Air duct medical application. Oropharyngeal airway insertion algorithm

Rice. 2 "Chain of Survival"

1. 
   Early activation of the ambulance service.
2. 
   Early onset of basic life support (stages A-B-C).
3. 
   Early defibrillation using automatic external defibrillators (Automated external defibrillators - AED).
4. 
   Early onset of further life support, including intubation and drug use.

1. 
   ^ STAGES OF CARDIO-PULMONARY AND CEREBRAL

P. Safar divided the whole complex of SLCR 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 breath.
3. 
   Artificial maintenance of blood circulation.

The goal is to restore spontaneous circulation

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

Purpose - cerebral resuscitation and post-resuscitation intensive

therapy

1. 
   Assessment of the condition (determination of the cause of circulatory arrest and its elimination) and the possibility of a full-fledged rescue of the patient, taking into account the degree of damage to the central nervous system.
2. 
   Restoration of normal thinking.
3. 
   Intensive therapy aimed at correcting impaired functions of other organs and systems.

Rice. 3 Airway management techniques

A. Control and restoration of airway patency

The "gold standard" for ensuring the patency of the respiratory tract is the "triple reception" according to P. Safar and tracheal intubation.

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

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

P. Safar developed a "triple dose" on the respiratory tract, including: tilting the head, opening the mouth and pushing the lower jaw forward(Fig. 3 D, C). Alternative methods of restoring airway patency are shown in fig. 3 B and 3 D.

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

1. 
   For car accidents(a person was hit by a car or was in a car during a collision);

1. 
   ^ When falling from a height (including the "divers").

Throwing the head back alone does not guarantee the restoration of airway patency. So, in 1/3 of unconscious patients, due to muscle atony, the nasal passages during exhalation are closed by a soft palate that moves like a valve. In addition, there may be a need to remove a foreign substance contained in the oral cavity (blood clots, vomit, fragments of teeth, etc.). Therefore, first of all, in persons with injuries, it is necessary to conduct an audit of 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 with the help of 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 pressed on the upper teeth, then the thumb is placed opposite the index finger on the lower teeth (Fig. 4 B) and the mouth is forcefully opened. In this way, a significant spreading force can be achieved, allowing the mouth to be opened and the oral cavity to be examined. In the presence of foreign bodies, 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. 4B). The right index finger is used to pull the right corner of the mouth down, which facilitates self-drainage of the oral cavity from liquid contents (Fig. 4 D). With one or two fingers wrapped in a handkerchief or other cloth, they clean the mouth and throat (Fig. 4 E). Solid foreign bodies are removed with the help of the index and middle fingers like tweezers or the index finger bent in the form of a hook.

Reception "finger behind the teeth" is used in the case of tightly clenched jaws. The index finger of the left hand is inserted behind the molars and the mouth is opened while resting on the head of the victim with the right hand placed on the forehead (Fig. 5 A).

In the case of a completely relaxed lower jaw, the thumb of the left hand is inserted into the mouth of the victim and the root of the tongue is lifted 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 by the method of crossed fingers.

Rice. 5 Forced mouth opening

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

Rice. 6 Guedel airway insertion technique

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

^ Rice. 7 Safar air duct insertion technique

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

These air ducts can be an adequate replacement for the two components of the "triple move" - ​​opening the mouth and protruding the lower jaw, but even with the use of air ducts, a third component, head tilting, is required. Tracheal intubation is the most reliable method for sealing the airways.

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

Rice.8 Double lumen duct insertion technique combitube. Airway patency is guaranteed at any location of the airway tube - both in the esophagus and in the trachea.

a. After selecting the laryngomask in accordance with the patient's body weight, lubricating the cuff with one hand, the patient's head is extended and the patient's neck is flexed. The laryngomask is taken as a writing pen (aperture upwards), the tip of the mask is placed in the center of the anterior incisors on the inner surface of the oral cavity, pressing it against the hard palate. Lower the lower jaw with the middle finger and examine the oral cavity. Pressing the tip of the cuff, move the laryngomask down (if the laryngomask begins to turn outward, it should be removed and reinstalled);

B. Continue to hold the laryngomask down, while pressing with the index finger in the area of ​​\u200b\u200bthe connection of 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;

C. With the index finger, leaning on the junction of the tube and the mask, the laryngomask is advanced further down, while performing a slight pronation with the brush. This allows you to quickly install it to the end. The resulting resistance means that the tip of the laryngomask is located opposite the upper esophageal sphincter

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

D-e. The cuff is inflated and the laryngomask is fixed.

