At the heart of the activities carried out in patients with circulatory and respiratory arrest, is the concept of "chain of survival". It consists of actions performed sequentially at the scene, during transportation and in medical institution. The most important and vulnerable link is the primary resuscitation complex, because in a few minutes from the moment of circulatory arrest, irreversible changes in the brain develop.

■ Both primary respiratory arrest and primary circulatory arrest are possible.

■ The cause of primary circulatory arrest can be myocardial infarction, arrhythmias, electrolyte disturbances, pulmonary embolism, aortic aneurysm rupture, etc. There are three options for cardiac arrest: asystole, ventricular fibrillation and electromechanical dissociation.

■ Primary respiratory arrest (foreign bodies in the airways, electrical injury, drowning, CNS damage, etc.) is less common. By the time the emergency medical service begins, as a rule, ventricular fibrillation or asystole has time to develop. The signs of circulatory arrest are listed below.

■ Loss of consciousness.

■ No pulse in the carotid arteries.

■ Respiratory arrest.

■ Pupil dilation and lack of reaction to light.

■ Change in skin color.

To confirm cardiac arrest, the presence of the first two signs is sufficient.

The primary resuscitation complex consists of the following activities (Fig. 2-1):

■ restoration of airway patency;

■ IVL and oxygenation;

■ indirect heart massage.

The specialized resuscitation complex includes the following activities:

■ electrocardiography and defibrillation;

■ provision of venous access and administration medicines;

■ tracheal intubation.

If you find an unconscious person, you should call out to him and shake his shoulder.

If the person does not open their eyes or respond, check for spontaneous breathing and a carotid pulse.

RESTORATION OF AIRWAY PERFORMANCE

In the event of an emergency, airway patency is often impaired as a result of retraction of the tongue, aspiration of vomit, blood. It is necessary to clean the oropharynx:

using a tupfer (gauze swab) or

using a mechanical or electric aspirator.

Then it is necessary to perform the Safar triple technique: straighten the head in the cervical spine, push the lower jaw forward and up and open the mouth. In cases where a fracture cannot be ruled out cervical the spine and unbend the head should not be limited to advancing the jaw and opening the mouth. If the denture is intact, it is left in the oral cavity, as this preserves the contour of the mouth and facilitates mechanical ventilation.

The technique for performing the Safar triple technique: throw back the head, push the lower jaw and open the mouth.

For airway obstruction foreign body the victim is laid on his side and 3-5 sharp blows are made with the lower part of the palm in the interscapular region, then they try to remove the foreign body from the oropharynx with a finger. If this method is ineffective, then the Heimlich maneuver is performed: the palm of the person providing assistance is placed on the stomach between the navel and the xiphoid process, the second hand is placed on the first and a push is made from the bottom up along the midline, and they also try to remove the foreign body from the oropharynx with a finger.

Due to the risk of infection of the resuscitator upon contact with the mucous membrane of the mouth and nose, as well as to improve the efficiency of mechanical ventilation, a number of devices are used:

■ Device "key of life".

■ Oral airway.

■ Transnasal airway.

■ Pharyngotracheal duct.

■ Double-lumen esophageal-tracheal airway (combitube).

■ Laryngeal mask.

Oropharyngeal airway is usually used. You can determine the appropriate size by measuring the distance from the corner of the mouth to the earlobe. The air duct is inserted with a bend down, inserted halfway, rotated 180 degrees and inserted to the end.

The laryngeal mask airway is an endotracheal tube that does not pass through the glottis into the trachea, but has a miniature mask at the distal end that is put on the larynx. The cuff adjacent to the edge of the mask is inflated around the larynx, providing a tight seal.

The laryngeal mask has many advantages, including the ability to avoid extension of the head in the cervical region, if there are contraindications for this.
Restoration of the airways can also be done with the help of a laryngeal tube.
Tracheal intubation is performed with prolonged resuscitation and can only be performed if you have good knowledge of the manipulation technique. Every emergency physician should be able to perform tracheal intubation. This method allows you to ensure optimal airway patency, reduce the likelihood of regurgitation during the complex resuscitation to provide higher intrapulmonary pressure. In addition, some drugs can be injected through the endotracheal tube.

ARTIFICIAL LUNG VENTILATION

Artificial respiration - blowing air or an oxygen-enriched mixture of gases into the lungs of a patient without or using special devices. The air exhaled by a person contains 16-18% oxygen, therefore, mechanical ventilation with atmospheric air or an oxygen-air mixture is more effective. Each breath should last 1-2 seconds. The adequacy of mechanical ventilation is assessed by periodic expansion of the chest and passive exhalation of air.

The media team usually administers ventilation either through an airway or face mask, or after tracheal intubation with an Ambu bag.

Straightening the Ambu bag (ADR - manual breathing apparatus)

Performing artificial lung ventilation using ADR. (Pay attention to the correct position of the hands.)

Artificial lung ventilation using an ADR with an oxygen hose connected to it.

INDIRECT HEART MASSAGE

After circulatory arrest for 20-30 minutes, automatism and conduction functions are preserved in the heart. The main purpose of heart massage is to create artificial blood flow. During an indirect heart massage, not only the heart is compressed, but also the lungs, which contain a large amount of blood. This mechanism is called the breast pump.

In patients with ventricular fibrillation, in the absence of a defibrillator prepared for work, it is recommended to apply a precordial blow (1-2 sharp punches to the border of the middle and lower third of the sternum from a distance of at least 30 cm).

When conducting a closed heart massage, the patient should be on a hard surface. One palm of the resuscitator is placed on the lower third of the sternum along the midline, the second rests against the back surface of the first. The time of pressing and releasing is 1 s, the interval between compressions is 0.5-1 s. The sternum in an adult should be “pushed through” to a distance of 5-6 cm. The interruption in chest compressions should not exceed 5-10 s when performing any therapeutic measures. level of 60-70 mm Hg, discoloration of the skin.

For 2 breaths of air, 30 chest compressions are performed.

ELECTRIC HEART DEFIBRILLATION

Electrical defibrillation of the heart - essential component cardiopulmonary resuscitation. The technique and algorithm for its implementation are described in the article "Sudden cardiac death" in the section "Emergency conditions in diseases of the cardiovascular system".

Energy set. Usually 360 joules are immediately set.

Lubrication of electrodes with gel.

Location of electrodes. The sternal electrode is located in the second intercostal space on the right. Apical - on the mid-axillary line.

To carry out the discharge, both red buttons are pressed simultaneously. Do not touch the patient while doing this.

VENOUS ACCESS AND DRUG INTRODUCTION FUNDS

If available peripheral vein, then use it, better after catheterization. If an experienced resuscitator is well versed in the puncture technique central vein, you can use this path, although this will have to interrupt resuscitation, and it is not advisable to do this for more than 5-10 s. Drugs are administered through the trachea if tracheal intubation is performed or, in extreme cases, drugs can be injected into the trachea through the cricoid membrane.

Drugs used in cardiopulmonary resuscitation.

■ Epinephrine 1 mg IV by bolus or endotracheal at a dose of 2 mg, diluted in 10 ml of 0.9% sodium chloride solution. Epinephrine remains the drug of choice in circulatory arrest. The administration of the drug can be repeated at intervals of 5 minutes, although the administration of doses exceeding 5 mg does not lead to an increase in survival. High doses of epinephrine may increase the severity of postresuscitation myocardial dysfunction,

contribute to the development of severe hypokalemia, one of the main pathogenetic factors of malignant ventricular arrhythmias.

Particular caution should be exercised when using epinephrine in the event of cardiac arrest associated with the abuse of cocaine or other sympathomimetics.

■ Atropine 1 mg (1 ml of 0.1% solution) in / in the stream or endotracheally (in this case, the dose is increased by 2-2.5 times). The introduction of atropine is indicated for bradysystole and asystole. The introduction can be repeated after 5 minutes, but the total dose should not exceed 3 mg during resuscitation.

TERMINATION OF RESUSCITATION

The reason for the termination of cardiopulmonary resuscitation is the absence of signs of restoration of blood circulation and respiration when using all available methods for 30 minutes.

In all cases of successful resuscitation, patients are subject to hospitalization in the intensive care unit of the hospital.

Clinical example

Man 50 years old. Does not make any complaints. (Unconscious).
According to a relative, he complained of chest pain for several hours, 2-3 minutes before the arrival of the ambulance, he lost consciousness, snored. There is no history of chronic diseases.
Objectively: he is lying on the couch on his back, single rare respiratory movements. The pulse on the carotid arteries is not determined. The skin is pale, moist. The pupils are wide. Beloglazov's sign is not detected.
The ECG revealed large-wave ventricular fibrillation.
Help: At 15.10 resuscitation began.
Indirect cardiac massage. Restored airway patency (laryngeal tube). Manual IVL.
15.15 Defibrillation with a 200 J discharge. Large-wave ventricular fibrillation is on the monitor.
15.17 Defibrillation with a 200 J discharge. Large-wave ventricular fibrillation is on the monitor.
15.18 Sol. Adrenalini 0.1%-1 ml IV.
15.20 Defibrillation with a 360 J discharge. Large-wave ventricular fibrillation is on the monitor.
15.22 Sol. Cordaroni 50 mg/ml – 6 ml IV
15.25 Defibrillation 360 J on the monitor small-wave ventricular fibrillation.
15.27 Sol. Adrenalini 0.1%-1 ml IV. On the monitor of the defibrillator, small-wave ventricular fibrillation.
15.30 There is an isoline on the monitor.
Sol. Adrenalini 0.1%-1 ml IV five times with an interval of 5 minutes.
Closed heart massage, IVL.
At 16.00On the ECG - isoline. RThe animation was found to be ineffective.

After 10 minutes, Beloglazov's symptom was detected. Declaration of death 16.10.
Ds . Ventricular fibrillation. clinical death. Resuscitation. Declaration of death.
Reported to the ROVD.

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Case Study #74

Patient X., 61 years old, was in the toxicological intensive care unit for 4 days. Clinical diagnosis. Main: 1. Poisoning with opiates, coma, complicated by respiratory failure of the central type. 2. IHD, HD-2, widespread atherosclerosis, postinfarction cardiosclerosis, recurrent myocardial infarction, deep vein thrombosis of the legs, pulmonary embolism.

Complications: purulent tracheobronchitis, aspiration pneumonia. Post-resuscitation disease, encephalopathy of mixed origin. Accompanying: cyst of the left kidney.

Pathological anatomical diagnosis: chronic exogenous (alcoholic) intoxication, micronodular fatty cirrhosis of the liver (fermentemia according to clinical data), splenomegaly, fatty myocardial dystrophy (uneven blood supply, foci of acute ischemic dystrophy of myocardiocytes), pancreatic lipomatosis. Condition after detoxification therapy (infusion, antidote), positive urine reaction to opiates.

