Cheat sheet: Algorithm for the provision of emergency care for cardiac diseases and poisoning. Reasons why acute coronary insufficiency and sudden death develop What is sudden coronary death

Concept definition

Sudden death- natural (non-violent) death, which occurred unexpectedly within 6 hours (according to some sources - 24 hours) from the onset of acute symptoms.

clinical death- this is a reversible state that lasts from the moment of cessation of vital functions (blood circulation, respiration) until the onset of irreversible changes in the cerebral cortex. This is the period when the viability of brain neurons is maintained under conditions of anoxia. Therefore, the defining criterion for the success of cardiopulmonary resuscitation is the restoration of full brain function.

The duration of the period of clinical death depends on the body temperature of the victim: when it rises, it is reduced to 1-2 minutes due to an increase in oxygen consumption by tissues due to the predominance of oxyhemoglobin dissociation processes over its formation; when lowered (under conditions of hypothermia), it lengthens to 12 minutes due to a decrease in oxygen consumption by tissues. In exceptional cases (drowning in ice water), the time of clinical death can be 30-60 minutes or more.

Under conditions of normothermia, the period of clinical death is 3-5 minutes, acting as a limiting factor in resuscitation: if cardiopulmonary resuscitation is started within 5 minutes from the moment of circulatory arrest and ends with the restoration of spontaneous blood circulation and respiration, there is every chance of restoring full-fledged thinking without neurological deficit.

social death- a partially reversible state characterized by an irreversible loss of functions of the cerebral cortex (decortication) while maintaining vegetative functions (synonym: vegetative state).

biological death characterized by an irreversible state of vital organs, when the revival of the body as an integral system is impossible.

With the development of resuscitation as a science and a branch of medicine, the concept "brain death"- complete and irreversible cessation of all brain functions, recorded with a beating heart against the background of artificial lung ventilation (ALV), infusion and drug therapy. In the modern sense, brain death is seen as the legal equivalent of human death.

The reasons

In the vast majority of cases, the cause of sudden death is coronary heart disease (acute coronary insufficiency or myocardial infarction), complicated by electrical instability. Less common are causes such as acute myocarditis, acute myocardial dystrophy (in particular, alcoholic etiology), pulmonary embolism, closed heart injury, electrical injury, heart defects. Sudden death occurs in neurological diseases, as well as during surgical and other interventions (catheterization of large vessels and heart cavities, angiography, bronchoscopy, etc.). There are cases of sudden death when using certain drugs (cardiac glycosides, procainamide, beta-blockers, atropine, etc.).

Risk factors for sudden death:

New onset Prinzmetal's angina

The most acute stage of myocardial infarction (70% of cases of ventricular fibrillation fall in the first 6 hours of the disease with a peak in the first 30 minutes)

Rhythm disturbances: rigid sinus rhythm (RR intervals less than 0.05 s.)

Frequent (more than 6 per minute), group, polytopic, allorhythmic ventricular extrasystoles

Prolongation of the QT interval with early extrasystoles of the R/T type and episodes of polymorphic ventricular tachycardia

Ventricular tachycardia, especially originating from the left ventricle, alternating and bidirectional

WPW syndrome with high frequency paroxysms of flutter and atrial fibrillation with aberrant QRS complexes

Sinus bradycardia

Atrioventricular blocks

Damage to the interventricular septum (especially in combination with damage to the anterior wall of the left ventricle)

The introduction of cardiac glycosides in the acute phase of myocardial infarction, thrombolytics (reperfusion syndrome)

Alcohol intoxication, episodes of short-term loss of consciousness.

Mechanisms of emergence and development (pathogenesis)

The most common mechanism of sudden death is ventricular fibrillation (flutter), much less often - asystole and electromechanical dissociation (the latter occur in shock, heart failure and AV blockade). Analysis of data from long-term ECG monitoring performed at the time of the onset of sudden circulatory arrest confirms that in 80-90% of cases, the mechanism of the latter is ventricular fibrillation, which is often preceded by episodes of paroxysmal ventricular tachycardia, turning into ventricular flutter. Thus, it has been shown that the most common cause of sudden cardiac death is ventricular fibrillation.

Circulatory failure causes rapid death due to anorexia of the brain if circulation and respiration are not restored within three to a maximum of five minutes. A longer break in the blood supply to the brain leads to irreversible changes in it, which predetermines an unfavorable prognosis even in the case of restoration of cardiac activity at a later period.

As we have already said, stressful situations, excessive excitation of the sympathoadrenal system, hypoxia and (or) myocardial ischemia, FRO activation, disturbances in the system of vascular-platelet hemostasis with the development of a microcirculatory block, an increase in the work of the heart, an increase in myocardial demand for oxygen and, as a consequence, the development of electrical instability of the myocardium.

Clinical picture (symptoms and syndromes)

Warning symptomatology:

- severe pain syndrome;

- tachycardia or bradycardia, accompanied by hemodynamic

disorders;

- respiratory disorders;

- sudden decrease in blood pressure;

- a rapid increase in cyanosis of the skin

Clinical signs of sudden cardiac arrest include:

Loss of consciousness;

Absence of pulse on large arteries (carotid and femoral);

Absence of heart sounds;

Stopping breathing or the appearance of agonal breathing;

Pupil dilation, lack of their reaction to light;

Change in skin color (gray with a bluish tinge).

Diagnostics

For the diagnosis of sudden cardiac arrest, it is sufficient to state the above four signs. Only immediate diagnosis and emergency medical care can save the patient. In any case of sudden loss of consciousness, the following scheme of urgent measures is recommended:

The patient is placed on his back without a pillow on a hard base;

Check for a pulse on the carotid or femoral artery;

Upon detection of cardiac arrest, immediately proceed to external cardiac massage and artificial respiration.

Treatment

Urgent care

Cardiopulmonary resuscitation begins in the presence of signs of clinical death.

1. Main features:

Absence of a pulse in the carotid artery;

Lack of breathing;

Dilated pupils that do not respond to light.

2. Additional features:

Lack of consciousness;

Paleness (earthy gray), cyanosis or marbling of the skin;

Atony, adynamia, areflexia.

According to the latest recommendations of the American Heart Association and the European Council for Resuscitation (2005), in case of sudden circulatory arrest, a complex of cardiopulmonary and cerebral resuscitation (LCPR) developed by P. Safar is performed, which consists of 3 successive stages.

Based on the foregoing, the provision of emergency care at the scene of the incident is of decisive importance. Its methods should be mastered not only by physicians, but also by persons who, due to their profession, are the first to be near the victim (law enforcement officers, transport drivers, etc.).

The initial stage of LPCR is an elementary life support activity, the main purpose of which is emergency oxygenation. It is carried out in three successive stages:

Control and restoration of airway patency;

Artificial maintenance of breath;

Artificial maintenance of blood circulation.

To restore airway patency, P. Safar's triple technique is used, which includes tilting the head back, opening the mouth and pushing the lower jaw forward.

The first thing to do is to make sure that the victim is unconscious: call out to him, ask loudly: “What happened?”, say: “Open your eyes!”, pat on the cheeks, gently shake his 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 laryngeal-pharyngeal region due to muscular atony. 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.

When carrying out manipulations on the respiratory tract, one must be aware of the possible damage to the spine in the cervical region. The greatest likelihood of such an injury can be observed with:

Road injuries (a person was hit by a car or was in a car during a collision);

Falls from a height (including divers).

Such victims should not be tilted (bend their neck forward) and turn their heads to the sides. In these cases, it is necessary to moderately stretch it towards yourself, followed by keeping the head, neck and chest in the same plane, excluding when performing a triple neck overextension technique, ensuring minimal tilting of the head and simultaneous opening of the mouth and protrusion of the lower jaw forward. When providing first aid, the use of “collars” fixing the neck area is shown.