^ Rice. 8 Technique for introducing a laryngeal mask.

Stable position on the side

If the victim is unconscious, but he has a pulse and adequate spontaneous breathing is maintained, 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 take it on the respiratory tract (Fig. 9).

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

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 it face down. Place his overhead hand under his cheek to maintain head position and avoid turning face down (Figure 9.4). At the same time, the hand of the victim, located behind his back, will not allow him to assume a supine position.

Algorithm for assisting with obturation of the respiratory tract by a foreign body

In case of partial airway obstruction (maintenance of normal skin color, the patient's ability to speak and the effectiveness of coughing), 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 in breathing, cyanosis), the following amount of assistance is recommended, depending on the presence or absence of consciousness in the patient:

^ Rice. 10 Technique for removing airway obstruction with foreign matter in conscious individuals

a) Conscious - 5 pats with the palm in the interscapular region (Fig. 10 A) or 5 abdominal compressions - the Heimlich maneuver (Fig. 10 B). In the latter case, the resuscitator stands behind the victim, compresses one of his hands into a fist and applies (with the side where the thumb is located) to the stomach along the midline between the navel and the xiphoid process. Firmly clasping the fist with the other hand, he presses the fist into the stomach with a quick upward pressure. The Heimlich maneuver is not performed in pregnant and obese individuals, replacing it with chest compressions, the technique of which is similar to that of 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. 
   Perform 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 step 6.1.
4. 
   In the event that attempts to administer artificial lung ventilation (ALV) are unsuccessful even after changing the position of the head, chest compressions should be started immediately to eliminate airway obstruction (because it creates a higher airway pressure to help remove foreign matter than patting in the interscapular region 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, make 2 artificial breaths.
6. 
   Evaluate efficiency.

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 - points 5-6.

After circulatory arrest and during CPR, there is a decrease in compliance (compliance) of the lungs. This in turn leads to an increase in the pressure required to insufflate an optimal tidal volume into the patient's lungs, which, against the background of a decrease in pressure, causing the gastroesophageal sphincter to open, allows air to enter the stomach, thus increasing the risk of regurgitation and aspiration of gastric contents. Therefore, when performing mechanical ventilation by the "mouth-to-mouth" method, each artificial breath should not be forced, but carried out for 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 % About 2 and 3.5-4 % CO2. After carrying out the "triple reception" on the respiratory tract, one hand is located on the forehead of the victim, providing tilting of the head and at the same time pinching the victim's nose with his fingers, after which, tightly pressing his lips around the victim's mouth, blows in air, following the excursion of the chest (Fig. 11 A ). If you see that the victim's chest has risen, let go of his mouth, giving the victim the opportunity to make a full passive exhalation (Fig. 11 B).

^ Rice. 10 Mouth-to-mouth artificial respiration technique

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

In the case of mechanical ventilation without airway protection, with a tidal volume of 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 of 500 ml. It has been shown that the use of low minute ventilation during mechanical ventilation can provide effective oxygenation during CPR. If air is noticed in 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 dose” is performed on the airways and breathing is continued “from mouth to mouth”.

Complications and errors during IVL.

• 
  Unobstructed airway patency
• 
  Air tightness not ensured

• 
  Underestimate (late start) or overestimate (start CPR with intubation) the value of ventilation

• 
  Lack of control of chest excursions
• 
  Lack of control of air entering the stomach
• 
  Attempts to medically stimulate breathing

precordial strike carried out when the resuscitator directly observes the onset of ventricular fibrillation or pulseless ventricular tachycardia (VF/Pulseless VT) on the monitor, 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 beat 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 ensure blood flow during chest compressions. The earliest was the theory of the heart pump(Fig. 11A), according to which blood flow is due to compression of the heart between the sternum and spine, resulting in increased intrathoracic pressure pushes blood out of the ventricles into the systemic and pulmonary channels. In this case, a prerequisite is the normal functioning of the atrioventricular valves, which prevent the retrograde flow of blood into the atria. In the phase of artificial diastole, the emerging negative intrathoracic and intracardiac pressure ensures venous return and filling of the ventricles of the heart. However, in 1980 J.T. Niemann, C.F. Babs et al. discovered that coughing, by increasing intrathoracic pressure, briefly maintains adequate cerebral blood flow. The authors called this phenomenon cough autoresuscitation. A deep rhythmic increased cough, with a frequency of 30-60 per minute, is able to maintain consciousness in trained patients (during cardiac catheterization) during the first 30-60 seconds from the onset of circulatory arrest, which is enough to connect and use a defibrillator.

