit and a neurologist with the same experience in the specialty. To conduct special research, the commission includes specialists in additional research methods with at least 5 years of experience in their specialty, including those invited from other institutions on an advisory basis. The appointment of the composition of the commission and approval of the “Protocol for establishing brain death” is made by the head of the intensive care unit where the patient is located, and during his absence by the responsible doctor on duty at the institution.

The commission cannot include specialists involved in organ retrieval and transplantation.

The main document is the “Protocol for Determining Brain Death,” which is important for all conditions, including organ removal. The “Protocol” must indicate the data of all studies, the surnames, first names and patronymics of the doctors - members of the commission, their signatures, the date and hour of registration of brain death and, consequently, the death of a person.

After brain death has been established and a “Protocol” has been drawn up, resuscitation measures, including mechanical ventilation, may be discontinued.

Responsibility for diagnosing a person’s death lies entirely with the doctors who determine brain death at the medical institution where the patient died.

^ H - Restoring normal thinking

I - Intensive therapy aimed at correcting impaired functions of other organs and systems

Post-resuscitation illness- this is a specific pathological condition that develops in the patient’s body as a result of ischemia caused by a total disturbance of blood circulation and reperfusion after successful resuscitation and is characterized by severe disorders of various parts of homeostasis against the background of impaired integrative function of the central nervous system.

During the clinical picture of post-resuscitation illness, 5 stages are distinguished (according to E.S. Zolotokrylina, 1999):

Stage I(6-8 hours of post-resuscitation period) is characterized by instability of the basic functions of the body. Main features: a 4-5-fold decrease in tissue perfusion, despite the stabilization of blood pressure at a safe level, the presence of circulatory hypoxia - a decrease in PvO 2 with relatively normal PaO 2 and SaO 2 values, with a simultaneous decrease in CaO 2 and CvO 2 due to anemia; lactic acidosis; increasing the level of fibrinogen degradation products (FDP) and soluble fibrin-monomer complexes (SFMC), which are absent normally.

^ Stage II(10-12 hours of post-resuscitation period) is characterized by stabilization of the basic functions of the body and an improvement in the condition of patients, although often temporary.

Severe disturbances in tissue perfusion and lactic acidosis persist, there is a further tendency to increase the level of PDP and the level of RKFM significantly increases, the fibrinolytic activity of plasma slows down - signs of hypercoagulation. This is the stage of “metabolic storms” with symptoms of severe hyperenzymemia.

^ Stage III(end of the 1st - 2nd day of the post-resuscitation period) - characterized by repeated deterioration of the patients’ condition according to the dynamics of clinical and laboratory data. First of all, hypoxemia develops with a decrease in PaO 2 to 60-70 mmHg, shortness of breath up to 30/min, tachycardia, increased blood pressure to 150/90-160/90 mmHg in young and middle-aged people, anxiety. Those. signs of acute pulmonary injury syndrome or acute respiratory distress syndrome (ARDS/ARDS) appear, with increasing shunting of the blood. Thus, the already existing gas exchange disorder deepens with the formation of mixed type hypoxia.

The most pronounced signs of DIC syndrome are: thrombinemia, hypercoagulation, an increase in the level of PDP against the background of a progressive decrease in the fibrinolytic activity of blood plasma, leading to the development of microthrombosis and blocking of organ microcirculation.

Damage to the kidneys (36.8%), lungs (24.6%) and liver (1.5%) prevails, however, all these disorders are still functional in nature and, therefore, are reversible with adequate therapy.

^ Stage IV(3-4 days of the post-resuscitation period) - has a twofold course: 1) either it is a period of stabilization and subsequent improvement of body functions with recovery without complications; 2) or this is a period of further deterioration in the condition of patients with an increase in multiple organ failure syndrome (MODS) due to the progression of the systemic pro-inflammatory response. It is characterized by hypercatabolism, the development of interstitial edema of the tissue of the lungs and brain, subcutaneous tissue, deepening hypoxia and hypercoagulation with the development of signs of multiple organ failure: bleeding from the gastrointestinal tract, psychosis with hallucinatory syndrome, secondary heart failure, pacreatitis and liver dysfunction.