IVL is carried out by the mouth-to-mouth method.

After a triple intake on the respiratory tract, one hand is placed on the forehead of the victim, providing a tilting of the head. Having pinched the nose of the revived person with your fingers and tightly pressing your lips around his mouth, you need to blow in air, following the excursion of the patient's chest (Fig. 3a). When it is raised, it is necessary to release the mouth of the victim, giving him the opportunity to make a full passive exhalation. The tidal volume should be 500-600 ml (6-7 ml/kg) with a respiratory rate of 10 per minute to prevent hyperventilation.

Errors during IVL.

Unobstructed airway patency

Air tightness not ensured

Underestimation (late onset) or overestimation (beginning of LPCR with intubation) of the value of mechanical ventilation

Lack of control of chest excursions

Lack of control of air entering the stomach

Attempts to medically stimulate breathing

To ensure artificial maintenance of blood circulation, an algorithm for conducting chest compression (indirect heart massage) is used.

1. Correctly lay the patient on a flat hard surface. Determine the points of compression - palpation of the xiphoid process and retreat two transverse fingers up. Place the hand with the palmar surface on the border of the middle and lower thirds of the sternum, fingers parallel to the ribs, and on it - the other hand.

2. Option for the location of the palms - "lock".

3. Proper compression: pushes are performed with arms straightened in the elbow joints with the transfer of part of the weight of your body to them.

The ratio of compressions to rescue breaths for both one and two rescuers should be 30:2. Compression of the chest is carried out at a frequency of 100 clicks per minute, a depth of 4-5 cm, pausing for breaths (in non-intubated patients, it is unacceptable to blow air at the time of chest compression - there is a risk of air entering the stomach).

Criteria for termination of resuscitation.

1. The appearance of a pulse on the main arteries (stop chest compression) and / or breathing (stop mechanical ventilation) is a sign of restoration of spontaneous circulation

2. Ineffective resuscitation within 30 minutes. The exceptions are the conditions in which it is necessary to prolong resuscitation:

hypothermia (hypothermia);

Drowning in ice water;

Overdose of drugs or drugs;

Electrical injury, lightning strike.

Signs of the correctness and effectiveness of compression is the presence of a pulse wave on the main and peripheral arteries.

To detect a possible restoration of spontaneous circulation in the victim, every 2 minutes of the ventilation-compression cycle, a pause (for 5 seconds) is made to determine the presence of a pulse on the carotid arteries.

After the restoration of blood circulation, the patient, lying on a stretcher, is transported (under cardiac monitoring) to the nearest department of cardiological resuscitation, subject to the continuation of therapeutic measures that ensure vital activity.

Obvious signs of biological death: the maximum expansion of the pupils with the appearance of the so-called dry herring shine (due to the drying of the cornea and the cessation of tearing); the appearance of positional cyanosis, when cyanotic staining is detected along the posterior edge of the auricles and the back of the neck, on the back; stiffness of the muscles of the limbs, not reaching the severity of rigor mortis.

In conclusion, it should be noted that the most significant factor influencing the outcome of sudden cardiac arrest is the improvement in the organization of care for this condition. Therefore, the American Heart Association proposed an algorithm for organizing first aid, called the “chain of survival”. It will save the lives of many victims.

Conservative treatment

To date, this concept is based on the following factors that determine the maximum safety of human life. First of all, this is the definition of risk zones where emergencies can occur; definition of types of emergencies; creation of a system of primary medical care at the prehospital stage. The latter includes: mastering modern assistance skills; equipping the subjects of the primary health care system and risk areas with modern equipment that is necessary for providing assistance; coordinating the interaction of the primary health care system with specialized services. According to the derived sequence, a model was developed for analyzing factors that affect survival in an emergency, the so-called “survival chain”

A strict algorithm of actions of the resuscitator under the condition of cardiac arrest and / or loss of respiratory function in the victim is substantiated and presented. Groups of persons requiring special attention are identified - these are people aged 45 to 60 years and people whose professions are associated with great psycho-emotional stress.

1. With the development of a resuscitation situation, time plays the most important role in providing assistance, since only a few minutes separate the victim from death. Therefore, the first leading stage is early access to the victim. The purpose of this stage is to determine the condition of the victim with the subsequent choice of an algorithm for providing assistance.

2. The next step of the algorithm is the early start of cardiopulmonary resuscitation. This stage includes: the release of the respiratory tract, artificial ventilation of the lungs, chest compressions, oxygen supply. That is, at this stage, CPR is performed, which consists of two manipulations: closed heart massage and artificial ventilation of the lungs.

Closed heart massage (CMC) is a rhythmic compression of the chest. ZMS is performed in the absence of a pulse on the main arteries. Manipulation creates positive pressure in the chest during the compression phase. The valves of the veins and heart ensure the antegrade flow of blood into the arteries. When the chest takes its original shape, blood returns to it from the venous part of the circulatory system. A small amount of blood flow is provided by compression of the heart between the sternum and the spine. During chest compressions, blood flow is 25% of normal cardiac output. According to the recommendations, it is suggested to carry out one breath for every 5 compressions in the presence of two resuscitators. In the case of a single resuscitation, 15 compressions must be followed by one breath (combination 15:1 or 30:2). The frequency of compressions should be approximately 100 per minute. Studies have been conducted on the use of high-frequency chest compressions with a frequency of more than 100 compressions per minute. One of the studies, where indirect massage was performed at a frequency of 120 compressions per minute, showed that this technique was more effective, which made it possible to suggest the possibility of high-frequency CPR.

3. If the second stage is ineffective, it is recommended to proceed to the third stage of the chain - early defibrillation. During defibrillation, the heart is exposed to an electrical impulse that depolarizes the membrane of most myocardial cells and causes a period of absolute refractoriness - a period in which an action potential cannot be caused by a stimulus of any intensity. In case of successful defibrillation, the chaotic electrical activity of the heart is interrupted. In this case, pacemakers of the first order (cells of the sinus node) are the first to be able to depolarize spontaneously and provide sinus rhythm. During a discharge, only a portion of the induced energy produces an effect on the heart due to the varying level of chest resistance. The amount of energy required during defibrillation (defibrillation threshold) increases with increasing time since cardiac arrest, with various drug exposures. For defibrillation in resuscitation of adults, empirically selected discharges of 200 J are used for the first two discharges and 360 J for the subsequent ones. Direct current discharges should be applied with proper electrode placement and good skin contact. The polarity of the electrodes is not critical. In the anterior position (often used in resuscitation), the electrode applied to the sternum is placed on the upper part of the right half of the chest under the collarbone. The electrode placed on the apex of the heart is located slightly lateral to the point of normal projection of the apex beat, but not on the mammary gland in women. In case of failure, the anterior-posterior location of the electrodes can be used - on the anterior ("sternal" electrode) and the posterior surface of the chest. The shape of the pulse generated by the defibrillator is also important. The first defibrillators produced a pulse that had a rectangular shape and two differently directed phases.

The next step in the modification of the pulse shape was the removal of the negative phase and the formation of a monophasic rectangular pulse shape.

However, as a result of long-term use of devices that generate a pulse of this configuration, especially in implantable cardioverter-defibrillators, their inefficiency with an increase in the defibrillation threshold has been shown. Most patients with implanted cardioverter-defibrillators received cordarone, which increased the defibrillation threshold. In a certain number of patients, an increase in the defibrillation threshold occurred due to an inflammatory reaction at the site of electrode implantation and, accordingly, an increase in tissue resistance. It was noted that in such patients, despite the discharge produced when arrhythmia occurred, there was no relief of arrhythmia. This observation led to another modification of the pulse configuration. The return of the second negative phase of the pulse was determined first, and the rectangular shape was changed to a cone-shaped exponential curve in both phases of the pulse.