^ Rice. 11 Theories explaining the mechanisms of chest compression

A. Theory of the heart pump; 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 the direct method (in the radial artery) of blood pressure 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 on the curves are due to the rhythmic inflation of the lungs (Fig. 19).

Technique for chest compressions

1. 
   Proper laying of the patient on a flat hard surface.
2. 
   Determination of the compression point - palpation of the xiphoid process and retreat two transverse fingers up, after which the hand is placed with the palmar surface on the border of the middle and lower thirds of the sternum, fingers parallel to the ribs, and the other on it (Fig. 20 A).

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

During periods of cessation of mechanical ventilation, phase pressure disappeared, which indicated 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 due to an increase in intrathoracic pressure, which creates an arterio-venous 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. Confirmation of the theory of the chest pump was the data of transesophageal echocardiography, 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, and open during artificial diastole.

Thus, both mechanisms seem to be involved to some extent in the generation of blood circulation during CPR.

It should be noted that prolonged chest compression is accompanied by a progressive decrease in mitral valve mobility, 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. phenomena of the so-called "stone heart".

^ The ratio of compressions to rescue breaths for both one and two rescuers should be 30:2 .

Chest compression should be performed with a frequency of 100 compressions / min., to a depth of 4-5 cm, synchronized with artificial respiration- making a pause for its implementation (it is unacceptable for non-intubated patients to carry out air injection at the time of chest compression - there is a risk of air entering the stomach).

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

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

^ Chest compression.

The fundamental problem of artificial circulatory support is the very low level (less than 30% of normal) of cardiac output (CO) created by chest compressions. Properly performed compression ensures the maintenance of systolic blood pressure at the level of 60-80 mm Hg, while diastolic blood pressure rarely exceeds 40 mm Hg and, as a result, causes a low level of cerebral (30-60% of normal) and coronary (5-20% from normal) blood flow. During chest compressions, coronary perfusion pressure increases only gradually, and therefore, with each successive pause necessary for mouth-to-mouth breathing, it decreases rapidly. However, several additional compressions lead to the restoration of the initial level of cerebral and coronary perfusion. In this regard, significant changes have occurred in relation to the algorithm for performing chest compressions. A compression to respiratory rate ratio of 30:2 has been shown to be more effective than 15:2 in providing the most optimal ratio 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, and for two resuscitators should be 30:2 and carried out in sync;

B) with airway protection (tracheal intubation, use of a laryngomask or combitube) chest compressions should be given at a rate of 100/min, ventilation at a rate of 10/min, asynchronous(because chest compressions with concomitant lung inflation increase 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 (respectively 50% and 63-94% of the norm) than chest compression, however, there is no data on its ability to improve the outcome of LPCR, 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 intrathoracic bleeding.
3. 
   Suspicion of a violation of the abdominal circulation, due to clamping of the descending thoracic aorta.
4. 
   Massive pulmonary embolism.
5. 
   Circulatory arrest against the background of hypothermia (allows for direct warming of the heart).
6. 
   The inability of chest compressions to generate a pulse on the carotid and femoral arteries due to the presence of deformity in the bones of the chest or spine.
7. 
   Suspicion of a long period of unnoticed clinical death.

^ II. Further life support stage

D. Drug therapy

Route of drug administration.

BUT) Intravenous, into central or peripheral veins. The optimal route of administration is central veins - subclavian and internal jugular, since the delivery of the administered drug to the central circulation is ensured. To achieve the same effect when introducing 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, a 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 administration of the drug, it is necessary to stop chest compression, and to improve absorption, quickly inject air into the endotracheal tube several times.

^ Pharmacological support of resuscitation.