Stage V(5-7 days or more of the post-resuscitation period) - develops only with an unfavorable course of the post-resuscitation period: progression of inflammatory purulent processes (massive pneumonia, often abscessed, suppuration of wounds, peritonitis in operated patients, etc.), generalization of infection - development of septic syndrome, despite for early adequate antibiotic therapy. At this stage, a new wave of damage to parenchymal organs develops, and degenerative and destructive changes already take place. Thus, fibrosis develops in the lungs, sharply reducing the respiratory surface, which leads to the irreversibility of a critical condition.

Posthypoxic encephalopathy is the most common variant of the course of post-resuscitation syndrome, manifesting itself to one degree or another in all patients who have suffered circulatory arrest. There was a 100% correlation between the absence of cough and/or corneal reflexes 24 hours after resuscitation with poor cerebral outcome.

^ Management of the post-resuscitation period.

Extracerebral homeostasis. After restoration of spontaneous circulation, therapy in the post-resuscitation period should be based on the following principles:

1. 
   Immediately after restoration of independent circulation, cerebral hyperemia develops, but after 15-30 minutes. After reperfusion, total cerebral blood flow decreases and hypoperfusion develops. And since the autoregulation of cerebral blood flow is disrupted, its level depends on the level of mean arterial pressure (MAP). In the first 15 - 30 minutes of the post-resuscitation period, it is recommended to provide hypertension (SBP 150 - 200 mm Hg) for 1 - 5 minutes, followed by maintaining normotension (both severe hypotension and hypertension must be corrected).
2. 
   Maintaining normal levels of PaO 2 and PaCO 2.
3. 
   Maintaining normothermia of the body. The risk of poor neurological outcome increases for every degree >37°C.
4. 
   Maintaining normoglycemia (4.4-6.1 mmol/l) - persistent hyperglycemia is associated with poor neurological outcome. The threshold level upon reaching which it is necessary to begin correction with insulin is 6.1-8.0 mmol/l.
5. 
   Hematocrit level in the range of 30 - 35% - soft hemodilution, which ensures a decrease in blood viscosity, which increases significantly in the microvasculature as a consequence of ischemia.
6. 
   Control seizure activity by administering benzodiazepines.

A) Pharmacological methods. At the moment, from the point of view of evidence-based medicine, there are no effective and safe methods of pharmacological effects on the brain in the post-resuscitation period.

The conducted studies made it possible to establish the feasibility of using perftoran in the post-resuscitation period. Perftoran reduces cerebral edema, the severity of post-resuscitation encephalopathy and increases the activity of the cerebral cortex and subcortical structures, facilitating rapid recovery from a comatose state. Perftoran is recommended to be administered in the first 6 hours of the post-resuscitation period at a dose of 5-7 ml/kg.

In order to carry out neuroprotective therapy in the post-resuscitation period, it is recommended to use the drug Somazina (citicoline), which has a neurorestorative effect due to the activation of the biosynthesis of membrane phospholipids of brain neurons and, first of all, phosphatidylcholine, an antioxidant effect - by reducing the content of free fatty acids and inhibiting ischemic phospholipases cascade, as well as a neurocognitive effect, due to an increase in the synthesis and release of acetylcholine, as the main neurotransmitter of numerous cognitive functions. Somazine is prescribed at a dose of 500 - 1000 mg 2 times/day intravenously, followed by a transition to the oral route of administration 200 mg 3 times/day in the recovery period.

B) Physical methods. Unconscious patients who have suffered circulatory arrest in out-of-hospital conditions due to the mechanism of ventricular fibrillation must be provided with body hypothermia to 32-34 0 C for 12-24 hours. It is also indicated that this same hypothermia regimen may be effective in patients with other arrest mechanisms and in cases of in-hospital circulatory arrest.