Defibrillation is one of the most effective methods of restoring an adequate rhythm of myocardial contractions in the most common cause of SCD - ventricular fibrillation. An analysis of many studies on sudden death outside of hospitals shows that the survival rate of patients decreases by 10% for every minute of delay in electrical defibrillation, however, adequately performed primary resuscitation (second stage) can slow down the process and increase the time before the development of irreversible cardiac arrest. The world community has already taken the path of providing this stage through the use of simple automatic external defibrillators, the operation of which does not require high qualifications, special knowledge and skills. It is enough to place them in the areas of risk of an emergency, and the device, provided it is connected to the victim, will determine the need for a discharge, its magnitude, and even the need for further action. The effectiveness of the use of automatic external defibrillators has now been proven both in specially designed studies and according to statistical data.

4. The correct implementation of the first three stages allows you to save the life of the victim until the arrival of a specialized service and the provision of qualified assistance.

The fourth stage of the struggle for human life in SCD is the stage of specialized medical care, which consists in early treatment. At this stage, time will also be an important factor. This stage includes: adequate ventilation of the lungs (mainly with tracheal intubation), medical support (catecholamines, antiarrhythmic drugs, electrolyte and buffer solutions), and, if necessary, pacing.

Adequate ventilation by invasive mechanical ventilation using tracheal intubation has been shown to improve prognosis with CPR in some studies. However, early intubation is preferred but remains controversial.

Medication support consists of vasoactive therapy including: epinephrine, norepinephrine, dopamine, dobutamine, vasopressin, endothelin 1, isoproterenol, ephedrine, phenylephrine, angiotensin II, serotonin, nitroglycerin, and drug combinations. Of all the above drugs, the CPR protocol includes adrenalin as the standard for resuscitation. The second drug of choice in resuscitation, according to the latest recommendations in 2005, is vasopressin. The limitation of the study is the small number of observations (40 patients). Recommended use is 40 units per injection, corresponding to 1 mg of adrenaline. In one of the studies of the comparative effectiveness of epinephrine and vasopressin in resuscitation, a significant superiority of the use of vasopressin was shown.

Support with electrolyte and buffer solutions in daily practice is not recommended. Based on existing recommendations, the use of this type of drug support is used in a specific resuscitation situation. For solutions of potassium and magnesium, this is hypokalemia and -hypomagnesemia, for sodium bicarbonate - previous acidosis, hyperkalemia, the use of tricyclic antidepressants.

Antiarrhythmic support is one of the most important parts of CPR medical support, given the underlying cause of SCD, ventricular fibrillation or ventricular tachycardia. For a long time, the class 1B drug, lidocaine, was the standard of antiarrhythmic support, and only at the end of the resuscitation protocol was it possible to use novocainamide, bretylium tosylate, cordarone. To date, the ARREST and ALIVE studies have led to changes in recommendations for antiarrhythmic CPR support. Convincing data on the superiority of the use of cordarone in the medical support of resuscitation allowed us to recommend this technique for routine use instead of lidocaine.

One of the most interesting and controversial issues for many years has been the possibility and effectiveness of fibrinolytic therapy in case of ineffective resuscitation. Many small studies have been carried out on the use of fibrinolytic therapy for ineffective resuscitation, a website has been created where all cases of the use of fibrinolytic therapy are collected to optimize the effect of resuscitation. However, this issue has not been resolved to date. The use of fibrinolytic therapy for failed resuscitation is a matter of choice for the resuscitator and is not supported by guidelines.

The criteria for the effectiveness of resuscitation measures are:

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

The appearance of a pulse on the carotid and femoral arteries;

Determination of the maximum arterial pressure at the level of 60-70 mm Hg;

Reducing pallor and cyanosis;

Sometimes - the appearance of independent respiratory movements.

When a hemodynamically significant spontaneous rhythm is restored, 200 ml of a 2-3% solution of sodium bicarbonate (Trisol, Trisbuffer), 1-1.5 g of potassium chloride in dilution or 20 ml of panangin in a stream, 100 mg of lidocaine in a stream (then drip at a rate of 4 mg / min), 10 ml of a 20% solution of sodium oxybutyrate or 2 ml of a 0.5% solution of Relanium in a stream. In case of an overdose of calcium antagonists - hypocalcemia and hyperkalemia - 2 ml of a 10% solution of calcium chloride is administered intravenously.

In the presence of risk factors for sudden death (see above), the introduction of lidocaine (80-100 mg intravenously, 200-500 mg intramuscularly) in combination with ornid (100-150 mg intramuscularly) is recommended; with a decrease in blood pressure - 30 mg of prednisolone intravenously.

Cardiac glycosides are not administered in case of sudden death.

Sudden cessation of blood circulation (sudden death) - primary circulatory arrest in a healthy person or a patient in a satisfactory condition, in the first 6 (24) hours of the disease due to acute ischemia or myocardial infarction, pulmonary embolism, infections (meningitis), etc. The risk increases sharply against the background of alcohol intoxication.
Symptoms. Sudden loss of consciousness with or without tonic-clonic convulsions, absence of carotid pulse, respiratory arrest or sudden onset of agonal breathing, pupillary dilatation maximizing at approximately 105 s.
In 80% of cases, flutter and ventricular fibrillation (VT, VF) are observed: convulsions, wheezing breathing, asymmetry and cyanosis of the face occur more often. Harbingers of VT and VF can be frequent (> 6 per minute), group, polytopic, allorhythmic, early (where the ratio Q-R’/QT<0,85) желудочковые экстрасистолы; левожелудочковые, альтернирующие, двунаправленные, torsades de pointes желудочковые тахикардии; фибрилляция и трепетание предсердий на фоне синдрома WPW с ЧСС>240 per minute and functional blockade of the legs.

Rice. 1. Continuous electrical stimulation (?) of parasystole (4), R inhibitory stimulator (arrow indicates natural contractions of the ventricles)

Rice. 2. Ventricular flutter (frequency 240 per minute). Ventricular fibrillation, turning into asystole; P waves are recorded