Hypertonic disease and atherosclerosis: moderate atherosclerosis of the aorta, stenosing plaques of the coronary arteries of the heart, widespread reticular and focal replacement cardiosclerosis, myocardial hypertrophy - heart weight 660 g, hypertensive angioencephalopathy with foci of acute hypoxic changes in neurons. Chronical bronchitis. Pneumosclerosis. Left kidney cyst. Cortical adenoma of the adrenal gland. Foci of symmetrical ischemic softening in the subcortical formations of both hemispheres of the brain. Left-sided lower lobe confluent pneumonia. Condition after lower tracheostomy and prolonged mechanical ventilation.

Reasons for discrepancies in diagnoses: overdiagnosis of poisoning, underestimation of clinical and anamnestic data.

P.S. A positive urine test for opiates (qualitative test) is insufficient evidence for diagnosing poisoning (narcotic coma), since it does not give a quantitative (toxic) characteristic of the concentration of the toxicant in the patient's biological environment, but only indicates its presence. In this case, the reassessment of laboratory data led to an underestimation of clinical and anamnestic information about the presence of severe somatic pathology in the patient (CHD, myocardial infarction, pneumonia, thromboembolism). pulmonary artery etc.), which was the main cause of death of the patient.

Case Study #75

Patient M., aged 36, was in the toxicological intensive care unit for 8 hours. Clinical diagnosis. Primary: poisoning with caustic liquid (soldering acid). Suicide. Chemical burn of the upper respiratory tract, stomach III st. Exotoxic shock. Complications: gastrointestinal bleeding. Background disease: chronic alcohol intoxication, alcoholic cardiomyopathy, drunkenness.

Pathological anatomical diagnosis: dichloroethane poisoning: liquid brownish-pink contents in the intestine with the smell of dichloroethane, hemorrhages under the gastric mucosa, subendocardial hemorrhages, uneven myocardial blood supply, plethora and pulmonary edema, cerebral edema, dystrophic changes in the liver, kidneys. Non-stenosing coronary sclerosis. Fibrosis of the pancreas.

Reasons for discrepancies in diagnoses: a short stay in the hospital, the severity of the condition.

P.S. In this case, clinical and anamnestic data (ingestion of acid and Clinical signs chemical burns of the stomach and respiratory tract) served as the basis for the diagnosis of poisoning with caustic liquid, confirmed, by the way, by gastroscopic examination. However, in the presence of bleeding, hemorrhages under the gastric mucosa were not detected, which are a constant symptom of dichloroethane poisoning, which had a major influence in the thanatogenesis of death as a result of an irreversible exotoxic shock. An error in the diagnosis is associated with the failure to conduct a chemical-toxicological blood test in the presence of a distinct smell of dichloroethane.

Case Study #76

Patient A., 38 years old, spent 45 minutes in the toxicological intensive care unit. Clinical diagnosis: mixture poisoning medicines for the purpose of self-treatment (trichopolum, stugeron, spazgan). Chronic alcoholism. Drunken state. Decompensated metabolic acidosis. Purulent tracheobronchitis. Atelectasis of the right lung? Histonephropathy. Alcoholic cardiomyopathy. Cholecystopancreatitis. DIC syndrome. Pulmonary edema, cerebral edema, TBI. Condition after clinical death, tracheal intubation, mechanical ventilation, central vein catheterization, resuscitation.

Pathological anatomical diagnosis: croupous upper and middle lobe right-sided pneumonia in the stage of gray hepatization. Severe dystrophy of the kidneys. Hyperplasia of the pulp of the spleen. Edema of lungs and brain. Chronic alcoholism: soft tissue fibrosis meninges, diffuse liver steatosis, pancreatic fibrosis, cardiomyopathy: expansion of the heart cavities, focal fibrosis of the endocardium of the left ventricle of the heart, hypertrophy, fatty degeneration and uneven myocardial blood supply; non-stenosing coronary sclerosis. Weakly expressed atherosclerosis of the aorta. Liquid state of blood. Dystrophy and uneven blood filling of the kidneys.

Reasons for discrepancies in diagnoses: poor-quality x-ray examination.

P.S. In this case, one of the important reasons for the discrepancy between diagnoses is the distrust or underestimation of the classical data of percussion and auscultation of the lungs, which could (“hepatic dullness of sound”) suggest lobar pneumonia, despite an incorrect x-ray examination.

Case Study #77

Patient Sh., 87 years old, was admitted on April 16, 2008 to the department of toxic intensive care for poisoning with caustic liquid (T54.3). Delivered by a team from MP from home. According to the SMP doctor, a patient suffering from senile dementia accidentally drank a solution of a caustic liquid (“Mole” - caustic soda) 2 hours before admission. On DHE - the stomach was washed through a tube, symptomatic therapy.

The patient suffers from ischemic heart disease, atrial fibrillation, hypertension, varicose veins. On admission: the patient's condition is moderate. The tongue and visible mucous membranes of the oral cavity are edematous, hyperemic. There is hoarseness of voice, pain on palpation of the cervical esophagus and abdomen in the epigastrium. With endoscopy - swelling of the entrance to the esophagus.

In the department of toxic resuscitation, infusion therapy with homeostasis correction, anti-burn, antibacterial, antispasmodic, hemostatic, symptomatic therapy was carried out. On the R-gram of the chest from April 21, 2008, there is hypovenilation of the basal segments on the right. On the background of therapy, the patient's condition stabilized.

The department continued detoxification, antibacterial, symptomatic therapy, endoscopic laser therapy (only 2 sessions due to the patient's refusal). The course of the disease was complicated by the development of post-burn stricture of the esophagus. 07.05.08, the patient developed signs of acute purulent parotitis on the right, in connection with which she underwent drainage of the duct of the parotid gland, continued antibacterial, detoxification therapy.

On the R-gram of the chest from 07.05.08, the lung fields are transparent, pneumosclerosis; esophagus - post-burn cicatricial narrowing of the lower third of the esophagus with a minimum clearance of up to 0.5. The patient's condition remained stable. Continued anti-burn, symptomatic therapy. EGDS 16.05.08, necrotic widespread burn esophagitis in the phase of formation of non-epithelized subcompensated extended stricture of the middle and lower thoracic esophagus. Focal ulcerative burn gastritis against the background of mucosal atrophy. On May 21, 2008, at 07:50, she was found unconscious, pressure and pulse on the main vessels were not determined, there was no breathing. An indirect heart massage was started, mechanical ventilation with an AMBU bag - without effect. At 08:10 he was pronounced dead.

Clinical diagnosis. Primary: poisoning with caustic liquid ("Mole"). Random. Chemical burns of the oral mucosa, pharynx, esophagus, stomach. Senile dementia. Complications: acute heart failure. Pulmonary embolism. Post-burn stricture of the esophagus. Accompanying: coronary artery disease. Widespread atherosclerosis of the vessels of the brain, aorta, coronary arteries of the heart. Atrial fibrillation. permanent form. Coronary cardiosclerosis. Hypertonic disease. Pneumosclerosis. Acute purulent parotitis on the right. Varicose disease.

Pathological anatomical diagnosis: poisoning with caustic liquid ("Mole"): chemical burn of the mucous membrane of the oral cavity, pharynx, esophagus and stomach (according to the medical record of the inpatient).

Deep vein thrombosis of the legs, progressive pulmonary embolism, infarction-pneumonia of the lower lobe of the right lung. Ascites (1000 ml), bilateral hydrothorax (left 300 ml, right 600 ml). Cerebral edema.

Hypertension and atherosclerosis: expansion of the heart cavities, non-stenosing coronary sclerosis, focal sclerosis of the endocardium, focal cardiosclerosis, dystrophic changes and moderate myocardial hypertrophy (heart weight 300 g), arteriolonephrosclerosis, brown cysts in the subcortical formations of both hemispheres of the brain, ulcerative aortic atheromatosis. Right-sided purulent parotitis. Fibrosis of the pancreas. Steatosis of the liver (T54.3).

Conclusion: death from pulmonary embolism due to deep vein thrombosis of the legs at the time of hospitalization due to caustic fluid poisoning.

P.S. An example of severe poisoning with caustic soda (chemical burns of the pharynx, esophagus, stomach) in an elderly patient suffering from many chronic diseases, including varicose veins, which suffered the first most severe stage of burn disease and died suddenly from pulmonary embolism, ultimately as a result of a medical error - in last days(when the danger has passed stomach bleeding) prophylactic heparinization and bandaging of the legs, a common source of thromboembolism, from thrombosed deep veins was not performed (violation of the protocol for the treatment of patients with thrombophlebitis of the veins of the leg).

Case Study #78

Patient G., aged 32, was taken to the Poison Center of the Research Institute for Emergency Medicine. N.V. Sklifosovsky by a media team from the street, where he was found unconscious after drinking alcohol. On DGE without therapy. The anamnesis is not known.

On admission: the general condition is extremely serious, the patient is in a coma. There are no meningeal signs. Pupils OS=OD=2 mm, photoreaction is reduced. Breathing spontaneously through the natural airways, inadequate, in connection with which, and to prevent aspiration, the patient was intubated without technical difficulties and transferred to mechanical breathing using a Micro-vent ventilator in IPPV mode, is carried out in all parts of the lungs. Breathing is hard, conducted wheezing. Heart sounds are muffled, arrhythmic, heart rate - 50-56 beats per minute, blood pressure - 80/40 mm Hg. The introduction of pressor amines has begun.

In the department of toxicological resuscitation, biological media were taken from the patient: ethanol in the blood - 3.04%, in the urine - 4.45%. At 21:45, against the background of mechanical ventilation, intractable collapse, cardiac arrest occurred. Started resuscitation - without effect. The pupils are wide, there is no photoreaction. Reflexes are not called. On the monitor - the absence of electrical activity of the heart. BP is not determined. The pulse is not palpated in the main vessels. Declared dead on 21.10.06 at 22:30 (stayed in intensive care for 75 minutes).

Clinical diagnosis. Primary: ethanol poisoning (T51.0). General hypothermia of the body. Primary complication: exotoxic shock; coma, complicated by respiratory failure of a mixed type. Pathological anatomical diagnosis: combined underlying disease.

1. Acute subdural hematoma in the fronto-parietal-temporal region on the left 150 g; swelling and dislocation of the brain: foci of secondary circulatory disorders in the trunk at the level of the pons.
2. Acute alcohol poisoning: intravital detection of ethanol in the blood 3.04%, in the urine - 4.45% (according to the medical record).
3. General hypothermia of the body: hypothermia (body temperature at admission 34 ° C), small focal hemorrhages in the gastric mucosa (Vishnevsky spots).

Purulent bronchitis. Cardiomyopathy. Diffuse hepatic steatosis. Kidney dystrophy. Uneven blood filling of internal organs, pulmonary edema. Abrasions of the frontal region on the left, behind the ear region on the right, anterior-outer surface of the right knee joint with focal hemorrhages in the surrounding soft tissues. Condition after central venous catheterization, mechanical ventilation, resuscitation. Postresuscitation fractures of 5-6 ribs on the left.