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

B) Atropine - 3 mg IV once (sufficient to eliminate vagal influence on the heart) for asystole and pulseless electrical activity associated with bradycardia (HR
in) Amiodarone (Cordarone) is a first-line antiarrhythmic drug for
ventricular fibrillation/pulseless ventricular tachycardia (VF/VT) refractory to electrical impulse therapy after 3 ineffective discharges at an initial dose of 300 mg (diluted in 20 ml of saline or 5% glucose), if necessary, re-administer 150 mg. Subsequently, continue intravenous drip 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, additional bolus of 50 mg (in this case, the total dose should not exceed 3 mg / kg for 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 restoration of spontaneous circulation is not recommended (although most experts recommend administration at pH

• 
  circulatory arrest associated with hyperkalemia or an overdose of tricyclic antidepressants;
• 
  in the absence of the effect of SLCR for 20 - 25 minutes. after circulatory arrest in case of its ineffectiveness for the restoration of independent cardiac activity.

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

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

^ D. Electrocardiographic diagnosis of the mechanismcirculatory arrest

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

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

Often, when registering an ECG from the electrodes of a defibrillator, VF may look like asystole. Therefore, in order to avoid possible errors, 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 kinds 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 (PEAP), ventricular fibrillation or pulseless ventricular tachycardia (pulseless VF/VT), and asystole.

^ Indications for electrical defibrillation of the heart:

1. 
   Pulseless Electrical Activity (EABP), includes electromechanical dissociation and severe bradyarrhythmia (clinically, bradyarrhythmia manifests itself with heart rate
2. 
   ^ Pulseless Ventricular Tachycardia (Pulseless VT) characterized by depolarization of ventricular cardiomyocytes with a high frequency. There are no P waves on the ECG and wide QRS complexes are noted (Fig. 22).

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

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

c) large-wave.

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

^ Fig. 24 Asystole

E. Defibrillation.

The current ERC2005 defibrillation algorithm recommends an initial 1 shock instead of the three consecutive shocks strategy of the earlier ERC2000 recommendations. In case of non-restoration of spontaneous blood circulation, a basic CPR complex is performed for 2 minutes. After that, a second discharge is carried out, and in case of inefficiency, the cycle is repeated.

The energy of the first shock, 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 critical mass of the myocardium. The initial energy level for bipolar defibrillators should be 150-200 J, followed by energy escalation to 360 J with repeated discharges. With a mandatory assessment of the rhythm after each discharge.

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

2 MINUTES...

The meaning of defibrillation is to depolarize the critical mass of the myocardium, leading to the restoration of sinus rhythm by a 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 damaging effects on the myocardium. Only 4% of the transthoracic current passes through the heart, and 96% through the rest of the chest structures. 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 to primary, has a worse prognosis and a low survival rate (0 - 2%).

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

If more than 4-5 minutes have passed before the moment of electrical defibrillation during VF/VT without a pulse, disturbances occur in the functional state of cardiomycytes due to a decrease in the content of ATP in the myocardium, hyperproduction of lactate and extracellular accumulation of Na +, which leads to a decrease in the contractile function of the myocardium . Therefore, defibrillation in this case can adversely affect the myocardium and sharply reduce the effectiveness of defibrillation, since additional application of a 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 ^ VF/VT without pulse> 4-5 minutes, an initial 2-minute chest compression followed by electrical defibrillation is recommended.

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 an electrical impulse - for 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 for monophasic discharges). According to the latest data, the success of defibrillation with a bipolar sinusoidal pulse
2. 
   The second important factor affecting 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 rest of the structures of the chest, therefore, their adequate location is very important (Fig. 25).

^ Rice. 25 Technique for electrical defibrillation using chest electrodes

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

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

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

With an anterior-anterior location, one electrode is placed at the right edge of the sternum under the clavicle, the second is lateral to the left nipple along the mid-axillary line (Fig. 26A). With an anterior-posterior location, one electrode is placed medially to the left nipple, the other is placed under the left shoulder blade (Fig. 26B). If the patient has an implanted pacemaker, the defibrillator electrodes should be about 6-10 cm away from the patient.

Rice. 26 Location of electrodes during defibrillation A. Anterior-anterior variant. B. Anterior-posterior - one electrode is placed medially to the left nipple, the other is placed under the left shoulder blade.