ECG: QRS, ST, T are not differentiated, there is no isoline. In VT, the recorded complexes are rhythmic, sinusoidal in nature, while in VF they are of different amplitudes, arrhythmic. The frequency of complexes is 150-600 per minute.
Electromechanical dissociation (may be caused by a sharp increase in pre- or afterload, observed with hypovolemia, cardiac tamponade, tension pneumothorax, metabolic disorders): the presence of QRS on the ECG and symptoms of clinical death. With asystole (short attacks of asystole against the background of sick sinus syndrome, the appearance of bifascicular blockades, especially bilateral ones, sharply increase its risk): absence of QRS (it is necessary to make sure that the electrocardiograph is working). With asystole, the face is usually pale, convulsions are not characteristic (Fig. 2).
Urgent care. Indirect cardiac massage (frequency of compressions 80-100 per minute) and mechanical ventilation in a ratio of 5:1 (one resuscitator -15:2). If the mechanism of death is not established: EIT 3 J/kg, then take an ECG. With TG and VZh - EIT 200 J, 2-300 J, then 360 J (3-4-5 7 / kg) after 15 compressions. Adrenaline (1 mg / amp.) After three EITs (with the amplitude of VF waves< <10 мм перед ЭИТ 1 мг адреналина, 1 мг атропина, 30 мг преднизолона в/в) - 7,5-15 мкг/кг (05-1 мг) каждые 5 мин в/в. Дополнительно вводится 1 мг/кг лидокаина в/в, повторять по 05 мг/кг каждые 3-5 мин до общей дозы 3 мг/кг, или 5 мг/кг орнида в/в (препараты сочетаются), повторять по 10 мг/кг каждые 5 мин до общей дозы 30-35 мг/кг.
After the introduction of drugs - EIT after 1-2 minutes of massage. After 3-4 EIT - tracheal intubation (endotracheal administration of adrenaline, atropine, lidocaine in a double dose per 10 ml of saline). Calcium chloride (10% 10 ml, g / amp.) 02 g IV (max 2-4 mg / kg at 10-minute intervals) with an overdose of verapamil or other calcium blockers, potassium preparations If a defibrillator is not available, lidocaine and ornid applied independently; in their absence, novocainamide is used - 250-500 mg IV or 100-200 mg IV, propranolol - 5-10 mg IV or IV. With ineffective ventilation in / in 1 ml / kg (1 meq / kg) of trisamine (in the absence of trisamine - 1 meq of base which contains 2 ml of 4.2% sodium bicarbonate solution) once or 0.5 ml / kg with repetition every 10 min. If, after EIT, atrial fibrillation or flutter is recorded with a hemodynamically ineffective rhythm or ventricular tachycardia, repeat EIT.
After restoration of a hemodynamically significant rhythm - infusion of 1 g / h of potassium chloride, 2 g / h of magnesium sulfate (10 ml of panangin in a stream for 5-10 minutes), 30-50 mcg / kg / min of lidocaine, which is approximately 2-4 mg / min (if lidocaine was not administered - first 15 mg/kg IV bolus), 50-100 mg/kg sodium hydroxybutyrate (20% 10 ml, 2 g/amp.) or 10 mg to 03 mg/kg sibazon (10 mg / amp.) in / in the jet.
With asystole and electromechanical dissociation and the impossibility of pacing - intravenous bolus 05-1 mg of adrenaline every 3-5 minutes [for asystole, it can be replaced with orciprenaline in / in 05 mg every 3-5 minutes or intravenous infusion of isadrin (isolroterenol) 1-4 mcg / min, with electromechanical dissociation - mezaton in / in 5-10 mg every 3-5 minutes]. After a single injection of adrenaline, pulmonary intubation. Atropine - 1 mg IV every 5 minutes up to 0.04 mg / kg (more effective in reflex cardiac arrest). If resuscitation is ineffective - the introduction of 1 ml / kg of trisamine, repeated every 10 minutes at 05 ml / kg. Rhythmic blows to the middle part of the sternum with a frequency of 60 per minute can be used.
If more than 5 minutes have passed since the moment of circulatory arrest, then alternative methods of adrenaline administration can be recommended in all cases of sudden clinical death: intermittent doses - 2-5 mg every 3-5 minutes, increasing - 1-3-5 mg every 3 minutes, high doses - 0.1 mg / kg, but not more than 8 mg, every 3-5 minutes.
Intracardiac administration of drugs - only in the absence of the effect of intravenous administration
Hospitalization: as fast as possible to the intensive care unit, bypassing the emergency room, on a stretcher with the provision of intravenous administration of drugs, oxygen therapy and resuscitation in the car.

- this is asystole or ventricular fibrillation, which arose against the background of the absence in the anamnesis of symptoms indicative of coronary pathology. The main manifestations include the absence of respiration, blood pressure, pulse on the main vessels, dilated pupils, lack of reaction to light and any kind of reflex activity, marbling of the skin. After 10-15 minutes, the appearance of a symptom of a cat's eye is noted. Pathology is diagnosed on the spot according to clinical signs and electrocardiography data. Specific treatment is cardiopulmonary resuscitation.

ICD-10

I46.1 Sudden cardiac death, as described

General information

Sudden coronary death accounts for 40% of all causes of death in people over 50 but under 75 years of age without diagnosed heart disease. There are about 38 cases of SCD per 100,000 people annually. With the timely start of resuscitation in the hospital, the survival rate is 18% and 11% with fibrillation and asystole, respectively. About 80% of all cases of coronary death occur in the form of ventricular fibrillation. More often, middle-aged men with nicotine addiction, alcoholism, and lipid metabolism disorders suffer. Due to physiological reasons, women are less prone to sudden death from cardiac causes.

The reasons

Risk factors for VCS do not differ from those for ischemic disease. Among the provocative effects include smoking, eating a large amount of fatty foods, arterial hypertension, insufficient intake of vitamins in the body. Non-modifiable factors - old age, male gender. Pathology can occur under the influence of external influences: excessive power loads, diving into ice water, insufficient oxygen concentration in the surrounding air, and acute psychological stress. The list of endogenous causes of cardiac arrest includes:

Atherosclerosis of the coronary arteries. Cardiosclerosis accounts for 35.6% of all SCD. Cardiac death occurs immediately or within an hour after the onset of specific symptoms of myocardial ischemia. Against the background of an atherosclerotic lesion, AMI is often formed, which provokes a sharp decrease in contractility, the development of a coronary syndrome, and flicker.
Conduction disorders. Sudden asystole is usually observed. CPR measures are ineffective. Pathology occurs with an organic lesion of the conduction system of the heart, in particular the sinatrial, atrioventricular node or large branches of the His bundle. As a percentage, conduction failures account for 23.3% of total cardiac deaths.
Cardiomyopathy. They are detected in 14.4% of cases. Cardiomyopathies are structural and functional changes in the coronary muscle that do not affect the coronary artery system. They are found in diabetes mellitus, thyrotoxicosis, chronic alcoholism. May have a primary nature (endomyocardial fibrosis, subaortic stenosis, arrhythmogenic pancreatic dysplasia).
Other states. The share in the overall structure of morbidity is 11.5%. These include congenital anomalies of the cardiac arteries, left ventricular aneurysm, and cases of SCD, the cause of which could not be determined. Cardiac death can occur with pulmonary embolism, which causes acute right ventricular failure, in 7.3% of cases accompanied by sudden cardiac arrest.

Pathogenesis

The pathogenesis directly depends on the causes that caused the disease. With atherosclerotic lesions of the coronary vessels, one of the arteries is completely occluded by a thrombus, the blood supply to the myocardium is disturbed, and a focus of necrosis is formed. The contractility of the muscle decreases, which leads to the onset of an acute coronary syndrome and the cessation of cardiac contractions. Conduction disorders provoke a sharp weakening of the myocardium. Ned residual contractility causes a decrease in cardiac output, stagnation of blood in the chambers of the heart, and the formation of blood clots.

In cardiomyopathies, the pathogenetic mechanism is based on a direct decrease in myocardial performance. In this case, the impulse propagates normally, but the heart, for one reason or another, reacts poorly to it. The further development of the pathology does not differ from the blockade of the conduction system. With PE, the flow of venous blood to the lungs is disrupted. There is an overload of the pancreas and other chambers, stagnation of blood is formed in the systemic circulation. A heart overflowing with blood in conditions of hypoxia is unable to continue working, it suddenly stops.

Classification

Systematization of SCD is possible due to the causes of the disease (AMI, blockade, arrhythmia), as well as the presence of previous signs. In the latter case, cardiac death is divided into asymptomatic (the clinic develops suddenly against the background of unchanged health) and having previous signs (short-term loss of consciousness, dizziness, chest pain an hour before the development of the main symptoms). The most important for resuscitation is the classification according to the type of cardiac dysfunction:

ventricular fibrillation. Occurs in the vast majority of cases. Requires chemical or electrical defibrillation. It is a chaotic erratic contraction of individual fibers of the ventricular myocardium, unable to provide blood flow. The condition is reversible, well stopped with the help of resuscitation.
Asystole. Complete cessation of heart contractions, accompanied by a cessation of bioelectric activity. More often it becomes a consequence of fibrillation, but it can develop primarily, without prior flicker. Occurs as a result of severe coronary pathology, resuscitation measures are ineffective.