P.S. The reason for the partial discrepancy between the clinical and pathoanatomical diagnoses lies in the insufficiently detailed neurological examination of the patient, which made it impossible to determine the local symptoms of brain damage, to conduct lumbar puncture and instrumental examination (X-ray of the skull, CT scan of the brain). However, ultimately, all this is due to the extremely difficult condition of the patient and the short time (75 min) of his stay in the hospital, which did not allow him to perform all the necessary diagnostic measures in this case.

Case Study #79

Patient K., 70 years old, on September 4, 2007, was taken to the city hospital by an ambulance team due to a snake bite. Diagnosis at admission: acute poisoning of animal origin (snake bite in the left hand). Anamnesis: 3 days ago he was bitten by a snake in his left hand, he did not seek medical help. Complained of pain and swelling of the left hand. No general manifestations of intoxication were noted. Nevertheless, intravenous infusion therapy was prescribed and, as follows from the statement of relatives, a dropper was placed in the bitten hand. On the 2nd day of hospital stay, the patient's condition remained satisfactory, he was discharged on the 3rd day at his own request.

Clinical diagnosis: poisoning with snake venom - a snake bite in the left hand. On the same day, redness and purulent discharge appeared at home from the place where the drip needle was placed, then within 6 days the inflammation progressed, swelling, hyperemia, pain spread to the entire left forearm, the temperature rose to 39 ° C. The therapy was carried out on an outpatient basis until the patient's condition became critical and urinary retention was noted.

11 days after the bite, the patient is re-hospitalized due to urinary retention in the urology department, while his serious condition, the presence of phlegmon of the left hand and forearm is ignored. Over the next 3 days, the patient's condition progressively worsened due to the development of sepsis (there were signs of multiple organ failure) and the patient died on the 15th day after the bite. Clinical diagnosis: 1. Main: snake bite 01.09.07, in the left hand. 2. Complications of the main diagnosis: phlegmon of the left forearm, severe sepsis, endotoxic shock, multiple organ failure. Pathological examination confirmed the diagnosis.

P.S. A clinical example of the death of a patient with a snake bite from severe complications (sepsis, multiple organ failure) due to a number of treatment shortcomings: late admission to the hospital (due to the fault of the patient), intravenous infusion therapy (not needed) in the bitten hand (source of infection), a break in inpatient treatment (due to the fault of doctors who failed to foresee the obvious danger of infectious complications).

Case Study #80

Patient M., aged 17, was admitted to the toxicology department on 23.10.97 at 17:05. Delivered by ambulance from the house, where a few hours before admission to the department he was found unconscious. Presumably with suicidal intent, he could take a mixture of psychotropic pills. There was no treatment for DGE. Upon admission to the department, the patient's condition was severe: he was unconscious, screamed at painful stimuli (active movements of the limbs), opened his eyes, but quickly "exhausted" and fell into a coma. Breathing was independent, adequate. BP - 130/70 mm Hg. Pulse - 90 beats / min. The skin and mucous membranes of the lips are pink, dry. Amitriptyline and benzodiazepines were found in the patient's urine samples.

After catheterization of the central vein, the patient started infusion therapy. The patient was shown intestinal lavage (CL). When trying to antegrade sounding of the initial section small intestine, during the introduction of the gastroduodenoscope into the patient's stomach, vomiting and aspiration of gastric contents occurred. The patient's condition deteriorated sharply: respiratory arrest occurred, the skin became pale cyanotic, the mucous membranes of the lips became cyanotic. BP — 60/30 mm Hg, thready pulse. The fiberscope was removed from the stomach. An emergency tracheal intubation was performed, mechanical ventilation was started, and the tracheobronchial tree was sanitized. Then, under endoscopic control, a nasojejunal probe was placed and CL was started. Hemodynamics remained unstable, despite all attempts to stabilize it. Against the background of intractable collapse, cardiac arrest occurred 2.5 hours later. Resuscitation measures were ineffective.

Clinical diagnosis. Main: acute poisoning with psychotropic drugs (amitriptyline, benzodiazepines). Complications: coma (coma on the Glasgow scale — 3b). aspiration syndrome. Acute cardiovascular failure.

P.S. In this case, before probing the intestine, it was necessary to intubate the trachea, but this was not done due to the preservation of the cough reflex and the patient's motor activity. To prevent aspiration of gastric contents during bowel probing and subsequent CL, it was necessary to give tracheal intubation induction anesthesia with muscle relaxants of ultrashort action, without fear in this case during mechanical ventilation of their synergistic action with a deepening coma.

Case Study #81

A sick man, 65 years old, (disabled group I after leg amputation) was hospitalized in the city hospital on October 11, 2007 with a diagnosis of pneumonia. Upon admission, there were signs of moderate respiratory failure (shortness of breath), moderate tachycardia, arterial hypertension (BP - 160/100 mm Hg). Received treatment according to the diagnosis. In addition, digoxin tablets were prescribed. On October 15, 2007, in the morning, he complained to the nurse about pain in his side and vomiting. The nurse informed the attending physician that there were no records (examination and appointments) on this matter in the medical history. On 15.10.07, at 17:00, the state of health worsened, the pain in the abdomen intensified, he was examined by the on-call therapist, who noted a moderately swollen, painful abdomen, pallor of the skin. The surgeon on duty suspected intestinal obstruction or mesenteric thrombosis. At the same time, the patient reported that the pain in the abdomen began at 14:10, but he did not tell anyone about this.

An abdominal radiograph was ordered to determine free gas in the abdominal cavity. The patient was transported to the X-ray room while sitting in a chair. In the x-ray room, abdominal distention increased sharply, the presence of free gas in the abdominal cavity was confirmed. In the same place there was a cardiac arrest and clinical death.

After resuscitation and restoration of stable hemodynamics, a laparotomy was performed. After making an incision, a fountain of fetid brown foam hit from the abdominal cavity. Even before the laparotomy, severe subcutaneous emphysema appeared, spreading to the level of the neck, to the back. A rupture of the stomach wall, foamy contents in the abdominal cavity, and reactive changes in the peritoneum were revealed. The patient died 2 hours after the operation.

A forensic medical examination revealed a total chemical burn of the gastric mucosa and 10 cm of the lower 1/3 of the esophagus, a rupture of the stomach wall up to 10 cm long, and mediastinal emphysema.
The medical examiner sent fluid obtained from the abdominal cavity and stomach for chemical examination. Hydrogen peroxide was found. The cause - the source of the appearance of hydrogen peroxide in the stomach - has not yet been established by the investigation.

P.S. Judging by the severity of the burn, the abundance of foam, we can talk about either technical hydrogen peroxide (perhydrol, 33%), or hydroperite tablets. There are observations of the development of a stroke in this pathology due to air embolism of cerebral vessels.

Case Study #82

Patient I., aged 23, was admitted on 20.10.07. at 00:35, died on October 26, 2007 at 07:00, spent 6 bed-days. The patient was taken to the department of toxicological resuscitation of the Research Institute for Emergency Medicine. N.V. Sklifosovsky by the SMP team from the house on 20.10.07. According to the SMP doctor, the patient injected himself intravenously into the femoral vein for the purpose of drug intoxication solvent No. 646 and acetic anhydride. There were complaints of lack of air, dizziness. On DHE - prednisolone 300 mg, trisol - 400.0, disol - 200.0, sodium bicarbonate solution 5% - 200.0.

The condition after admission is extremely severe, GCS - 12 points. Stunning, on awakening complaints of difficulty in breathing, chills. The skin is sharply cyanotic, vascular pattern of the type of marbling. Multiple traces of injections in the groin. Visible mucous membranes are moist, cyanotic. Heart sounds are muffled, rhythmic. BP — 90/60 mm Hg, PS = HR = 108-112 bpm. Breathing is noisy, respiratory rate - 30-42 per minute, auscultatory - wet rales of various sizes, decrease in vesicular respiration in lower sections. After catheterization Bladder received 500 ml of dark red urine (possibly hemolyzed). In connection with respiratory failure of the mixed type, the patient underwent tracheal intubation and was transferred to a ventilator.

In the toxicological study of biological media in the blood / urine - ethanol was not detected, in the urine: free hemoglobin, acetone, isopropanol, ethyl acetate were found. An R-graph of the chest dated October 20, 2007 showed vascular plethora with elements of pulmonary edema, dilated roots, bilateral hydrothorax, and bilateral polysegmental pneumonia. Ultrasound of October 20, 2007 revealed bilateral hydrothorax (separation of the pleura at the level of the sinus on both sides up to 3.0 cm).

In toxicological resuscitation on October 20, 2007, hemodiafiltration No. 1 was performed due to the development of hyperhydration (increase in pulmonary edema, increased wet rales, increase in CVP to 180-200 mm of water column), azotemia (creatinine increased from 130 to 307), development of oliguria. Conducted: infusion and symptomatic therapy, due to unstable hemodynamics (decrease in blood pressure to 90/60 mm Hg), the introduction of vasopressors (S/Dopmini - at a rate of 5-7 mcg/kg/min) was started.

On October 21, 2007, taking into account the appearance of a rash in a patient, worsening of the neurological status (stunning, sharply inhibited), leukocytosis of 28.5 thousand, meningitis of unclear etiology cannot be excluded. He was consulted by a neurosurgeon, an infectious disease specialist - there are no data for an infectious disease. October 21, 2007 — repeated hemodiafiltration No. 2 was performed due to the persistence of hyperhydration, hyperazotemia, and oligoanuria. On October 22, 2007, against the background of persistent bilateral pulmonary edema, a repeated R-graphic study revealed bilateral hydrothorax, more on the right; ultrasound revealed separation of the pleura on the right up to 6.5 cm, on the left up to 1.8 cm, a puncture of the right pleural cavity, 600 ml of serous-hemorrhagic fluid and 600 ml of air were removed, a drainage of 5 m / r was installed.

A control R-logical study revealed a right-sided pneumothorax with mediastinal displacement, drainage of the right pleural cavity at 2 m/r was performed, the drains were connected to active aspiration. In the control R-logical study, liquid and air were not detected. The patient's condition remained extremely severe, without positive dynamics.

On October 23, 2007, hemodiafiltration No. 3 was performed (renal-hepatic insufficiency, hyperazotemia persist). Due to the need for mechanical ventilation, prevention of trophic disorders in the trachea, adequate sanitation of the TBD, the patient underwent n/tracheostomy. On October 24, 2007, and on October 25, 2007, hemodiafiltration Nos. 4 and 5 were performed for azotemia and AKI. Against the background of ongoing detoxification therapy, the condition remained extremely severe, with negative hemodynamics. Hypotension progressed, the rate of dopamine administration was constantly increasing, up to 15–20 µg/kg/min. 26.10.07 at 06:30 the patient's condition deteriorated sharply: there was a collapse with cardiac arrest. Cardiopulmonary resuscitation was started, which was unsuccessful. At 07:00 - death was declared.