3) The third factor affecting the effectiveness of defibrillation is chest resistance or transthoracic resistance. The phenomenon of transthoracic impedance (resistance) is of great clinical importance, since it is precisely this that explains the difference in current energies between the current energy gained on the scale of the apparatus and allocated 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 in the expiratory phase, because. transthoracic resistance under these conditions is reduced by 16%, the optimal force applied to the electrodes is 8 kg for adults and 5 kg for children aged 1-8 years. However, 84% of the reduction in transthoracic resistance is accounted for by ensuring good contact between the interface 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, conductive gel or gauze moistened with hypertonic solution are used. In an extreme situation, the electrode surface can simply be moistened with any conductive solution (water).

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

Thus, the obligatory fulfillment in clinical practice, first of all, of three main 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 hypertonic solution, are important conditions that ensure the effectiveness of the electrical defibrillation.

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

Most frequent mistakes during defibrillation:

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

B) poor skin-electrode contact;

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

Prevention of the recurrence of VF is one of the priorities after the restoration of effective cardiac activity. Preventive therapy for recurrent VF should be differentiated as far as possible. The number of discharges to eliminate refractory (especially rapidly relapsing) VF is not limited if resuscitation is started in a timely manner and there is hope for the restoration of cardiac activity.

Until recently, lidocaine was considered the drug of first choice for the prevention and treatment of VF. Currently, there is insufficient evidence to consider lidocaine as a useful adjunct to electrical defibrillation. At the same time, data have been obtained that amiodarone (cordarone) is an alternative to lidocaine, which is recommended to be administered during early defibrillation (1-2 min VF), if the first three discharges are not effective, at a dose of 300 mg intravenously as a single bolus after the first dose. epinephrine (greater recovery success compared to lidocaine); cordarone is recommended to be administered with 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 left ventricular myocardial dysfunction, amiodarone is preferable compared to other antiarrhythmics; in these cases it is either more effective or less arrhythmogenic.

It should be noted that after the discharges (especially the maximum values), an "isoelectric" line is often recorded on the monitor screen for several seconds. Usually this is a consequence of the rapidly 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. after it, a coordinated rhythm appears 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 more 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 persists or any other pulseless rhythm is recorded (but not VF/VT), a new dose of epinephrine should be administered and CPR should be performed for another 2 minutes, then the rhythm and pulse should be reassessed. Further tactics of resuscitation will depend on the type of electromechanical activity of the heart: stable (persistent) asystole, its transformation into VF/VT, development of EMD or hemodynamically efficient rhythm.

The likelihood of a favorable outcome of CPR in PAPA/asystole (as in refractory VF/VT) can only be increased if there are potentially reversible, treatable causes of circulatory arrest. 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 continuous monitoring of the effectiveness of ongoing activities
• 
  Lack of clear accounting of therapeutic measures and control over their implementation
• 
  Reassessment of violations of CBS, uncontrolled infusion of NaHCO 3
• 
  Premature termination of resuscitation
• 
  Weakening of control over the patient after the restoration of blood circulation and respiration.

^ Criteria for terminating resuscitation

1. 
   Restoration of spontaneous circulation by the appearance of a pulse on the main arteries (then stop chest compression) and / or respiration (stop mechanical ventilation).
2. 
   failure of resuscitation during 30 minutes.

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

^ III. long-term maintenance stage

G-assessment of the patient's condition

The first task after the 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 of a full recovery of the patient); 2) determining the severity of homeostasis disorders 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 found out even during the first two stages of cardiopulmonary and cerebral resuscitation, since it is often impossible to restore independent blood circulation without this. The assessment of the severity of homeostasis disorders also helps to prevent repeated episodes of circulatory arrest, since severe disorders in such systems as the respiratory and cardiovascular systems, as well as in the water-electrolyte balance and acid-base balance, in themselves can be causes of clinical death.

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

1. General information

Decisive for ascertaining brain death is the combination of the fact of the cessation of the functions of the entire brain with proof of the irreversibility of this cessation.

The right to establish a diagnosis of brain death gives the presence of accurate information about the causes and mechanisms of development of this condition. Brain death can develop as a result of its primary or secondary 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 trauma, 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 a sharp deterioration in systemic circulation, due to a long-lasting shock, etc.

2. Conditions for establishing a diagnosis of brain death

The diagnosis of brain death is not considered until the following effects are excluded: intoxications, including drugs, primary hypothermia, hypovolemic shock, metabolic endocrine coma, and the use of narcotic drugs and muscle relaxants.