Symptoms of sudden cardiac death

40-60 minutes before the development of a stop, the appearance of previous signs may occur, which include fainting lasting 30-60 seconds, severe dizziness, impaired coordination, a decrease or increase in blood pressure. Characterized by pain behind the sternum of a compressive nature. According to the patient, the heart seems to be clenched in a fist. Precursor symptoms are not always observed. Often the patient simply falls during the performance of any work or exercise. Sudden death in a dream without previous awakening is possible.

Cardiac arrest is characterized by loss of consciousness. The pulse is not determined both on the radial and on the main arteries. Residual breathing can persist for 1-2 minutes from the moment the pathology develops, but breaths do not provide the necessary oxygenation, since there is no blood circulation. On examination, the skin is pale, cyanotic. There is cyanosis of the lips, earlobes, nails. The pupils are dilated and do not react to light. There is no reaction to external stimuli. With tonometry of blood pressure, Korotkoff's tones are not auscultated.

Complications

Complications include a metabolic storm that occurs after successful resuscitation. Changes in pH due to prolonged hypoxia lead to disruption of the activity of receptors and hormonal systems. In the absence of the necessary correction, acute renal or multiple organ failure develops. The kidneys can also be affected by microthrombi, which are formed during the onset of DIC, myoglobin, the release of which occurs during degenerative processes in the striated muscles.

Poorly performed cardiopulmonary resuscitation causes decortication (brain death). In this case, the patient's body continues to function, but the cerebral cortex dies. Recovery of consciousness in such cases is impossible. A relatively mild variant of cerebral changes is posthypoxic encephalopathy. It is characterized by a sharp decrease in the mental abilities of the patient, a violation of social adaptation. Somatic manifestations are possible: paralysis, paresis, dysfunction of internal organs.

Diagnostics

Sudden cardiac death is diagnosed by a resuscitator or other specialist with a medical background. Trained representatives of emergency response services (rescuers, firefighters, policemen), as well as people who happened to be nearby and have the necessary knowledge, are able to determine circulatory arrest outside the hospital. Outside the hospital, the diagnosis is made solely on the basis of clinical signs. Additional techniques are used only in the ICU, where they require minimal time to apply. Diagnostic methods include:

hardware allowance. On the heart monitor, to which each patient of the intensive care unit is connected, large-wave or small-wave fibrillation is noted, ventricular complexes are absent. An isoline may be observed, but this rarely happens. Saturation indicators quickly decrease, blood pressure becomes undetectable. If the patient is on assisted ventilation, the ventilator signals that there are no spontaneous breath attempts.
Laboratory diagnostics. It is carried out simultaneously with measures to restore cardiac activity. Of great importance is a blood test for acid-base balance and electrolytes, in which there is a shift in pH to the acid side (a decrease in the pH value below 7.35). To exclude an acute infarction, a biochemical study may be required, in which increased activity of CPK, CPK MB, LDH is determined, and the concentration of troponin I increases.

Urgent care

Assistance to the victim is provided on the spot, transportation to the ICU is carried out after the restoration of the heart rhythm. Outside the hospital, resuscitation is carried out by the simplest basic techniques. In a hospital or ambulance setting, complex specialized electrical or chemical defibrillation techniques may be used. For revival, the following methods are used:

Basic CPR. It is necessary to lay the patient on a hard, flat surface, clear the airways, tilt the head back, and protrude the lower jaw. Pinch the victim's nose, put a tissue napkin over his mouth, clasp his lips with his lips and take a deep breath. Compression should be done with the weight of the whole body. The sternum should be pressed through by 4-5 centimeters. The ratio of compressions and breaths is 30:2 regardless of the number of rescuers. If the heart rate and spontaneous breathing are restored, you need to lay the patient on his side and wait for the doctor. Self-transportation is prohibited.
Specialized assistance. In the conditions of a medical institution, assistance is provided in a comprehensive manner. If ventricular fibrillation is detected on the ECG, defibrillation is performed with discharges of 200 and 360 J. It is possible to administer antiarrhythmics against the background of basic resuscitation. With asystole, adrenaline, atropine, sodium bicarbonate, calcium chloride are administered. The patient must be intubated and transferred to mechanical ventilation, if this has not been done before. Monitoring is shown to determine the effectiveness of medical actions.
Help after rhythm recovery. After the restoration of sinus rhythm, IVL is continued until consciousness is restored or longer if the situation requires it. According to the results of the analysis of acid-base balance, the electrolyte balance, pH is corrected. It requires round-the-clock monitoring of the patient's vital activity, assessment of the degree of damage to the central nervous system. Rehabilitation treatment is prescribed: antiplatelet agents, antioxidants, vascular drugs, dopamine for low blood pressure, soda for metabolic acidosis, nootropics.

Forecast and prevention

The prognosis for any type of SCD is unfavorable. Even with timely CPR, there is a high risk of ischemic changes in the tissues of the central nervous system, skeletal muscles, and internal organs. The probability of successful rhythm recovery is higher in ventricular fibrillation, complete asystole is less favorable prognostically. Prevention consists in the timely detection of heart disease, the exclusion of smoking and alcohol consumption, regular moderate aerobic training (running, walking, jumping rope). Excessive physical activity (weightlifting) is recommended to be abandoned.

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Sudden death

Protocol code: E-003

Purpose of the stage: restoration of the function of all vital systems and organs.

Code (codes) according to ICD-10:

R96 Other sudden death of unknown cause

Ruled out:

sudden cardiac death so described (I46.1)

sudden death of an infant (R95)

Definition:

Death occurs suddenly or within 60 minutes after the onset of symptoms of deterioration in well-being in persons who were previously in a stable condition, in the absence of signs of a specific disease.

VS do not include cases of violent death, death as a result of trauma, asphyxia, drowning and poisoning.

VS can be cardiogenic or non-cardiogenic.

The main cardiac causes of OEC: ventricular fibrillation, pulseless ventricular tachycardia, complete AV block with idioventricular rhythm, electromechanical dissociation, asystole, severe vascular dystonia with a critical drop in blood pressure.

Ventricular fibrillation.

Discoordinated and disintegrated contractions of myocardial fibers leading to the impossibility of SW formation.

It accounts for 60-70% of all cases of OEC.

VF is more often observed in acute coronary insufficiency, drowning in fresh water, hypothermia, electric shock.

Harbingers of VF: early, paired and polytopic ventricular extrasystoles.

Prefibrillatory forms of VT: alternating and pirouette VT, polymorphic VT.

The rate of ventricular tachycardia is so high that during diastole the ventricular cavities are unable to fill with sufficient blood, resulting in a sharp decrease in cardiac output (no pulse) and hence inadequate circulation.

Pulseless ventricular tachycardia is predicted to equate to ventricular fibrillation.

Asystole

Absence of cardiac contractions and signs of electrical activity, confirmed in three leads on the ECG.

It accounts for 20-25% of all cases of effective circulatory arrest.

They are divided into sudden (especially unfavorable in terms of prognosis) and delayed (occurring after previous rhythm disturbances).

Severe depression of myocardial contractility with a drop in cardiac output and blood pressure, but with persistent cardiac complexes on the ECG.

It accounts for about 10% of all cases of AEC.

Primary EMD - the myocardium loses the ability to perform effective contraction in the presence of a source of electrical impulses.

The heart quickly switches to an idioventricular rhythm, which is soon replaced by asystole.

Primary EMDs include:

1) acute myocardial infarction (especially its lower wall);

2) the state after repeated, debilitating myocardium, episodes of fibrillation, eliminated by CMRT;

3) the final stage of severe heart disease;

4) myocardial depression by endotoxins and drugs in case of overdose (beta-blockers, calcium antagonists, tricyclic antidepressants, cardiac glycosides).