Clinical diagnosis. Main: 1. Poisoning with solvent No. 646 (T52.9) and acetic anhydride administered intravenously. Suicide. 2. Complication of the main one: exotoxic shock, acute hemolysis, hemoglobinuric nephrosis, purulent tracheobronchitis, bilateral pleuropneumonia, hydropneumothorax, acute renal failure. Related: drug addiction. Pathological anatomical diagnosis: combined poisoning with opiates, solvent 646 and acetic anhydride: acute hemolysis - the concentration of free hemoglobin in the urine is 3.39 mg / ml. Hemoglobinuric nephrosis. Acute kidney failure(according to clinical data). Purulent tracheobronchitis. Bilateral focal confluent pleuropneumonia. Post-catheterization thrombophlebitis of the right femoral vein thromboembolism of small branches of the pulmonary artery. Uneven blood filling of internal organs, cerebral edema.
Drug addiction: multiple traces of medical injections in the left inguinal region, phlebitis of the left femoral vein. chronic hepatitis.

Condition after lower tracheostomy, mechanical ventilation, resuscitation. Conclusion: death occurred from bilateral pleuropneumonia and thromboembolism of the pulmonary artery branches, which complicated the course of combined poisoning with opiates, solvent 646 and acetic anhydride.

P.S. In this case of severe poisoning, which required a number of complex detoxification and resuscitation measures, there was no targeted treatment of widespread thrombophlebitis post-injection (probably after repeated drug administration) and post-catheterization (carrying out 5 hemodiafiltration), namely, the establishment of a trap in the inferior vena cava, anticoagulant therapy , which led to thromboembolism of the branches of the pulmonary artery, which, along with toxic pneumonia, became one of the main causes of death of the patient.

Case Study #83

Patient M., aged 31, was admitted to the Poison Center of the Research Institute for Emergency Medicine. N.V. Sklifosovsky on February 17, 2001, was discharged on April 12, 2001 (54 bed days). Diagnosis: suicidal attempt to poison with metal mercury from 01.02.01, Mercury intoxication. On admission: complaints of weakness, general malaise, pain in the joints, limbs, lower abdomen, hyperthermia.

The patient was delivered by the toxicological team of the SMP from the 15th City Clinical Hospital. 02/01/01 For suicidal purposes, mercury was injected from 9 mercury thermometers intravenously, after which there was an increase in temperature to 38 ° C, chills, a metallic taste in the mouth, transient stomatitis, pain throughout the body, which gradually localized in the joints and in the lower sections of the abdomen.

She was hospitalized in the gynecological department of City Clinical Hospital No. 15 with a diagnosis of salpingo-oophoritis (confirmed by laparoscopy), a course of treatment with ampiox, against which an allergic reaction developed. In connection with the increase in weakness, general malaise, the appearance of cramps in the limbs, she was transferred to the therapeutic department, where the fact of the introduction of mercury was revealed. R-graphy was carried out - on the images of the abdominal cavity, lungs - multiple dense blackouts. After consultation with a toxicologist, she was transferred to the Center for Health Protection on February 17, 2001.

On admission: serious condition. Consciousness is clear, contact, oriented. The skin is pale. Visible mucous membranes are pale, moist. There is an increase in the submandibular, axillary and inguinal lymph nodes, which are painful on palpation. The phenomena of stomatitis, hyperthermia. There are no focal neurological symptoms and meningeal signs. Pupils of medium size, photoreaction saved. Tendon reflexes are evenly reduced.

Breathing spontaneous, adequate. Chest of the correct form. Both halves participate in the act of breathing evenly. BH - 20 per minute. Auscultatory - carried out over all departments, no wheezing.
The area of ​​the heart is not changed. The heart sounds are clear, the rhythm is correct. PS=HR — 116 bpm, BP — 110/70 mm Hg.

Oral mucosa with symptoms of stomatitis. The abdomen is of the correct form, not swollen, participates in the act of breathing, soft on palpation, without reaction to palpation; liver - along the edge of the costal arch.
The kidneys are not palpable. The symptoms of effleurage are negative on both sides. Diuresis is preserved, there are no dysuric manifestations.

Conducted infusion-detoxification therapy with the introduction of unithiol in / in, / m. On February 26, 2001, the result of blood and urine tests for mercury content was obtained: in urine — 1.25 mg/l (N — 0.015), in blood — 0.48 mg/l (N — 0.02). Hemodialysis No. 1 — 6 hours was performed. Then, on 03/01/01 and 03/05/01, magnetic blood treatment, hemosorption and 2 hemodialysis for 6 hours were performed.

As a result of the treatment, the condition improved, weakness, temperature decreased, and against the background of antihistamine therapy, the manifestations of dermatitis were stopped. The content of mercury in biological media remained elevated due to the depot of mercury in the lungs and in the cavity of the heart. On March 16, 2001, after appropriate preparation, an attempt was made to remove mercury by the endovascular route from the heart cavity under angiography control using a catheter installed in the right atrium. 250 ml of blood with fibrin and drops of mercury were removed (2 ml in total).

In the control R-graphy, the presence of metal in the cavity of the right ventricle is preserved. After 10 days, a second attempt was made to remove the mercury, as a result of which it was completely removed.
On April 6, 2001, due to a pronounced increase in the content of mercury: in the blood - 0.25 mg/l, in the urine - 1.075 mg/l, magnetic blood processing, hemodialysis No. 4 - 6 hours, and ultraviolet blood processing were performed. Again, the phenomena of an allergic reaction were noted - itching, hyperemia of the skin, puffiness of the face. After taking antihistamines, the manifestations of dermatitis disappeared, the general condition improved, pulse, blood pressure were within normal limits. Weakness lessened.

Survey. Clinical blood test on April 10, 2001: - erythrocytes - 3.8 x 1012 / l, hemoglobin - 103, leukocytes - 7.5 x 109 / l, eosinophils - 2%, stab neutrophils - 3%, segmented neutrophils - 54% , lymphocytes - 30%, monocytes - 11%. General analysis urine 04/05/01: color light yellow, transparency - incomplete; relative density - 1.014, protein - no, leukocytes - 1-3 in the field of view, erythrocytes - no. Biochemical blood test on March 29, 2001: total protein - 74; urea - 5.7; creatinine - 87; bilirubin - 9.2.

The patient was discharged home. Recommended: to continue restorative therapy, taking cuprenil. Clinical diagnosis: 1. Acute metal mercury poisoning with intravenous administration. 2. Toxic nephropathy and encephalopathy. Toxicoallergic reaction. 3. Enlargement of the thyroid gland. Eutherios. Foreign bodies (mercury) in the cavities of the heart and bronchial system of the lungs.

Subsequent clinical examinations(2002) showed persistent signs of toxic nephropathy and encephalopathy with a generally satisfactory condition and a significant decrease in the concentration of mercury in the urine. Subsequently, the patient gave birth to a healthy child, but the connection with her was cut off and her fate is unknown.

P.S. The interest of this case lies in the fact that the patient, having hidden the fact of poisoning, only after 16 days came to the specialized toxicological department for treatment due to incorrect diagnosis of the disease on the DGE and in the hospital before confessing to the deed already with a pronounced clinic acute poisoning.

Case Study #84

Patient W, 28 years old, was taken to the Center for the Treatment of Poisoning of the Research Institute for Emergency Medicine named after. N.V. Sklifosovsky on December 12, 2007 with a diagnosis of acute poisoning with Azaleptin. According to the media doctor, she was found unconscious in an apartment with a geyser next to her mother's corpse.

On admission: a serious condition, depression of consciousness was assessed as a superficial coma (according to the Glasgow scale — 6b). Pupils OD=OS=3 mm. Focal neurological symptoms and traumatic injuries were not revealed. Breathing is independent, noisy, respiratory rate - 18-20 per minute, is carried out in all fields of the lungs, auscultatory - a large number of wet rales. Hemodynamic parameters: BP — 110/60 mm Hg, heart rate — 62 beats/min. Due to inefficient breathing, the patient was transferred to mechanical ventilation after tracheal intubation.

Preliminary diagnosis: poisoning with psychotropic drugs stage IIB. Coma, complicated by respiratory disorders of a mixed type. Chemical-toxicological examination revealed benzodiazepines in the urine.

Started infusion (glucose, albumin), detoxification (tube gastric lavage, intestinal lavage), symptomatic (actovegin) and antibiotic therapy. No positive dynamics of consciousness was noted. The patient was examined by a neurosurgeon who found signs of cerebral edema. A CT scan of the brain was performed, signs of diffuse ischemia in the cortex, subcortical formations and ventricular expansion were identified. Lumbar puncture reduced intracranial pressure and ruled out traumatic brain injury.

By the 3rd day, it became known that a forensic chemical study in the blood of the deceased mother of the patient revealed carboxyhemoglobin in a lethal concentration of 70%. Taking into account this addition to the clinical and anamnestic data in patient Sh., although carboxyhemoglobin was not detected in the blood, toxicohypoxic encephalopathy of the mixed type was diagnosed, due to combined poisoning with benzodiazepines and carbon monoxide.

Nootropic and antihypoxic drugs were added to the treatment: carnitine chloride, gliatilin, acyzol, B vitamins, three sessions of hyperoxybarotherapy were performed. Against the background of the treatment, a positive trend was noted: the restoration of consciousness, spontaneous breathing. On the 20th day, a repeated CT scan of the brain revealed an arachnoid cyst in the left temporal region (0.5 cm3). After stabilizing her condition, she was transferred to the rehabilitation department. Clinical diagnosis at discharge. Primary: benzodiazepine and carbon monoxide poisoning. Toxicohypoxic encephalopathy. Complications: purulent tracheobronchitis. Arachnoid cyst of the left temporal region of the brain.

P.S. A rare observation of paired suicidal acute poisoning with benzodiazepines and carbon monoxide, due to which the patient developed severe cerebral edema, which is not typical for poisoning with benzodiazepines alone, as a result of which a comprehensive clinical and laboratory study had to be carried out, which made it possible to exclude craniocerebral trauma and detect the consequences of toxic damage carbon monoxide, determine the correct diagnosis and complex treatment(detoxification and symptomatic), contributing to the complete recovery of a severe patient. It is possible that the protective antihypoxic effect of benzodiazepines found in the blood of the daughter, in contrast to the deceased mother.

Case Study #85

Patient G., 73 years old, was taken to the Center for the Treatment of Poisoning of the Research Institute for Emergency Medicine named after V.I. N.V. Sklifosovsky by a media team from the house, where 24 hours before admission with a suicidal intent, she took up to 140 tab. tizercine, was discovered by relatives in an unconscious state. On DGE - stupor, the stomach was washed through a tube, is registered with the IPA, a repeated suicide attempt.

Upon admission to the toxic intensive care unit: the patient's condition was severe - in a coma, a weak motor reaction to a painful stimulus (according to the Glasgow scale 5b). Bruised wound of the left brow. BP — 105/60 mm Hg, heart rate — 110 bpm. Breathing independent, inadequate, in connection with which the patient was intubated, transferred to a ventilator.

In the laboratory: ethanol in the blood, urine - not detected, phenothiazines, benzodiazepines were found in the urine. In the department of the patient, infusion, detoxification, symptomatic therapy, forced diuresis, administration of laxatives, and pharmacological stimulation of the intestine were started. To rule out neurosurgical pathology, the patient was consulted by a neurosurgeon, and a CT scan of the brain was performed; there are no data for neurosurgical pathology. The course of the disease was complicated by the development of purulent tracheobronchitis, pneumonia.