3. A set of clinical criteria, the presence of which is mandatory for establishing the diagnosis of brain death

1. 
   Complete and permanent absence of consciousness (coma).
2. 
   Atony of all muscles.
3. 
   Lack of response to strong pain stimuli in the area of ​​trigeminal points and any other reflexes that close above the cervical spinal cord.
4. 
   Lack of pupillary response to direct bright light. In this case, it should be known that no drugs that dilate the pupils were used. The eyeballs are immobile.

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

3.7 Absence of oculovestibular reflexes.

To study oculovestibular reflexes, a two-sided caloric test is performed. Before it is carried out, it is necessary to make sure 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, the external auditory canal is slowly irrigated with cold water (t + 20°C, 100 ml) for 10 s. With preserved function of the brain stem after 20-25 s. there is nystagmus or deviation of the eyes towards the slow component of nystagmus. The absence of nystagmus and deviation of the main apples during a caloric test performed on both sides indicates the absence of vestibular reflexes.

1. 
   The 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 to aspirate the secret.
2. 
   Lack of spontaneous breathing.

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

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

C) after the execution of 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. At this time, there is an accumulation of endogenous carbon dioxide, controlled by sampling arterial blood. The stages of blood gas control are as follows: before the start of the test under mechanical ventilation conditions; 10-15 minutes after the start of mechanical ventilation with 100% oxygen, immediately after disconnecting 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 the functions of the respiratory center of the brainstem. At emergence of the minimum respiratory movements IVL immediately resumes.

4. Additional (confirmatory) tests to the complex of clinical criteria in establishing the diagnosis of brain death

4.1. Establishment of the absence of electrical activity of the brain is carried out in accordance with the international provisions of the electroencephalographic study in conditions of brain death. Needle electrodes are used, at least 8, located according to the "10-20%" system and 2 ear electrodes. The interelectrode resistance must be at least 100 Ohm and not more than 10 kOhm, the interelectrode distance - at least 10 cm. It is necessary to determine the safety of switching and the absence of unintentional or deliberate 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 at least 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 must be maintained for at least 30 minutes of continuous recording. If there are doubts about the electrical silence of the brain, re-registration of the EEG is necessary. Assessment of EEG reactivity to light, loud sound and pain: the total time of stimulation with light flashes, sound stimuli and painful stimuli
for at least 10 minutes. The source of flashes supplied with a frequency of 1 to 30 Hz should be at a distance of 20 cm from the eyes. The intensity of sound stimuli (clicks) - 100 dB. The speaker is located near the patient's ear. Stimuli of maximum intensity are generated by standard photo- and phonostimulators. For painful irritations, strong pricks of the skin with a needle are used. An EEG recorded over the phone cannot be used to determine the electrical silence of the brain.

4.2. Determination of the absence of cerebral circulation.

Contrast double panangiography of 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 mmHg.

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

5. Duration of observation

In case of primary brain damage, in order to establish the clinical picture of brain death, the duration of observation should be at least 12 hours from the moment the signs described in paragraphs 3.1-3.9 were first established; with a secondary lesion, 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 the loss of brain functions in accordance with paragraphs. 3.1-3.8. At the same time, it should be taken into account that spinal reflexes and automatisms can be observed under conditions of continued mechanical ventilation.

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

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 neuropathologist with the same work 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 a consultative basis. The appointment of the composition of the commission and the approval of the "Protocol for establishing brain death" is carried out by the head of the intensive care unit where the patient is located, and during his absence by the responsible doctor on duty of the institution.

The commission cannot include specialists involved in the collection and transplantation of organs.

The main document is the "Brain Death Establishment Protocol", which is relevant for all conditions, including organ harvesting. The "Protocol" must contain the data of all studies, the surnames, names and patronymics of the doctors - members of the commission, their signatures, the date, hour of registration of brain death and, consequently, the death of a person.

After the establishment of brain death and the execution of the "Protocol", resuscitation, including mechanical ventilation, may be terminated.

The responsibility for diagnosing the death of a person lies entirely with the doctors who establish brain death at the medical institution where the patient died.