5) atrial thrombosis, heart tumor.

Secondary EMD - a sharp decrease in cardiac output, not associated with a direct violation of the processes of excitability and contractility of the myocardium.

Causes of secondary EMD:

1) pericardial tamponade;

2) pulmonary embolism;

4) severe hypovolemia;

5) thrombus occlusion of a prosthetic valve.

EMD can be caused by:

sinus bradycardia, atrioventricular block, slow idioventricular rhythm. Mixed forms of EMD

Marked with the progression of toxic-metabolic processes:

1) severe endotoxemia;

2) hypoglycemia;

3) hypo- and hypercalcemia;

4) severe metabolic acidosis;

Principles of Cardiopulmonary Resuscitation (CPR)

The brain experiences the absence of blood flow only for 2-3 minutes - it is for this period of time that glucose reserves in the brain are enough to ensure energy metabolism during anaerobic glycolysis.

Resuscitation should begin with prosthetics of the heart, the main task is to provide blood perfusion to the brain!

sudden death resuscitation

The main tasks of the first resuscitation aid:

1. Restoration of effective hemodynamics.

2. Restoration of breathing.

3. Restoration and correction of brain functions.

4. Prevention of recurrence of the terminal state.

5. Prevention of possible complications.

The main symptoms of a sudden stop of effective blood circulation:

1. Loss of consciousness develops within 8-10 seconds from the moment of circulatory arrest.

2. Convulsions usually appear at the moment of loss of consciousness.

3. Absence of pulsation on large main arteries.

4. Respiratory arrest often occurs later than other symptoms - by about 20 - 30 - 40 s. Sometimes agonal breathing is observed for 1-2 minutes or more.

5. Pupil dilation appears after 30-90 seconds from the onset of circulatory arrest.

6. Paleness, cyanosis, "marbling" of the skin.

Indications for resuscitation:

1. Absence and severe weakness of pulsation in the carotid (or femoral and brachial) arteries.

2. Lack of breath.

3. Inadequate breathing (pathological forms of breathing, shallow, rare, fading breathing).4. Lack of consciousness.

5. Lack of photoreactions and dilated pupils.

Contraindications for resuscitation:

1. Terminal stages of an incurable disease.

2. Significant traumatic destruction of the brain.

3. Early (drying and clouding of the cornea, a symptom of "cat's eye") and late (cadaveric spots and rigor mortis) signs of biological death.

4. Documented refusal of the patient from resuscitation.

5. Being in a state of clinical death for more than 20 minutes before the arrival of qualified assistance.

What manipulations should not be carried out in order to avoid wasting time:

1. Auscultate the heart.

2. Search for pulsation on the radial artery.

3. Carry out the algorithm - "feel, see, hear."

4. Determine corneal, tendon and pharyngeal reflexes.

5. Measure blood pressure.

The main criteria for continuing resuscitation:

1. Pulse on the carotid arteries, synchronous with chest compressions - indicates the correct execution of a heart massage and maintaining tone

myocardium.

2. Change in the color of the skin (pink).

3. Constriction of the pupil (improvement of oxygenation in the region of the midbrain).

4. High "artifact complexes" on the ECG.

5. Recovery of consciousness during resuscitation.

Indicators of the futility of further resuscitation:

1. Areactivity of dilated pupils.

2. Absence or steady decrease in muscle tone.

3. Absence of reflexes from the upper respiratory tract.

4. Low deformed "artifact complexes" on the ECG.

The term "closed heart massage" is invalid, because. by pushing the sternum 4-5 cm in the anteroposterior direction, it is impossible to squeeze the heart between the sternum and the spinal column - the indicated size of the chest is 12-15 cm, and the size of the heart in this area is 7-8 cm.

In chest compressions, the effect of thoracic

pumps, i.e. an increase in intrathoracic pressure during compression and a decrease in intrathoracic pressure during decompression.

precordial strike

1. 4-5 sharp punches are applied to the patient in the zone of the border of the middle and lower third of the sternum from a distance of at least 30 cm.

2. The blow must be strong enough, but not extremely powerful.

3. Indications for precordial beats are ventricular fibrillation and pulseless ventricular tachycardia.

4. Efficiency of impact in case of ventricular tachycardia without pulse ranges from 10 to 25%.

5. With ventricular fibrillation, rhythm recovery occurs much less frequently.

6. It is used only in the absence of a defibrillator prepared for work and

patients with significant circulatory arrest.

7. Precordial shock should not be used as a substitute for electrical cardiac defibrillation (EMF).

8. Precordial beat can translate ventricular tachycardia into asystole, ventricular fibrillation or EMD, respectively, VF - into asystole or EMD.

9. In asystole and EMD, the precordial beat is not used.

Thoracic pump technique:

1. The palmar surface of the right hand is placed on the middle of the sternum or 2-3 cm above the xiphoid process of the sternum, and the palm of the left hand on the right.

2. You can not take your hand off your chest in pauses.

3. Compression is carried out due to the gravity of the body of the rescuer.

4. The depth of excursion of the sternum towards the spine should be 4-5 cm in adults.

5 . The rate of pressure should be 60-80 in 1 min.

6. To assess the effectiveness of the thoracic pump, periodically palpate the pulse on the carotid arteries.

7. Resuscitation is suspended for 5 seconds at the end of 1 minute and then every 2-3 minutes to assess whether the restoration of spontaneous breathing and circulation has occurred.

8. Resuscitation should not be stopped for more than 5-10 seconds for additional therapeutic measures and for 25-30 seconds for tracheal intubation.

9. The compression-to-inspiration ratio should be 20:2 with any number of rescuers prior to tracheal intubation, then 10:1.

Auxiliary techniques that increase the effect of the thoracic pump:

1. Carrying out a thoracic pump only on a solid basis.

2. Raising the legs by 35-40° reduces the "functioning" vascular bed at the expense of the lower extremities. This leads to the centralization of blood circulation and an increase in BCC by 600-700 ml. The inflowing blood accelerates the closure of the aortic valves in the phase of cessation of chest compressions, thereby improving coronary blood flow.

The Trendelenburg position is dangerous, because it contributes to the development of hypoxic cerebral edema.

1. Infusion of plasma substitutes increases venous pressure and increases venous backwater.

2. Insertion abdominal compression consists in compressing the abdomen after the cessation of chest compression. By this action, as it were, blood is squeezed out of the vascular bed of the abdomen. Carry out only in intubated patients because of the danger of regurgitation.

Thoracic pump mechanism:

1. Thoracic pump - compression of the chambers of the heart and lungs by increasing pressure in the entire chest cavity.

2. In the phase of chest compression, all chambers of the heart, coronary arteries and large vessels are compressed.

3. The pressure in the aorta and the right atrium equalizes and the coronary circulation stops.

4. When the chest is expanded, blood flow to the heart improves, a small pressure gradient is established between the aorta and the right atrium.

5. An increase in pressure in the aortic arch leads to the closure of the semilunar valves, behind which the orifices of the coronary arteries depart, and, consequently, to the restoration of blood flow through the coronary arteries.

Thoracic pump efficiency:

1. Creates a low pressure gradient and low diastolic pressure (the driving force for coronary blood flow) by evenly distributing pressure on the structures of the chest cavity.

2. Cardiac index is less than 20-25% of the norm, which is lower than that observed in severe cardiogenic shock.

3. The performance of the thoracic pump rapidly decreases, which, even in the absence of severe myocardial damage, leads to the disappearance of efficiency by 30-40 minutes. Increasing hypoxia and mechanical trauma of the heart in a short time lead to a drop in myocardial tone.