25.10.08, the patient noted cardiac arrest, resuscitation was carried out with a positive effect. On October 25, 2008, the patient underwent n/tracheostomy for long-term mechanical ventilation and adequate sanitation of the patient's TBD. On the R-gram of the chest organs dated October 28, 2008, there were signs of right-sided polysegmental pneumonia. Against the background of ongoing therapy, the patient's condition remained extremely severe. On October 28, 2008, at 18:00, abdominal distention was noted, abdominal ultrasound showed separation of the peritoneal sheets in all departments by 2-3 cm. The patient was examined by a responsible surgeon, laparocentesis was performed, and 1500 ml of bile was excreted.

In connection with bile peritonitis, the patient was examined by an anesthesiologist and, according to vital indications, was transferred to an emergency operating unit for laparotomy, but in the operating room, cardiac arrest suddenly occurred against the background of intractable collapse. On the monitor - the absence of electrical activity of the heart. Resuscitation measures - without effect. At 21:20, death was declared.

Clinical diagnosis. Main: 1. Poisoning with phenothiazines, benzodiazepines (T42.4, T 43.4). Suicide. Exotoxic shock. 2. Biliary peritonitis of unknown etiology. 10/25/08 - n / tracheostomy. Complications of the main: coma, complicated by respiratory failure of a mixed type. Purulent tracheobronchitis. Bilateral polysegmental pneumonia. Hepatonephropathy. Acute vascular and respiratory failure.

Concomitant: ischemic heart disease. Atherosclerotic cardiosclerosis. Hypertension II stage. Circulatory failure IIB. Abrasions of the superciliary region on the left. Forensic medical diagnosis: poisoning with psychotropic drugs (late admission) - lifetime detection of phenothiazines and benzodiazepines in the urine (according to the medical record); condition after catheterization of the right subclavian vein, infusion and detoxification therapy, mechanical ventilation, clinical death, resuscitation.

Acute bulb ulcer duodenum with perforation, common bile peritonitis (more than 2500 ml). Purulent-necrotic tracheobronchitis, right-sided focal confluent pneumonia. Dystrophy of the myocardium, kidneys. Uneven blood filling of the internal organs, swelling of the brain, lungs with focal intrapulmonary hemorrhages. Mild atherosclerosis of the aorta; arterionephrosclerosis, multiple kidney cysts. Focal steatosis of the liver. Fibrosis of the pancreas. Obliteration of the left pleural cavity, pneumosclerosis. Condition after laparocentesis, recatheterization of the right subclavian vein with damage to the wall of the right ventricle of the heart, development of hemopericardium (370 ml), repeated resuscitation; post-resuscitation fractures of 2-5 ribs on the left. Abrasion of the left eyebrow.

Conclusion: death occurred on October 28, 2008 at 21:20 from poisoning with psychotropic drugs, the clinical course of which was complicated by the development of right-sided pneumonia, acute duodenal ulcer with perforation and diffuse peritonitis.

P.S. In this example, due to the severe condition of the patient, only conservative methods of detoxification were used - infusion therapy, stimulation of diuresis. During resuscitation for repeated clinical death during recatheterization of the right subclavian vein, the wall of the right ventricle of the heart was damaged with the development of hemopericarditis (370 ml of blood). To avoid such complications, always use any other vein (eg, jugular or femoral) away from the area of ​​hand pressure on the chest during chest compressions to assist catheter movement.

E. A. Luzhnikov, G. N. Sukhodolova

L. E. Elchinskaya, A. Yu. Shchurov, N. I. Sesina, M. I. Yurshevich

This article presents an overview of clinical cases of medical care for patients with complicated forms of myocardial infarction of the anterior wall of the left ventricle in men of the same age group (50-60 years old) without a previous history of coronary artery disease, with a different course of complications in a specialized resuscitation and cardiology team of the City Emergency Medical Station. aid of St. Petersburg.

Purpose - to emphasize the importance and necessity of a differential approach to therapy and tactics of medical care in acute myocardial infarction, treatment of patients in a specialized resuscitation and cardiology team (RCB) with complicated forms of myocardial infarction on prehospital stage.

Let us consider several clinical cases of providing medical care to patients with a complicated course of acute myocardial infarction, in the conditions of a specialized resuscitation and cardiological team of the city ambulance station of St. Petersburg.

1st case

A call to a man K., 57 years old, to help an ambulance medical team. Reason for the call: "Acute myocardial infarction, candidate for thrombolysis". From the anamnesis it is known that against the background physical activity sudden chest pains of a pressing nature. The patient called an ambulance 10 minutes after the onset of pain. Arriving medical team diagnosed acute myocardial infarction. Taking into account the time of onset of the pain syndrome and the estimated time of delivery to the on-call hospital, which has a vascular center, I called the RCH for a possible STLT. RCH arrived at 45 minutes from the onset of pain.

At the time of arrival of the resuscitation cardiology team:

With active questioning, he does not complain.

The patient was conscious, hemodynamically stable, without signs of microcirculation disorders, blood oxygenation was satisfactory, there were no signs of heart failure.

Prior to the arrival of the SCD, the ECG doctor recorded an ECG, which has the following changes - subepicardial damage to the anterior wall of the left ventricle

(ST elevation in V1-V4 up to 5 mm.)

Pain syndrome, accompanied by general weakness, dizziness, sweating, was stopped by the introduction of fentanyl (100 μg IV). Also, before the SCD, the following were prescribed: aspirin 250 mg, heparin 5000 U, oxygen inhalation was carried out.

On the ECG of the registered RSC, there is a positive trend compared to the previous ECG: a decrease in ST to the isoline, a rise in V2-V3 up to 1 mm remains). When monitoring ECG - single supraventricular extrasystoles. These changes were regarded as spontaneous thrombolysis, given the duration of the pain syndrome (1 hour). The idea that the patient has AMI of the anterior LV wall has not changed.

The therapy was carried out according to WHO recommendations. The patient was prescribed clopidogrel 300 mg, anaprilin 20 mg (BP=120/80 mmHg, heart rate=85 per minute), heparin infusion 1000 IU/h using an infusion pump. The patient was prepared for transport to the hospital.

A few minutes later, without a previous deterioration in the condition, life-threatening rhythm disturbances, ventricular fibrillation occurred, which was regarded as a reperfusion syndrome.

Started resuscitation under the protocol "ventricular fibrillation" recommended by ERS (2010). Tracheal intubation was performed, the patient was transferred to mechanical ventilation, local hypothermia of the head was performed as part of cerebroprotection. Refractory VF persisted. Resuscitation continued for 15 minutes, VF was stopped after the 7th defibrillation, the total dose of cordarone was 450 mg, HMS was performed by the LUCAS 2 chest compression system, which is available on the equipment of the resuscitation and cardiological teams of the St. Petersburg State Health Budgetary Healthcare Institution. When using the LUCAS 2 apparatus, the effectiveness of chest compressions increases, due to stable and uniform chest compressions, cardiac output is up to 50% of the initial value according to various sources. At 16 minutes, effective blood circulation was restored, there is a tendency to arterial hypotension due to postresuscitation syndrome. Hemodynamics was quickly stabilized with dopamine inotropic support at a dose of 7 µg/kg/min. A central venous catheter was installed, a moderate increase in CVP was noted. For neuroprotective purposes, anesthesia was performed with fentanyl 100 μg, Relanium 10 mg, propofol infusion at a dose of 4 mg/kg/h, cytoflavin was prescribed against the background of stabilized hemodynamics, prolonged mechanical ventilation was performed using the Drager apparatus (against the background of FiO - 1 - 0.5). Bladder catheterization was performed, 200 ml of “pre-shock” urine was obtained. The rate of diuresis is reduced. Furosemide 20 mg IV was prescribed to prevent prerenal acute renal failure as part of the treatment of postresuscitation syndrome. According to the i-STAT gas analyzer, which is equipped with the resuscitation teams of the GSSMP, (Na 137 mmo / L, K 2.9 mmo / L, CL 110 mmo / L, pH 7.109, PCO 44.0 mmHg, HCO3 9.2 mmo / L, BEecf -20 mmo/L), metabolic acidosis was confirmed, which inevitably develops in critical conditions, sodium bicarbonate 5% - 100 ml was prescribed for correction, mechanical ventilation parameters were selected in the mode of moderate hyperventilation.

Electrolytes (K, Mg) were infused, since hypokalemia often developing in AMI can be one of the reasons provoking life-threatening arrhythmias, which in this situation was proven laboratory (data from the i-STAT system).

After stabilization of the patient's condition, he was taken to the nearest hospital with a vascular center. The patient was transferred to prolonged mechanical ventilation, in deep medical sedation, minimal inotropic support. ECG without negative dynamics.

In the future, it is known that the patient in the shortest possible time, within an hour, according to emergency indications, underwent coronary angioplasty with stenting of the infarct-dependent artery (LAD). According to the CAG data, there is a parietal thrombus in the area of ​​the permanent ligament, angiographic criteria for the thrombolysis that took place. The patient was on a ventilator during the day, inotropic support in minimal doses. On the second day, he was extubated, in a clear mind, stable hemodynamics, minimal neurological deficit (post-hypoxic encephalopathy). He was hospitalized for 18 days, after which he was sent for sanatorium treatment.

Due to the fact that medical care was provided in a specialized resuscitation team, it was possible to cope with the complications of acute myocardial infarction. Perform CPR effectively. Start targeted, rather than symptomatic, correction of metabolic acidosis, implement neuroprotection, choose the right ventilation mode, stabilize the patient's condition and deliver him to a specialized vascular center.

2nd case

A call to a 60-year-old man S. to help an ambulance team with AMI, cardiogenic shock.

At the time of arrival of the SCD - 3.5 hours from the onset of a typical anginal pain syndrome. The patient is in depressed consciousness (E-3, M-6, V-4, 13b. on the GLAZGO scale - stunning). BP=60/40 mm Hg, heart rate=120 per minute, sinus tachycardia. Auscultatory moist coarse rales over all lung fields, RR=24 per minute, SpO2=88%. The skin is cold to the touch, moist, pale gray in color. On the ECG - subepicardial damage, necrosis of the anterior-lateral wall of the left ventricle (QS in V1-V4, ST elevation up to 8 mm in V1-V6).

Prior to SCD, the following was administered: fentanyl 100 mcg, heparin 5000 units, aspirin 500 mg, dopamine infusion was started. Moderate pain persists.