^ Z - Restoration of 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 due to ischemia caused by a total violation 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 postresuscitation disease, 5 stages are distinguished (according to E.S. Zolotokrylina, 1999):

I stage(6-8 hours post-resuscitation period) is characterized by instability of the main body functions. 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, with a simultaneous decrease in CaO 2 and CvO 2 due to anemia; lactic acidosis; an increase in the level of fibrinogen degradation products (PDF) and soluble fibrin-monomer complexes (RKFM), which are absent in the norm.

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

Severe disorders of tissue perfusion, 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 the plasma slows down - signs of hypercoagulability. This is the stage of "metabolic storms" with manifestations of pronounced hyperenzymemia.

^ Stage III(the end of the 1st - 2nd day of the postresuscitation period) - is characterized by a repeated deterioration in the condition of patients 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, an increase in blood pressure to 150/90-160/90 mmHg in young and middle-aged people, anxiety. Those. there are signs of acute lung injury syndrome or acute respiratory distress syndrome (ARDS/ARDS), with increasing blood shunting. Thus, there is a deepening of the already existing violation of gas exchange with the formation of mixed type hypoxia.

The signs of DIC are maximally pronounced: thrombinemia, hypercoagulability, an increase in the level of PDP against the background of a progressive decrease in the fibrinolytic activity of the 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 this is a period of stabilization and subsequent improvement of body functions with recovery without complications; 2) either 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 a systemic pro-inflammatory response. It is characterized by hypercatabolism, the development of interstitial edema of the lung and brain tissue, subcutaneous tissue, deepening of hypoxia and hypercoagulation with the development of signs of multiple organ failure: bleeding from the digestive tract, psychosis with hallucinatory syndrome, secondary heart failure, pancreatitis and liver dysfunction.

V stage(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 abscessing, suppuration of wounds, peritonitis in operated patients, etc.), generalization of infection - the development of septic syndrome, despite for early appropriate antibiotic therapy. At this stage, a new wave of damage to parenchymal organs develops, while degenerative and destructive changes take place. Thus, fibrosis develops in the lungs, which sharply reduces the respiratory surface, which leads to the irreversibility of a critical condition.

Posthypoxic encephalopathy is the most common variant of the course of postresuscitation syndrome, which manifests itself to one degree or another in all patients who have undergone circulatory arrest. A 100% correlation was found 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 the restoration of spontaneous circulation, the therapy of the post-resuscitation period should be based on the following principles:

1. 
   Immediately after the restoration of independent blood circulation, cerebral hyperemia develops, but after 15-30 minutes. reperfusion, the total cerebral blood flow decreases and hypoperfusion develops. And since there is a breakdown in the autoregulation of cerebral blood flow, 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 maintenance of normotension (both severe hypotension and hypertension should be corrected).
2. 
   Maintaining a normal level of PaO 2 and PaCO 2.
3. 
   Maintain body normothermia. The risk of poor neurological outcome increases for every degree >37°C.
4. 
   Maintenance of normoglycemia (4.4-6.1 mmol/l) - persistent hyperglycemia is associated with poor neurological outcome. The threshold level at which it is necessary to start correction with insulin is 6.1-8.0 mmol/l.
5. 
   Hematocrit level within 30 - 35% - mild hemodilution, which reduces blood viscosity, which increases significantly in the microvasculature as a result of ischemia.
6. 
   Control of seizure activity with benzodiazepines.

BUT) 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 allowed to establish the expediency of using perftoran in the post-resuscitation period. Perftoran reduces cerebral edema, the severity of postresuscitation encephalopathy and increases the activity of the cerebral cortex and subcortical structures, contributing to a rapid exit from a coma. 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 conduct neuroprotective therapy in the postresuscitation period, it is recommended to use the drug Somazine (citicoline), which has a neuro-restorative effect due to the activation of the biosynthesis of membrane phospholipids of brain neurons and, primarily, 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. Somazin is prescribed at a dose of 500-1000 mg 2 times / day intravenously, followed by a transition to the oral route of administration of 200 mg 3 times / day in the recovery period.

B) Physical methods. Unconscious patients who have undergone out-of-hospital circulatory arrest due to the mechanism of ventricular fibrillation should be provided with body hypothermia up 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 the case of in-hospital circulatory arrest.

Therapy of edema-swelling of the brain 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 pro-inflammatory reaction during and after CPR, as a component of postresuscitation disease.