4. Provides no more than 5-10% of normal coronary circulation.

5. Cerebral blood flow during the production of a thoracic pump does not exceed 10-20% of the norm, while most of the artificial blood flow is carried out in the soft tissues of the head.

6. The minimum blood circulation in the brain that a thoracic pump is able to create is a 10-minute time barrier. After the specified period of time, the entire supply of oxygen in the myocardium completely disappears, energy reserves are completely depleted, the heart loses tone and becomes flabby.

The effectiveness of open heart massage (OMS):

1. OMS provides greater survival with full restoration of brain function. Most patients recover with restoration of cerebral life, even after two hours of CMPR.

2. Infection is not a major problem after thoracotomy, even under non-sterile conditions.

3. OMS provides more adequate cerebral (up to 90% of normal) and coronary (more than 50% of normal) blood flow than a thoracic pump, because the latter increases intrathoracic pressure, blood pressure and venous pressure.

4. OMS creates a higher arterio-venous perfusion pressure.

5. With thoracotomy, the heart can be directly observed and palpated, which helps to evaluate the effect of drug therapy and PMF in SIMR.

6. An open chest allows you to stop intrathoracic bleeding.

7. In case of intra-abdominal bleeding, it allows temporary clamping of the thoracic aorta above the diaphragm.

8. The mechanical irritation of the heart provided by direct massage contributes to the appearance of myocardial contractions.

OMS should be started as early as possible in cases where an adequately performed thoracic pump does not restore spontaneous circulation. The discrediting of CHI depends on the delay in its use.

After an unsuccessful long-term production of a thoracic pump, the transition to OMS is equivalent to a massage of a deceased heart.

The main indications for direct heart massage:

1. Pericardial tamponade in most cases can be eliminated only by direct emptying of the pericardial cavity from fluid.

2. Extensive pulmonary thromboembolism.

3. Deep hypothermia - persistent VF occurs. Thoracotomy allows you to warm the heart with warm saline during direct massage.

4. Penetrating wounds of the chest and abdominal cavity, blunt trauma with a clinical picture of cardiac arrest.

5. Loss of elasticity of the chest - deformity and rigidity of the chest and spine, mediastinal displacement.

6. Unsuccessful attempts (within 3-5 minutes) of external defibrillation (at least 12 discharges of maximum energy).

7. Sudden asystole in young people and inefficiency of the thoracic pump.

8. Massive hemothorax.

10. Exudative pleurisy.

11. Ruptured aortic aneurysm.

12. Severe emphysema.

13. Multiple fractures of the ribs, sternum, spine.

Defibrillation Success Factors:

1. Efficient production of a thoracic pump, ventilation of the lungs with a maximum supply of oxygen in the respiratory mixture.

2. Defibrillation after the introduction of adrenaline is more effective. Small-wave fibrillation is transferred to large-wave fibrillation with the help of adrenaline. Defibrillation with small wave fibrillation is ineffective and can cause asystole.

3. With the introduction of cardiotonic or antiarrhythmic drugs, the discharge should be applied no earlier than 30-40 seconds after the administration of the drug. Follow the pattern: medicine > thoracic pump and ventilator > defibrillation > medicine > thoracic pump and ventilator > defibrillation.

4. It is necessary to observe the density and uniformity of pressing the electrodes to the skin: the pressure is about 10 kg.

5. The location of the electrodes should not be close to each other.

6. To overcome the resistance of the chest, which averages 70-80 ohms, and to receive more energy from the heart, three discharges with increasing energy are applied: 200 J > 300 J > 360 J.

7. The interval between discharges should be minimal - only for the time of pulse control or ECG (5-10 seconds).

8. The polarity of the applied pulse is not of fundamental importance.

9. The application of the discharge should be carried out in the patient's exhalation phase. This reduces lung coverage of the heart and reduces ohmic resistance by 15-20%, which increases the efficiency of the defibrillator discharge.

9. In the event of repeated episodes of fibrillation, the discharge energy that previously had a positive effect is used.

10. If ECG control is not possible, applying a “blind” discharge in the first minute of cardiac arrest is quite acceptable.

11. Avoid placing electrodes over an artificial pacemaker.

12. With a significant thickness of the patient's chest wall, the initial discharge of the EIT should be 300 J, then 360 J and 400 J.

Mistakes and complications of electropulse therapy (EIT)

1. It is impossible to carry out EIT during asystole.

2. Accidental exposure of others to electrical discharge may be fatal.

3. After EIT (cardioversion), there may be a temporary or permanent disruption of the artificial pacemaker.

4. Do not allow long breaks in resuscitation while preparing the defibrillator for discharge.

5. Loose pressing of the electrodes is not allowed.

6. Do not use electrodes without sufficient wetting of their surface.

7. Do not leave tracks (liquid, gel) between the defibrillator electrodes.

8. You can not be distracted during the EIT.

9. Do not apply low or excessive voltage discharge.

11. You can not provide resuscitation at the time of the EIT.

Indications and contraindications for manipulation

The use of an oral airway is not recommended for:

1) unresolved obstruction of the upper respiratory tract;

2) trauma to the oral cavity;

3) fracture of the jaw;

4) loose teeth;

5) acute bronchospasm.

Complications when using the oral airway:

1) bronchospastic reaction;

2) vomiting followed by regurgitation;

3) laryngospasm;

4) aggravation of airway obstruction.

Indications for tracheal intubation:

1. Ineffective ventilation of the lungs by other means.

2. Great resistance to air blowing (unresolved laryngospasm, large weight of the mammary glands in obesity, with toxicosis in pregnant women).

3. Regurgitation and suspected aspiration of gastric contents.

4. The presence of a large amount of sputum, mucus and blood in the oral cavity, in the trachea, bronchi.

6. Absence of pharyngeal reflexes.

7. Multiple fractures of the ribs.

8. Transition to open heart massage.

9. The need for prolonged mechanical ventilation.

Remember, that:

If a defibrillator is available for VF, the shocks are delivered prior to intravenous access.

When peripheral veins are available, catheterization of the main veins is not performed to avoid complications (tension pneumothorax, injury to the subclavian artery and thoracic lymphatic duct, air embolism, etc.).

In case of a fracture of the ribs and / or the sternum of the patient, the frame of the chest is disturbed, which sharply reduces the effectiveness of the thoracic pump.

Drugs (adrenaline, atropine, lidocaine) can be injected into the endotracheal tube or directly into the trachea by conicopuncture, increasing the dose by 2-3 times and diluting 10-20 ml of isotonic sodium chloride solution, followed by 3-4 forced breaths to pulverize the drug.

Intracardiac injections "in the blind" are not used, due to the risk of damage to the coronary vessels and pathways, the development of hemopericardium and tension pneumothorax, injection of the drug directly into the myocardium.

Classification:

Sudden death:

1. Cardiogenic: asystole, ventricular fibrillation, pulseless ventricular tachycardia, electromechanical dissociation;

2. Non-cardiogenic: asystole, ventricular fibrillation, pulseless ventricular tachycardia, electromechanical dissociation.

Diagnostic criteria:

Signs of a sudden stop of effective blood circulation:

1. Consciousness is absent.

2. Pulsation on large main arteries is not determined.

3. Breathing is agonal or absent.

4. The pupils are dilated, do not react to light.

5. The skin is pale gray, occasionally with a cyanotic tint.

List of main diagnostic measures:

1) reveal the presence of consciousness;

2) check the pulse on both carotid arteries;

3) establish the patency of the upper respiratory tract;

4) determine the size of the pupils and their reaction to light (in the course of resuscitation);

5) determine the type of effective circulatory arrest on the defibrillator monitor (ECG) (in the course of resuscitation);

6) assess the color of the skin (in the course of resuscitation).