The SKB team started oxygen insufflation, dose adjustment of dopamine according to the level of blood pressure, fentanyl 100 mcg was administered, clopidogrel 300 mg was prescribed. Shock persists, refractory to inotropic support. Treatment options for pulmonary edema due to arterial hypotension are limited. Despite the time from the onset of AMI more than 3 hours, the presence of a zone of myocardial necrosis, taking into account the preservation of a large zone of myocardial damage, uncorrected true cardiogenic shock, and the absence of contraindications, a decision was made to perform STL (Metalysis). The 2nd peripheral vein was catheterized, 10,000 units were injected. Metalise (calculated by body weight), heparin infusion 1000 U/h was started. ECG monitoring was carried out. Prepared for EIT. Within 35 minutes after administration of the thrombolytic, the patient remained in an unstable, grave condition. ECG without dynamics. At the 35th minute - the appearance of reperfusion arrhythmias in the form of an accelerated ideoventricular rhythm of 80 per minute

Against this background, there was a positive trend in hemodynamics, stabilization of blood pressure at the level of 100/70 mm Hg, clarification of consciousness. The skin is dry, moderately pale. ECG - decrease in ST elevation, persists in V2-V4 up to 4 mm.

Subsequently, the dose of dopamine was adjusted, a positive reaction to inotropic support was observed (reperfusion in the zone of viable myocardium, which was in a state of stagnant and hibernating, due to which it is possible to improve myocardial contractility stimulated by β-agonists, an increase in EF). BP stabilized at 130/80 mmHg, dopamine - 7 µg/kg/min. Pulmonary edema therapy was started: fractional administration of morphine, furosemide, slow infusion of nitrates, against the background of dopamine infusion under BP control. Auscultation in the lungs - a decrease in the caliber and prevalence of wheezing, respiratory rate - 18-20 per minute, SpO2 - 94%. Consciousness is clear.

The patient was transported to the nearest vascular center, where CAG was performed as soon as possible, coronary anatomy with stenting of the infarct-dependent LAD (according to CAG - angiographic criteria for effective thrombolysis). The patient was installed IABP (intra-aortic balloon counterpulsation). For several days he was on the support of IABP, inotropic support, in a clear mind, on spontaneous breathing. The phenomena of OSSN were stopped. The patient was discharged for outpatient treatment after 21 days.

Thanks to the tactics correctly chosen by the resuscitator, conducting STLT at the prehospital stage, intensive care managed to stabilize the extremely serious condition of the patient and safely deliver him to the hospital.

3rd case.

A call to a 54-year-old M. man to help an ambulance paramedic team with AMI, cardiogenic shock.

According to the patient's relatives, he did not experience pain in the chest. Felt bad about 19 hours ago, there was a general weakness, sweating, according to relatives noted unsteadiness of gait, oddities in behavior during the day, there were repeatedly pre-syncope. He was abroad, in this state he drove a vehicle, then moved to the passenger seat, because. was unable to drive further. Upon returning to the city, the relatives called the ambulance. From the anamnesis it is known that the patient long time suffers from diabetes, type 2 on insulin therapy.

At the time of arrival of the SCD, the patient is in a clear mind, there are intellectual-mnestic disorders, the patient is euphoric, underestimates the severity of his condition.

There are no focal neurological, meningeal symptoms. The skin is moderately pale, moist, cold to the touch. BP=80/60 mmHg, HR=130/min, sinus tachycardia, SpO2=83%, RR=26/min. auscultatory breathing hard, carried out in all parts of the lungs, no wheezing. On the ECG - subepicardial damage, necrosis of the anterior LV wall (QS, ST elevation in V1-V5 5-8mm).

The above symptoms were regarded as a manifestation of prolonged hypoxia of mixed genesis (hypoxic, circulatory) against the background of the development of complicated AMI.

A qualitative test was performed for markers of myocardial necrosis, which is available on the equipment of cardioresuscitation teams of the St. Petersburg GBUZGSSMP (troponin, myoglobin, CPK-MB) - positive, which confirms the prescription of MI. A decrease in saturation in the absence of moist rales in the lungs indicates interstitial pulmonary edema.

Heparin 5000 units, aspirin 500 mg were introduced before SCD. Narcotic analgesics were not administered. Oxygen insufflation, dopamine infusion 7 mcg/kg/min, fractional administration of morphine, furosemide, zylt 300 mg were started. BP=115/70 mmHg, HR=125/min, RR=26/min, SpO2=92%. Given the tendency to arterial hypotension, the introduction of nitrates is impossible. Consciousness without dynamics. Against the background of a long-term shock, according to the parameters of the gas analyzer, compensated acidosis was determined, however, in this case, taking into account spontaneous respiration, the administration of sodium bicarbonate is dangerous. Taking into account the correction of respiratory failure with medication, there are no indications for transfer to mechanical ventilation. With the development of ARF due to pulmonary edema against the background of cardiogenic shock, indications for mechanical ventilation should be determined very biasedly, because. respiratory therapy for pulmonary edema involves aggressive settings to expel extravascular lung water, which greatly reduces cardiac output and exacerbates hemodynamic disturbances). : according to Echocardiography (performed at the prehospital stage, available on the equipment of cardio-resuscitation teams of the St. Petersburg State Budgetary Healthcare Institution of Healthcare, akinesia of the proximal and distal segments of the anterior and lateral walls, the apex of the left ventricle, a sharp decrease in EF.

Despite the prescription, the patient has urgent indications for CAG

The patient was transported to the vascular center. At the time of transfer, the state is the same.

In the first hour after admission, CAG was performed, revascularization in the basin of the infarct-dependent artery, IABP was installed. The next day the patient was on IABP support, combined inotropic support, spontaneous breathing. In this case, the catamnesis is unknown.

Having considered the above cases, we see the need for specialized cardio-resuscitation teams in the structure of the ambulance station. In order to provide effective assistance to patients with complicated forms of myocardial infarction, in addition to drugs, special training of a doctor (anesthesiology-resuscitation, cardiology), additional diagnostic and medical equipment is necessary. According to the statistics of the St. Petersburg State Budgetary Healthcare Institution of Healthcare, the number of cases with stabilization of the vital functions of patients in an extremely serious and terminal condition in the conditions of specialized teams is 15%-20% higher than in linear ambulance teams.

After analyzing the provision of care to patients with complicated forms of myocardial infarction by specialized cardio-resuscitation teams, we came to the following conclusions:

1. When providing medical care to patients with ACS at the prehospital stage, despite the reasonable need to deliver the patient as soon as possible to the nearest vascular center for early PCI. In some cases, the risk of death during transportation is extremely high in the absence of specialized cardio-resuscitation care; in order to stabilize the patient and prepare for transportation, the doctor must have a specialization in anesthesiology and resuscitation, and the brigade must have additional diagnostic and therapeutic equipment.
2. When providing specialized resuscitation care to seriously ill patients in full at the prehospital stage, the “door-balloon” time in the hospital is reduced and the patient’s prognosis is improved.
3. According to studies, the widespread use of STL at the prehospital stage increases survival and improves the long-term prognosis of patients with ACS with nonST. However, in some cases, a balanced and individual approach is required to determine the indications for STL.
4. The presence of a gas analyzer in the equipment of the SKB facilitates work with patients in serious and critical condition, providing objective data for the correction of EBV, BOS, determining indications for transfer to mechanical ventilation, selection of ventilation parameters, and also assessing the contribution of the hemic component in a mixed version of hypoxia. These features facilitate the stabilization of the condition of these patients.
5. The presence of a qualitative and quantitative analyzer for determining myocardial damage allows timely and more accurate treatment of patients with ACS.

Conclusion:

Given the trend towards a reduction in the number of medical teams in the structure of ambulance stations, in order to reduce the mortality rate from acute myocardial infarction, it is necessary to increase the number of specialized resuscitation teams. The presence of expensive equipment on the equipment of resuscitation teams: ventilators / IVs, gas analyzers, ECHO, systems for closed heart massage, pacemakers, etc., is justified by the high number of stabilized patients and a favorable prognosis for the further course of the disease.

Literature:

1. Diagnosis and treatment of patients with acute myocardial infarction with ST elevation ECG. Russian recommendations. - M; 2007

2. Diagnosis and treatment of myocardial infarction with ST segment elevation. Guidelines from the American Heart Association and the American College of Cardiology. - M; 2004

3. Guide to emergency medical care / ed. S.F. Bagnenko, A.L. Vertkina, A.G. Miroshnichenko, M.Sh. Khubutii. - M.: GEOTAR-Media, 2007. - 816 p.

4. Ruksin V.V. Emergency cardiology / V.V. Ruksin. - St. Petersburg: Nevsky dialect; M.: Publishing House "Laboratory of basic knowledge", 2003. - 512 p.

7. The ASSENT 3 Investigators. Efficacy and safety of tenecteplase in combination with enoxaparin, abciximab, or unfractionated heparin: the ASSENT 3 randomized trial. Lancet 2001;358:605-13.

Ambulance. A guide for paramedics and nurses Vertkin Arkady Lvovich

16.19. Cardiopulmonary resuscitation

Cardiopulmonary resuscitation – This is a set of measures aimed at reviving the body in the event of circulatory and / or respiratory arrest, that is, upon the onset of clinical death.

clinical death – this is a kind of transitional state between life and death, which is not yet death, but can no longer be called life. Pathological changes in all organs and systems are reversible.

Graph of effective cardiopulmonary resuscitation versus time to clinical death.

As you can see from the graph, the chance of being successfully resuscitated decreases by 10% every minute if primary care is not provided. The duration of the period of clinical death is 4-7 minutes. With hypothermia, the period is extended to 1 hour.

There is an algorithm of actions aimed at maintaining the life of the victim:

Assess the reaction of the victim;

Call for help;

Open airways;

Assess breathing;

Call a doctor on duty or a resuscitator;

Do 30 compressions;

Perform 2 breaths;

Evaluate the effectiveness of actions.

Evaluation of pulsation in the main arteries is not carried out due to frequent diagnostic errors; it is used only as a technique for assessing the effectiveness of ongoing cardiopulmonary resuscitation. First aid for patients with cardiopulmonary attacks includes providing breathing with special medical equipment, defibrillation, emergency drug injections.

Evaluation of the reactions of the victim

Gently shake him by the shoulders and ask out loud, "Are you all right?"

If it responds, then:

Leave it in its original position, making sure that it is not in danger.

Try to find out what happened to him and call for help if necessary.

Re-evaluate its condition periodically.

If he doesn't respond, then follows:

Call someone to help you;

Turn the victim onto their back.

Opening of the airways

With your head thrown back and your palm on your forehead, gently tilt the patient's head back, leaving your thumb and forefinger free to cover your nose if rescue breathing is required.

Hooking your fingers on the hole under the chin, move the victim's chin up to open the airway.

Breath assessment

See if your chest is moving.

Listen to see if the victim is breathing.

Try to feel his breath on your cheek.

During the first few minutes after cardiac arrest, the victim may continue to breathe weakly or infrequently noisy breaths. Do not confuse this with normal breathing. Look, listen, feel for at least 10 seconds to determine if the casualty is breathing normally. If you have any doubt that your breathing is normal, consider it not.

If the casualty is breathing normally:

Rotate it to a stable lateral position;

Ask someone or go for help yourself / call a doctor;

Keep checking for breath.

Doctor call

Have someone go get help, or if you are alone, leave the casualty and call the on-call or emergency doctor, then come back and start chest compressions as follows.