In patients in the postresuscitation period, computed tomography or magnetic resonance imaging can be used to diagnose the development of diffuse cerebral edema. At the same time, 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), is more characteristic of the postresuscitation period.

^ Edema of the brain

The purpose of anti-edematous therapy is: a) reduction of ICP; b) maintaining an adequate CPP; c) prevention of secondary brain damage due to swelling.

Decongestive therapy should be based on the following principles:

• 
  limiting the volume of injected infusion media (introduction of 5% glucose is unacceptable);
• 
  exclusion of factors that increase ICP (hypoxia, hypercapnia, hyperthermia):
• 
  normoventilation and normoxia: p and CO 2 34-36 mm Hg, p v CO 2 40-44 mm Hg, S and O 2 \u003d 96%: on mechanical ventilation: alveolar ventilation (AV) AV \u003d 4.8 - 5, 2 l/min., AV = MOD - (BH 150 ml), where MOD is the minute volume of breathing, BH is the respiratory rate;
• 
  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, then cerebral perfusion pressure (CPP) should be maintained >70 mm Hg (CPP = SBP - ICP, mm Hg, thus SBP = 70 + ICP, mm Hg.

• 
  GCS > 12 points: ICP = 10, SBP = 80, mm Hg;
• 
  GCS = 8 - 12 points: ICP = 15, SBP = 85, mm Hg;
• 
  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 these moderate doses of the drug, tk. 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 prolonging the administration of this drug 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 cerebral volumetric 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 saponin escin from horse chestnut seeds and the amino acid L-lysine. In the blood serum, the salt of L-lysine aescinate 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 anti-exudative and rapid anti-edematous action. The drug is administered strictly intravenously at a dose of 10 ml (8.8 mg of escin) 2 times in the first 3 days, then 5 ml - 2 times / day. The maximum daily dose of the drug should not exceed 25 ml - 22 mg of escin. The course - until a stable clinical effect is obtained, as a rule, 7-8 days.

1. 
   Writing an abstract based on a review of current literature data on the pathophysiology of circulatory arrest and the latest developments in methods for resuming spontaneous circulation and higher brain functions in the postresuscitation period.

1. 
   Clinical signs of pre-agony, 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 stop.
4. 
   Stages of cardiopulmonary and cerebral resuscitation according to P. Safar.
5. 
   Modern method of basic life support.
6. 
   Methods for resuming and maintaining airway patency during resuscitation.
7. 
   Medications used in continued life support and routes of administration.
8. 
   Types of circulatory arrest and features of measures to resume independent blood circulation.
9. 
   Methodology and safety precautions for defibrillation.
10. 
    Criteria for termination of resuscitation.
11. 
    Clinical and laboratory methods for diagnosing brain death.
12. 
    Auxiliary methods for diagnosing brain death.
13. 
    Post-resuscitation disease - definition and stages.
14. 
    Stages of exit from a coma after clinical death.
15. 
    General principles of intensive care of postresuscitation disease.

1. 
   Viewing training videos:

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

1. 
   Mastering the practical skills of SIMR on a mannequin:

• 
  implementation of the triple reception of P. Safar;
• 
  the use of povіtrovodіv;
• 
  application of a face mask or "key of life";
• 
  performance of SHVL by methods "from mouth to mouth" and "from mouth to nose";
• 
  performing SHVL on a baby mannequin using the “mouth to mouth and nose” method;
• 
  performing an indirect heart massage on an adult mannequin;
• 
  performing an indirect heart massage on a baby mannequin;
• 
  performing indirect massage using a cardiopamp;
• 
  performing basic life support by two rescuers;
• 
  performing defibrillation on a mannequin;
• 
  using an automatic defibrillator on a manikin.

1. 
   Determination of the type of circulatory arrest by ECG
2. 
   Solution of clinical situations with circulatory arrest using the simulator program "Cardiac Arrest!" (or analogues).
3. 
   Diagnosis of "brain death":

• 
  in the intensive care unit and resuscitation in patients with atonic comma;
• 
  in the training room (in the absence of patients with an exorbitant comma) when parsing educational copies of case histories.

A) Main:

1. 
   Anesthesiology and intensive therapy: 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 Sciences, 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 honey. publishing house, 2002. - 672 p.