First aid tactics:

Principles of treatment:

1. The effectiveness of restoring the effective work of the heart depends on the time of the start of CIRT and on the adequacy of the measures taken.

2. Creating a rigid support under the patient's head and torso improves the efficiency of the chest pump.

3. Raising the legs by 30-40° increases the passive return of blood to the heart - increases the preload.

4. Insertion of abdominal compression in the interval between successive chest compressions increases preload and increases coronary perfusion pressure.

5. Open heart massage after tracheal intubation creates an effective pressure gradient and significantly increases the perfusion of the brain and heart, which allows prolonging CIRT up to 2 hours or more with the restoration of biological and social life. Produced at the pre-hospital stage only by a trained medical worker!

ventricular fibrillation

1. Apply precordial shocks during the preparation of the defibrillator for work, if no more than 30 seconds have passed since the effective blood circulation stopped. Remember that the precordial beat itself can lead to the development of asystole and EMD!

6. Defibrillator shock is applied only in the presence of large-wave fibrillation: 200 J - 300 J - 360 J. Discharges should follow each other without continuing CIRT and checking the pulse.

7. If unsuccessful: epinephrine (0.1%) IV 1.0 ml (1 mg) per 10 ml isotonic solution

NaCl, after which SLMR is performed and EIT is repeated - 360 J.

8. In case of failure: intravenous bolus amiodarone (cordarone) 300 mg per 20 ml of 5% glucose; if amiodarone is not available, lidocaine 1.5 mg/kg IV bolus. SLMR - EIT (360 J). Search for a removable cause of VF.

9. If unsuccessful: epinephrine 3.0 mg IV, sodium bicarbonate 2 ml 4% solution per 1 kg (1 mmol / kg) IV, amiodarone 300 mg per 20 ml 5% glucose (lidocaine 1.5 mg / kg w/w). SLMR - EIT (360 J).

10. If unsuccessful: magnesium sulfate 5-10 ml 25% solution IV and / or propranolol 0.1% - 10 ml IV. SLMR - EIT (360 J).

11. In case of failure: thoracotomy, open heart massage with medical support and EIT.

12. If VF is eliminated: evaluate hemodynamics, determine the nature of the post-conversion rhythm. Continue maintenance infusion

antiarrhythmic agent, which gave a positive effect.

Ventricular tachycardia without pulse

Treatment is similar to that for ventricular fibrillation.

Asystole

1. Do not use precordial beats with established or suspected asystole!

2. Compression of the chest (60-80 in 1 min).

3. IVL. First, "from mouth to mouth", with an Ambu bag. After tracheal intubation, use 100% oxygen.

4. Venepuncture or venocatheterization.

6. Epinephrine (0.1%) IV 1.0 ml (1 mg) per 10 ml isotonic NaCl solution (repeat every 3 minutes). Increase the dose to 3 mg, then 5 mg, then 7 mg if the standard does not work. SRMR between injections.

7. Atropine (0.1%) IV 1.0 ml (1 mg), repeat every 3 minutes. Increase the dose to 3 mg if the standard dose is ineffective up to a total dose of 0.04 mg/kg. SLMR.

8. Eliminate the possible cause of asystole (hypoxia, acidosis, hypokalemia and hyperkalemia, drug overdose, etc.).

9. Aminophylline (2.4%) IV 10 ml for 1 min. SLMR.

10. External pacing is effective while maintaining myocardial function.

11. Sodium bicarbonate (4%) 1 mmol/kg IV is indicated if asystole occurs against the background of acidosis.

Electromechanical dissociation (EMD)

1. Do not use precordial beats with established or suspected EMD!

2. Compression of the chest (60-80 in 1 min).

3. IVL. First, "from mouth to mouth", with an Ambu bag. After tracheal intubation, use 100% oxygen.

4. Venepuncture or venocatheterization.

6. Epinephrine (0.1%) IV 1.0 ml (1 mg) per 10 ml isotonic NaCl solution (repeat

every 3 minutes). Increase the dose to 3 mg, then 5 mg, then 7 mg if the standard does not work. SRMR between injections.

7. Identify the cause (shock, hypokalemia, hyperkalemia, acidosis, inadequate ventilation, hypovolemia, etc.) and eliminate it.

8. Infusion therapy - 0.9% NaCl solution or 5% glucose solution up to 1 l / h.

9. With low heart rate - atropine 1 mg IV every 3 minutes, bringing up to 3 mg.

10. Sodium bicarbonate (4%) 1 mmol/kg IV in the development of acidosis.

11. Electrocardiostimulation.

Note:

Sodium bicarbonate is administered at 1 mmol / kg (2 ml of a 4% solution per 1 kg of body weight), and then at 0.5 mmol / kg every 7-10 minutes. Applied with prolonged SIMR (10 minutes or more), the development of sudden death on the background of acidosis, hyperkalemia, overdose of tricyclic antidepressants.

With hyperkalemia, the introduction of calcium chloride is indicated at the rate of 20-40 ml of 10%

solution in / in.

List of basic and additional medicines:

1) epinephrine

2) atropine

3) amiodarone

4) aminophylline

5) 0.9% sodium chloride solution

6) 4% sodium bicarbonate solution

7) lidocaine

8) 25% magnesium sulfate solution

9) propranolol

Indicators of the effectiveness of medical care:

The main criteria for continuing resuscitation:

1) pulse on the carotid arteries;

This indicates the correctness of the heart massage and the preservation of myocardial tone.

2) discoloration of the skin (pink discoloration);

3) constriction of the pupil (improvement of oxygenation in the area of the midbrain);

4) high "artifact complexes" on the ECG.

5) recovery of consciousness during resuscitation.

List of used literature

1. Guide to emergency medical care. Bagnenko S.F., Vertkin A.L., Miroshnichenko A.G., Khabutia M.Sh. GEOTAR-Media, 2006

2. First aid in emergency critical conditions. I.F. Epiphany. St. Petersburg, "Hippocrates", 2003

3. Secrets of emergency care. P. E. Parsons, J. P. Wiener-Kronisch. Moscow, MEDpress-inform, 2006

4. Pulmonary-cardiac and cerebral resuscitation. F.R. Akhmerov et al. Kazan, 2002

5. Intensive care of threatening conditions. Ed. V.A. Koryachkin and V.I. Strashnova. St. Petersburg, 2002

6. Guide to intensive care. Ed. A.I. Treshchinsky and F.S. Glumcher. Kyiv, 2004

7. Intensive care. Moscow, GEOTAR, 1998

8Henderson. emergency medicine. Texas, 2006

9. Vital Signs and Resuscitation. Stewart. Texas, 2003

10 Rosen's Emergency Medicine. Mosby, 2002

5. Birtanov E.A., Novikov S.V., Akshalova D.Z. Development of clinical guidelines and protocols for diagnosis and treatment, taking into account modern requirements. Guidelines. Almaty, 2006, 44 p.

No. 883 "On Approval of the List of Essential (Essential) Medicines".

7. Order of the Minister of Health of the Republic of Kazakhstan dated November 30, 2005 No. 542 “On amendments and additions to the order of the Ministry of Health of the Republic of Kazakhstan dated December 7, 2004 No. 854 “On approval of the Instructions for the formation of the List of essential (vital) medicines”.

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Cheat sheet: Algorithm for the provision of emergency care for cardiac diseases and poisoning. Reasons why acute coronary insufficiency and sudden death develop What is sudden coronary death

The reasons

Mechanisms of emergence and development (pathogenesis)

Clinical picture (symptoms and syndromes)

Diagnostics

Treatment

ICD-10

General information

The reasons

Pathogenesis

Classification

Symptoms of sudden cardiac death

Complications

Diagnostics

Urgent care

Forecast and prevention

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