30 chest compressions:

Kneel at the side of the victim;

Place the base of the palm in the middle of the victim's chest;

The base of the second palm, place on top of the first;

Interlace your fingers in the lock and make sure that the pressure will not fall on the ribs of the victim. Do not press on the upper abdomen or on the end of the sternum;

Stand vertically above the victim's chest and press on the chest with straight arms (compression depth 4-5 cm);

After each compression, do not take your hands off the chest, the frequency of compressions is 100 per minute (slightly less than 2 per 1 second);

Compressions and the intervals between them should take about the same amount of time.

2 breaths

After 30 compressions, open the victim's airway again by tilting his head back and raising his chin.

Putting your hand on your forehead, squeeze the soft tissues of your nose with your thumb and forefinger.

Open the patient's mouth while keeping the chin up.

Take a normal breath and place your lips tightly around the patient's mouth, ensuring a tight seal.

Exhale evenly into his mouth for one second, as if you were breathing normally, following the movement of his chest, this will be (sufficient) artificial respiration.

Leaving the patient's head in the same position and straightening up a little, follow the movement of the patient's chest during exhalation.

Take a second normal breath and exhale into the patient's mouth (there should be 2 breaths in total). Then immediately place your hands on the victim's chest, in the manner described above, and give another 30 chest compressions.

Continue chest compressions and ventilation at a ratio of 30:2.

Evaluation of the effectiveness of actions

Perform 4 sets of "30 compressions - 2 breaths", then place your fingertips over the carotid artery and evaluate its pulsation. If it is absent, continue to perform the sequence: 30 compressions - 2 breaths, and so 4 complexes, after which evaluate the effectiveness again.

Continue resuscitation until:

Doctors will not arrive;

The victim will not begin to breathe normally;

You will not lose strength completely (you will not be completely tired).

A stop to assess the patient's condition can be made only when he begins to breathe normally; Until then, do not interrupt resuscitation.

If you are not alone in resuscitation, change every one to two minutes to avoid overworking.

Stable lateral position – optimal patient position

There are several options for the optimal position of the patient, each of which has its own advantages. There is no universal provision suitable for all victims. The position should be stable, close to this lateral position with the head down, without pressure on the chest, for free breathing. There is the following sequence of actions to place the victim in a stable lateral position:

Remove goggles from the victim.

Kneel next to the victim and make sure both legs are straight.

Place the patient's arm closest to you at a right angle to the torso, bending the elbow so that the palm is pointing up.

Swing your far arm across your chest, pressing the back of his hand against the victim's cheek on your side.

With your free hand, bend the victim's leg farthest from you, taking it slightly above the knee and keeping his foot on the ground.

Keeping his hand pressed to his cheek, pull the far leg to turn the victim to your side.

Adjust the top leg so that the hip and knee are bent at a right angle.

Tilt your head back to make sure your airway remains open.

If it is necessary to keep your head tilted, rest it with your cheek on the palm of his bent arm.

Check for breath regularly.

If the victim must remain in this position for more than 30 minutes, he is turned to the other side to relieve pressure on the lower arm.

In most cases, providing emergency care in the hospital associated with fainting and falling . In such cases, it is also necessary to first conduct an inspection according to the algorithm described above. Help the patient back to bed if possible. In the patient's card, it is necessary to make a record that the patient fell, under what conditions this happened and what assistance was provided. This information will help your doctor decide on treatment that will prevent or reduce your risk of fainting and falls in the future.

Another common cause requiring emergency care is - respiratory disorders . Their cause may be bronchial asthma, allergic reactions, pulmonary embolism. When examining according to the indicated algorithm, it is necessary to help the patient cope with anxiety, find the right words to calm him down. To facilitate the patient's breathing, raise the head of the bed, use oxygen bags, masks. If the patient is more comfortable breathing while sitting, be close to prevent a possible fall. A patient with respiratory problems should be referred for X-ray, to measure the level of arterial gases in him, to conduct an ECG and calculate the respiratory rate. The patient's medical history and reasons for hospitalization will help determine the causes of respiratory problems.

Anaphylactic shock - a type of allergic reaction. This condition also requires emergency care. Uncontrolled anaphylaxis leads to bronchoconstriction, circulatory collapse, and death. If a patient is transfused with blood or plasma at the time of an attack, it is necessary to immediately stop their supply and replace it with a saline solution. Next, you need to raise the head of the bed and carry out oxygenation. While one person from the medical staff monitors the patient's condition, the other must prepare adrenaline for injection. Corticosteroids can also be used to treat anaphylaxis. antihistamines. To a patient suffering from such severe allergic reactions, you must always carry an ampoule of adrenaline and a bracelet with a warning about possible anaphylaxis or a reminder for the ambulance doctors.

Loss of consciousness

There are many reasons why a person can lose consciousness. The patient's medical history and reasons for hospitalization provide information about the nature of the disorder. Treatment for each is selected strictly individually, based on the causes of loss of consciousness. Some of these reasons are:

taking alcohol or drugs: Do you smell alcohol from the patient? Are there clear signs or symptoms? What is the reaction of the pupils to light? Is it shallow breathing? Does the patient respond to naloxone?

attack(apoplexy, cardiac, epileptic): have there been seizures before? Does the patient experience urinary or intestinal incontinence?

metabolic disorders : Does the patient suffer from renal or hepatic insufficiency? Does he have diabetes? Check your blood glucose levels. If the patient is hypoglycemic, determine if intravenous glucose is required;

traumatic brain injury: The patient has just suffered a traumatic brain injury. Be aware that an elderly patient may develop a subdural hematoma days after a TBI;

stroke: if a stroke is suspected, computed tomography of the brain should be performed;

infection: whether the patient has signs or symptoms of meningitis or sepsis.

Remember that loss of consciousness is always very dangerous for the patient. In this case, it is necessary not only to provide first aid, to carry out further treatment, but also to provide emotional support.

Airway obstruction by a foreign body (suffocation) is a rare but potentially avoidable cause of accidental death.

- Give five blows to the back as follows:

Stand to the side and slightly behind the casualty.

While supporting the chest with one hand, tilt the victim so that the object that has exited the respiratory tract would fall out of the mouth rather than enter the respiratory tract.

Make about five sharp blows between the shoulder blades with the base of the palm of the other hand.

– After each stroke, monitor whether the obstruction has decreased. Pay attention to efficiency, not the number of hits.

- If five blows to the back have no effect, give five abdominal thrusts as follows:

Stand behind the casualty and wrap your arms around him at the top of his abdomen.

Tilt the victim forward.

Squeeze one hand into a fist and place it on the area between the navel and the xiphoid process of the victim.

Grabbing your fist with your free hand, make a sharp push in an upward and inward direction.

Repeat these steps up to five times.

Currently, the development of cardiopulmonary resuscitation technology is carried out through simulation training (simulation - from lat. . simulation -"pretense", a false image of the disease or its individual symptoms) - the creation of an educational process in which the student acts in a simulated environment and knows about it. The most important qualities of simulation training are the completeness and realism of modeling its object. As a rule, the biggest gaps are identified in the field of resuscitation and management of the patient in emergency situations, when the time for making a decision is minimized, and the development of actions comes to the fore.

This approach makes it possible to acquire the necessary practical and theoretical knowledge without harming human health.

Simulation training allows: to teach how to work in accordance with modern algorithms for providing emergency care, to develop teamwork and coordination, to increase the level of performing complex medical procedures, to evaluate the effectiveness of one's own actions. At the same time, the training system is based on the method of obtaining knowledge “from simple to complex”: starting from elementary manipulations, ending with practicing actions in simulated clinical situations.

The simulation training class should be equipped with devices used in emergency situations (breathing equipment, defibrillators, infusion pumps, resuscitation and traumatic placements, etc.) and a simulation system (dummies of various generations: for practicing primary skills, for simulating elementary clinical situations and actions of the prepared group).

In such a system, with the help of a computer, the physiological states of a person are simulated as fully as possible.

All the most difficult stages are repeated by each student at least 4 times:

At a lecture or seminar;

On the mannequin - the teacher shows;

Self-execution on the simulator;

The student sees from the side of his fellow students, marks the mistakes.

The flexibility of the system allows it to be used for training and simulation of many situations. Thus, the simulation technology of education can be considered an ideal model for teaching care at the prehospital stage and in the hospital.

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The article discusses the main errors in the conduct of CPR, identified in the analysis of emergency call cards of the State Budgetary Institution of Health of the Republic of Moldova "Ambulance Station" in Saransk, as well as a number of practical issues that arise when providing medical care to patients in terminal condition.

Indications and conditions for cardiopulmonary resuscitation

When determining indications for CPR, one should be guided by the following regulatory legal acts:

Federal Law No. 323-FZ dated November 21, 2011 “On Citizens in Russian Federation”(Article 66 “Determination of the moment of death of a person and termination of resuscitation measures”); Decree of the Government of the Russian Federation of September 20, 2012 No. 950 “On approval of the Rules for determining the moment of death of a person, including the criteria and procedure for determining the death of a person, the Rules for the termination of resuscitation measures and the form of the protocol for establishing the death of a person.”

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Indications for carrying out CPR are all cases of clinical death (hereinafter referred to as CS), regardless of the cause of its development, with the exception of those cases when resuscitation is not carried out.

The diagnosis of CS is based on three main and three additional criteria.

Basic (mandatory) criteria:

1) lack of consciousness (the patient has no reaction to examination and pain);

2) lack of pulsation in the main arteries (on the carotid - in children over 1 year old and adults, on the femoral - in children under 1 year old);

3) lack of breathing or agonal type of breathing (complete cessation of breathing occurs on average 20-30 seconds after cardiac arrest).

Additional (optional) criteria:

1) dilated pupils (maximum pupillary dilation (up to 5 mm) occurs within 1 min 45 from the onset of CS; if the patient has maximal pupillary dilation, this means that almost 50% of the time has passed from everything that was released before the beginning CPR);

2) areflexia (no corneal reflex and pupillary reaction to light);

3) discoloration of the skin (pallor, cyanosis, acrocyanosis).

10-15 seconds are allotted to identify the main criteria of the COP, if they are established, it is necessary to immediately start CPR.

For your information, the ECG during CS is very informative, since it often allows you to determine the sequence of CPR (for example, perform electrical defibrillation or refrain from it, etc.) and its effectiveness. However, given that time is the most important factor in CS care, the ECG should only be recorded after CPR has been started, when extra hands appear.

Resuscitation measures are not carried out in the following cases:

the presence of signs of biological death; the presence of a pre-documented (legally formalized) refusal of the patient to undergo CPR, due to religious or other reasons; the onset of CS against the background of the progression of reliably established incurable diseases (the last stages malignant neoplasms, atonic coma in violation of cerebral circulation in elderly patients) or incurable consequences of an acute injury incompatible with life. The futility of CPR in such patients should be determined in advance by a council of physicians and recorded in the medical history. Carrying out the entire complex of CPR in such patients will not lead to the prolongation of life, but to the prolongation of dying. The senile age of the patient cannot be a reason for refusing resuscitation.