Therapy of cerebral edema-swelling after resuscitation

Pathophysiological mechanisms of brain damage after circulatory arrest and resuscitation include primary damage due to the development of global ischemia and secondary damage in the form of a proinflammatory reaction during and after CPR, as a component of post-resuscitation illness.

In patients in the post-resuscitation period, the development of diffuse cerebral edema can be diagnosed using computed tomography or magnetic resonance imaging. Moreover, the post-resuscitation period is more characterized by the development of predominantly cytotoxic cerebral edema, i.e. the development of intracellular edema (neurons, glial cells) with the preservation of an intact blood-brain barrier (BBB).

^ CEREBRAL EDEMA

The goal of decongestant therapy is: a) reducing ICP; b) maintaining adequate CPP; c) preventing secondary brain damage due to swelling.

Decongestant therapy should be built on the following principles:

• 
  limiting the volume of administered infusion media (administration of 5% glucose is unacceptable);
• 
  exclusion of factors that increase ICP (hypoxia, hypercapnia, hyperthermia):
• 
  normoventilation and normoxia: p a CO 2 34-36 mm Hg, p v CO 2 40-44 mm Hg, S a O 2 =96%: on mechanical ventilation: alveolar ventilation (AV) AB = 4.8 – 5, 2 l/min., AB = MOD – (RR·150 ml), where MOD is the minute volume of respiration, RR is the respiratory frequency;
• 
  giving an elevated position (20-30 0) to the head end of the bed (patients with severe stroke do not turn their heads to the sides in the first 24 hours);
• 
  If ICP monitoring is available, cerebral perfusion pressure (CPP) should be maintained >70 mm Hg (CPP = SBP - ICP, mm Hg, so SBP = 70 + ICP, mm Hg.

• 
  GCS > 12 points: ICP = 10, SBP = 80, mmHg;
• 
  GCS = 8 – 12 points: ICP = 15, SBP = 85, mmHg;
• 
  GCS 20, SBP = 95 – 100, mmHg)

Hyperosmolar solutions. These drugs mobilize free fluid into the intravascular space and reduce intracranial pressure.

A) mannitol - 25-50 g (0.25-0.5 g/kg) (1370 mOsmol/l) every 3-6 hours (osmotherapy is effective for 48-72 hours), under the control of plasma osmolarity (should not exceed 320 mOsm/l). It has been shown that the decongestant effect is achieved when using the indicated moderate doses of the drug, because the use of high doses of mannitol (1.5 g/kg) leads to a paradoxical increase in cerebral edema due to the accumulation of osmotically active particles in the brain substance, due to damage to the BBB or when the administration of this drug is prolonged for more than 4 days. Mannitol reduces ICP by 15-20%, increases CPP by 10% and, unlike furosemide, improves cerebral blood flow by reducing hematocrit, increasing volumetric cerebral blood flow, by mobilizing extracellular fluid and improving the rheological properties of blood by reducing blood viscosity by 16% ( furosemide, on the contrary, increases blood viscosity by 25%):

B) rheosorbilact (900 mosmol/l), sorbilact (1670 mosmol/l) at a dose of 200-400 ml/day;

• 
  furosemide - bolus 40 mg intravenously;
• 
  L-lysine escinate is a complex of water-soluble salt of escin saponin from horse chestnut seeds and the amino acid L-lysine. In blood serum, L-lysine aescinate salt quickly dissociates into lysine and aescin ions. Escin protects glycosaminoglycans in the walls of microvessels and the surrounding connective tissue from destruction by lysosomal hydrolases, normalizing increased vascular tissue permeability and providing an antiexudative and rapid decongestant effect. The drug is administered strictly intravenously in a dose of 10 ml (8.8 mg of escin) 2 times in the first 3 days, then 5 ml - 2 times a day. The maximum daily dose of the drug should not exceed 25 ml - 22 mg of escin. The course is until a lasting clinical effect is obtained, usually 7-8 days.