The senile age of the patient cannot be a reason for refusing to perform CPR, although, of course, there is a certain relationship between the patient's age and the effectiveness of resuscitation.

Resuscitation measures are terminated in the following cases:

ascertaining the death of a person on the basis of brain death, including against the background of ineffective use of a full range of measures aimed at maintaining life; inefficiency of resuscitation measures aimed at restoring vital functions within 30 minutes; Note Before starting CPR, it is very important to record the time. At the same time, it is not enough to look at the clock, it is necessary to loudly call it to others. Such a mark can provide an invaluable service in the struggle for the life of the victim, and besides, it is important for the subsequent retrospective analysis of the correctness of actions, the reliability of conclusions, etc. ”1. The duration of CPR can be more than 30 minutes (up to 40-60 minutes) if the patient is under the influence of sedatives, hypnotics, narcotic drugs, with hypothermia. If ventricular fibrillation persists within 30 minutes of the start of resuscitation, resuscitation should be continued. In case of electrical injury, the duration of CPR is at least 45 minutes (preferably until signs of biological death), since the victim may be in a state of “imaginary death”. Resuscitation of victims of electric shock and lightning is usually more successful than in the case of cardiac arrest due to other causes, and an attempt to resuscitate may be effective even with a late start of assistance. multiple cardiac arrests that are not amenable to any medical influence; if during the course of CPR it turned out that it was not indicated for the patient (if a CS occurred in a person with an unknown history, CPR is started immediately, anamnesis is collected during resuscitation and, if it turns out that resuscitation was not indicated, it is stopped).

It must be remembered that resuscitation should be started in all cases when it is necessary. “Starting to save a person, the doctor does not have the right to act half-heartedly. Having done this once, he will unwittingly let go of the internal mechanism of self-control, which should be especially developed among resuscitators, like no other category of doctors, and subsequently begin to decide the fate of patients, taking on the functions of God, and not a doctor.

The reason for the refusal to conduct CPR cannot be a reference to the impossibility of resuscitation under the existing conditions.

The reason for the refusal to conduct CPR cannot be a reference to the impossibility of resuscitation under the existing conditions - CPR should be carried out in any conditions (unless, of course, there is a danger to the health or life of the EMS staff themselves)!

Before starting resuscitation, it is very important to assess the risk for medical workers and the patient: it is necessary to identify, evaluate and, if possible, eliminate various hazards - heavy traffic; the threat of explosion, collapse, electric discharge, exposure to aggressive chemicals and other damaging factors. Only by securing yourself and the patient, you can think about helping him!

The above regulations do not address the following situations:

conditions for refusing to perform CPR, if it is reliably known that the CS occurred more than 30 minutes ago (but there are no signs of biological death - cadaveric spots, rigor mortis); when the patient's relatives refuse to resuscitate (for example, with CS in people suffering from mental disorders).

In these difficult situations for the EMS doctor, in our opinion, a win-win solution is to carry out CPR in full. It must be understood that in the future, if any claims arise from the relatives of the deceased or inspection organizations, it will be much easier to justify the need for resuscitation than to refuse them.

In addition, EMS staff should be aware that if a patient has HIV infection, an open form of tuberculosis, meningococcal infection or other contagious infectious diseases cannot be a reason for refusing CPR. EMS personnel must take into account the risk to themselves and use the protective equipment available in the brigade packs.

The procedure for resuscitation is detailed in the CPR guidelines of the American Heart Association (2010) and the recommendations of the European Council on Resuscitation (2010). In addition, the order of the Ministry of Health of Russia dated December 20, 2012 No. 1113n approved the standard for emergency medical care for sudden cardiac death. Interested readers are advised to refer to these documents, within the framework of this article we will focus only on common mistakes CPR, since the cost of any mistake during CPR during the EMS phase is very high.

Common Mistakes in Cardiopulmonary Resuscitation

Seven tactical mistakes:

1) any delay in starting CPR;
2) initiation of CPR without taking into account the three-phase temporal model of sudden cardiac death;
3) the absence of a single leader, the presence of outsiders;
4) lack of accounting for ongoing activities, control over the implementation of all appointments, their effectiveness and time;
5) ignoring the possibility of eliminating reversible causes of CS;
6) weakening of control over the patient's condition in the post-resuscitation period;
7) negligent completion of medical records.

Seven mistakes during defibrillation:

1) any unreasonable delay in defibrillation;
2) insufficient conductive gel under the defibrillator electrodes, as well as very wet skin or a large amount of chest hair, which leads to a decrease in the effectiveness of the electrical discharge;
3) incorrect location of the defibrillator electrodes, the electrodes are not pressed against the chest wall strongly enough;
4) the discharge energy is incorrectly selected;
5) repetition of an electric discharge without previous closed heart massage and artificial ventilation of the lungs for 2 minutes;
6) non-observance of safety precautions when working with a defibrillator, use of a faulty defibrillator;
7) unreasonable defibrillation: conducting defibrillation during asystole according to the principle “it will not get worse” (in this case, defibrillation is ineffective, since it can lead to an increase in parasympathetic tone, suppression of the activity of natural pacemakers).

Seven mistakes when performing a closed heart massage:

1) the patient is on a soft, bending base;
2) violation of the technique of closed heart massage (the hands of the resuscitator are incorrectly positioned: the resuscitator leans on his fingers, bends his arms in elbow joints or tears them from the sternum; harsh and therefore too short chest compressions);
3) the first pressure on the sternum is carried out too weakly;
4) unreasonable interruptions in conducting a closed heart massage;
5) an attempt to assess the heart rate earlier than 2 minutes after defibrillation without performing a closed heart massage and mechanical ventilation during this time;
6) violation of the frequency and depth of massage movements;
7) non-compliance with the ratio between closed heart massage and artificial ventilation of the lungs (30: 2).

Seven mistakes during artificial ventilation of the lungs:

1) the patency of the upper respiratory tract has not been restored (if it is impossible to intubate the trachea, the head has not been tilted back);
2) an attempt to restore the patency of the upper respiratory tract by pushing the lower jaw forward;
3) tightness is not ensured when air is blown in (the nose is not clamped, the mask does not fit snugly, the cuffs of the endotracheal tube are not sufficiently inflated);
4) underestimation (late start, poor quality) or overestimation of the value of artificial lung ventilation (the beginning of cardiopulmonary resuscitation with tracheal intubation, sanitation of the tracheobronchial tree);
5) lack of control over chest excursions;
6) lack of control over the ingress of air into the stomach, with overdistension of the stomach, there is a risk of regurgitation;
7) blowing air at the time of chest compression without reliable protection respiratory tract, which leads to air entering the stomach.

Seven mistakes in drug therapy:

1) lack of a reliable route of administration (intravenous or intraosseous) of drugs;
2) the introduction of drugs into the "small" veins;
3) non-compliance with the method of administration of drugs (dilution in 20 ml of 0.9% sodium chloride solution, bolus injection, final jet injection of 20 ml of 0.9% sodium chloride solution);
4) non-compliance with the intervals of administration and dosage of drugs;
5) the use of atropine and other non-indicated drugs (for example, dopamine, norepinephrine, prednisolone, etc.);
6) stopping CPR in order to administer drugs;
7) non-use of pathogenetically justified drugs (for example, infusion therapy with CS against the background of hypovolemia).

Requirements for the preparation of primary medical documentation

Analyzing court cases on claims of patients against medical organizations, it can be concluded that some of the decisions were made in favor of patients only because medical organizations could not confirm or refute any fact due to improper filling of primary medical documentation.

Consideration of patients' claims to the EMS service always begins with the study and analysis of the EMS call card. Based on the high importance of the EMS call card as a legal document, it is possible to formulate the main requirements for its execution during CPR.

The call card should clearly indicate the main criteria for the diagnosis of "clinical death": lack of consciousness, absence of pulsation on the main arteries (it is necessary to indicate specifically on which artery the pulsation was determined), lack of breathing. At the SMP stage, the identification and description of additional criteria for the CS is optional. Moreover, the indication in the call card of such signs as the absence of corneal reflexes and / or pupillary reactions to light, especially the absence of heart sounds and breathing during auscultation, the absence of blood pressure, suggests that the doctor performed an examination, which led to an unjustified delay in CPR and could cause a poor outcome.

When issuing an EMS call card, the resuscitation allowance must be described in detail and consistently, indicating the exact time for each manipulation. Particular attention should be paid to the timing of the start and end of CPR. At the same time, the termination of CPR should be justified by the phrase: “Carrying out cardiopulmonary resuscitation was terminated due to the impossibility of restoring vital functions. At __ h __ min, death was declared in the presence of the ambulance brigade.

Only ECGs on paper, registered at the place of call, have legal force.

It is important to remember that only ECGs on paper, registered at the place of the call, have legal force. Therefore, all ECGs reflecting the main points of CPR should be attached to the EMS call card.

When formulating a diagnosis in the EMS call card, it is necessary to indicate not only the disease that led to the development of CS, but also the fact of CPR and its complications, since complications during CPR in the future may become an object of litigation in controversial cases of establishing the nature of damage - criminal or iatrogenic (for example, chest burns - as a result of defibrillation, rib fractures - as a result of a precordial blow or closed heart massage, etc.).

In cases where CPR was not performed, the EMS call card should clearly justify the reason: the patient has signs of biological death; Availability legally registered refusal of the patient to perform CPR; the onset of CS against the background of the progression of reliably established incurable diseases.

When indicating the signs of biological death, the SMP physician should be aware that the indisputable criteria for biological death at the SMP stage are cadaveric changes, which can be early (symptom of the "cat's pupil", drying and clouding of the cornea) and late (cadaveric spots and rigor mortis). The most obvious sign of biological death is cadaveric spots, which begin to appear after 40-60 minutes and fully manifest themselves 6-12 hours after the onset of death. Cadaveric spots are bluish or bluish-purple diffuse spots in sloping areas of the body (for example, if a person lies on his back, they are determined in the back, buttocks, back of the legs). Rigor mortis can be detected in the masticatory muscles and muscles of the hands by the end of the first hour after death, then rigor mortis spreads throughout the body.

Textbooks and guidelines often contain a requirement that the corpse be delivered to the mortuary only if there are late signs of biological death. The expediency of such a requirement is justified by cases of medical errors in ascertaining biological death, therefore, to date, it is carried out in many hospitals. However, at the EMS stage, for example, in the event of the death of a patient in the EMS car, this requirement is not feasible. In this regard, the EMS physician should be aware that, in accordance with the Procedure for conducting pathoanatomical autopsies, approved by order of the Ministry of Health of Russia dated 06.06.2013 No. 354n, “the direction of the bodies of the dead, as well as stillborns, for pathoanatomical autopsy ... is carried out after ascertaining the biological death of a person by a medical worker medical organization or visiting brigade of the SMP. Thus, the delivery of the corpse to the mortuary is permissible at any time after death.

1 Guide to clinical resuscitation / ed. T. M. Darbinyan. Moscow: Medicine, 1974. 284 p. 2 Piradov M.A. The problem of persistent vegetative state in resuscitation // Surgeon. 2006. No. 7. S. 32.