1. 
   Writing an abstract based on a review of modern literature data regarding the pathophysiology of circulatory arrest and the latest developments in methods for restoring spontaneous circulation and higher cerebral functions in the post-resuscitation period.

1. 
   Clinical signs of preagonia, terminal pause and agony.
2. 
   Signs of clinical and biological death.
3. 
   Factors in the development of clinical death and the reliability of the resumption of spontaneous circulation with different mechanisms of its arrest.
4. 
   Stages of cardiopulmonary and cerebral resuscitation according to P. Safar.
5. 
   Modern methods of basic life support.
6. 
   Methods for restoring and maintaining airway patency during resuscitation measures.
7. 
   Medicines used for continued life support and routes of their administration.
8. 
   Types of circulatory arrest and features of measures to restore spontaneous circulation.
9. 
   Methodology and safety precautions for defibrillation.
10. 
    Criteria for terminating resuscitation measures.
11. 
    Clinical and laboratory methods for diagnosing brain death.
12. 
    Auxiliary methods for diagnosing brain death.
13. 
    Post-resuscitation illness - definition and stages.
14. 
    Stages of recovery from a comatose state after clinical death.
15. 
    General principles of intensive care of post-resuscitation illness.

1. 
   Watching educational videos:

• 
  Padre reanimazzioni (about academician V.O. Negovsky).
• 
  Cardiopulmonary resuscitation: basic life support.
• 
  Cardiopulmonary resuscitation: basic life support using an automatic defibrillator.
• 
  Apallic syndrome.
• 
  Diagnosis of brain death.

1. 
   Mastering practical CPR skills on a mannequin:

• 
  performing the triple maneuver of P. Safar;
• 
  use of pipelines;
• 
  use of a face mask or “key of life”;
• 
  performing shvl using the “mouth to mouth” and “mouth to nose” methods;
• 
  performing SHVL on a baby dummy using the “mouth to mouth and nose” method;
• 
  performing chest compressions on an adult mannequin;
• 
  performing chest compressions on a baby dummy;
• 
  performing indirect massage using a cardio pump;
• 
  performing basic life support by two resuscitators;
• 
  performing defibrillation on a mannequin;
• 
  using an automatic defibrillator on a mannequin.

1. 
   Determining the type of circulatory arrest using an ECG
2. 
   Solving clinical situations with circulatory arrest using the “Cardiac Arrest!” simulator program. (or analogues).
3. 
   Diagnosis of “brain death”:

• 
  in the intensive care unit and resuscitation department for patients with atonic comma;
• 
  in the training room (in the absence of patients with extreme comma) when analyzing educational copies of medical histories.

A) Main:

1. 
   Anesthesiology and intensive care: Pidruchnik / L.P. Chepkiy, L.V. Novitska-Usenko, R.O. Tkachenko. – K.: Vishcha School, 2003. – 399 p.
2. 
   Usenko L.V., Tsarev A.V. Cardiopulmonary and cerebral resuscitation. Dnepropetrovsk: 2008. – 43 p.
3. 
   Neuroreanimatology: neuromonitoring, principles of intensive care, neurorehabilitation: [monograph]/ ed. Corresponding member NAS and AMS of Ukraine, Dr. med. sciences, prof. L.V. Usenko and Doctor of Science, prof. L.A. Maltseva. – Volume 2. – Dnepropetrovsk: ART-PRESS, 2008. – 278 p.

1. 
   Negovsky V.A., Gurvich A.M., Zolotokrylina E.S. Post-resuscitation illness. M.: Medicine, 1987. – 480 p.
2. 
   Starchenko A.A. Clinical neuroreanimatology. SPb: SPb med. publishing house, 2002. – 672 p.