What is neurological shock. Pain shock

The circulatory disorder is based on direct damage to the spinal cord in trauma of the lower cervical and upper thoracic spine by intraneron swelling and extracellular edema, accompanied by dysfunction of sympathetic neurons, which leads to a decrease in vascular tone, vasodilation and blood deposition in the periphery.

There is a relative deficit of BCC due to a discrepancy between the volume of circulating blood and the capacity of the vascular bed, and venous return decreases. Due to the defeat of the sympathetic centers, the sympathetic reaction is not realized, therefore, hypotension is not accompanied by tachycardia, but bradycardia may increase due to the predominance of the tone of the parasympathetic nervous system.

Clinical features of neurogenic shock: no tachycardia and pallor of the skin, no "white spot" symptom. Decreased sensitivity and motor activity complete the picture and correspond to the level of the lesion.

burn shock

There are 3 degrees of OR:

Compensated OR - occurs when the burn area is up to 15-20% of the body surface. The patient groans, rushes about, complains of pain in burn wounds, chills, thirst, nausea. With an inhalation burn, breathing is difficult.

Excitation is replaced by adynamia, confusion, oliguria.

Subcompensated OS - develops when the burn area is from 20 to 45% of the body surface. Excitation is replaced by adynamia, confusion, oliguria. Characterized by instability of hemodynamics, hypotension 90 mm Hg, vomiting Mortality up to 40% of burn disease.

Decompensated OR - develops when the burn surface is over 45%.

Hypothermia, vomiting of “coffee grounds”, black urine with a burning smell, anuria, intestinal paresis, pulse pressure is sharply reduced, sometimes not caught. Lethality approaches 100%.

Thermal inhalation injury is manifested by shortness of breath, hoarseness, cyanosis.

External signs - nose burn, singed hair. Violation of microcirculation in the lungs, microembolism of pulmonary capillary blood flow, pulmonary infarction, atelectasis, extensive pneumonia.

The severity index of the process is determined using the Frank index.

General principles of first aid for shock at the prehospital stage:

Start anti-shock measures as soon as possible.

Eliminate the cause of the shock.

3. Offer the patient bed rest, cover it warmly or overlay with heating pads.

4. Remove the pillow from under the head and raise the legs at an angle of 35-45 degrees.

5. Put a cold compress on the patient's head

Ventilate the room or give the patient an oxygen-air mixture

Bring a swab moistened with ammonia to the patient's nose

8. Offer the patient hot, strong, sweet tea (coffee).

9. Reassure the patient and inspire him with the idea of quickly eliminating the problem.

10. Immediately call a doctor or an ambulance

Pharmacotherapy at the prehospital stage

Rehydration and detoxification therapy for rapid recovery of BCC

In case of hypovolemic, septic and anaphylactic shock, it is necessary to start BCC replacement and detoxification as soon as possible.

Crystalloid solutions for enteral administration: Regidron, Glucosolan, Citroglucosolan and others. The solution is given in a warm form, 30-50 milliliters 3-4 times per hour.

Crystalloid solutions for parenteral administration: Lactosol, Chlosol, Quatrasol, Trisol, Trisomin, Ringer, Ringer-Lock, Philips 1, Philips 2 and others.

Colloidal solutions for parenteral detoxification: Albumin, Polyglucin, Rheomacrodex, Reopoliglyukin, Plasmafusin, Gelatinol, Oxypolygelatin, Zhelifundol, Physiogel, Refortan, Stabizol and others.

Parenteral therapy is carried out at the rate of 3:1 per day.

The criterion of effectiveness is an increase in systolic pressure up to 100 mm. rt. Art.

Treatment of respiratory failure

Objectives of treatment: to ensure airway patency, ventilation of the lungs and tissue oxygenation.

In cardiogenic and neurogenic shock, oxygen inhalation is usually sufficient; in hypovolemic and septic shock, they often switch to mechanical ventilation.

Tracheal intubation is used:

To ensure the patency of the respiratory tract with oppression of consciousness.

For the prevention of aspiration of gastric contents in case of depression of consciousness.

For the release of the respiratory tract from sputum in pneumonia.

To stimulate the respiratory and vascular centers administered : Caffeine; Cordiamin; Sulfocamphocaine.

Treatment of kidney failure

Restoration of blood flow through the kidneys and stimulation of diuresis is carried out by dopamine (increase in cardiac output and renal blood flow). With oliguria and anuria, the introduction of diuretics is not effective. Eufillin slightly stimulates renal blood flow.

Heart failure treatment

With cardiogenic, neurogenic and septic shock (not amenable to infusion therapy), Dopamine or Dobutamine is administered parenterally and very rarely Adrenaline or Norepinephrine. Isoprenaline, Amrinon, Ditoxin are used in the intensive care unit for their intended purpose

General information

Shock is the response of the body to the action of external aggressive stimuli, which may be accompanied by disorders of blood circulation, metabolism, nervous system, respiration, and other vital functions of the body.

There are such causes of shock:

1. Injuries resulting from mechanical or chemical effects: burns, lacerations, tissue damage, limb avulsions, current exposure (traumatic shock);

2. Concomitant trauma loss of blood in large quantities (hemorrhagic shock);

3. Transfusion to the patient of incompatible blood in a large volume;

4. Entry of allergens into a sensitized environment (anaphylactic shock);

5. Extensive necrosis of the liver, intestines, kidneys, heart; ischemia.

Diagnosis of shock in a person who has suffered a shock or injury can be based on the following signs:

anxiety;
blurred consciousness with tachycardia;
reduced blood pressure;
disturbed breathing
reduced volume of urine;
skin is cold and moist, marbled or pale cyanotic

Clinical picture of shock

The clinical picture of shock differs depending on the severity of exposure to external stimuli. To correctly assess the condition of a person who has undergone shock, and to provide assistance for shock, several stages of this condition should be distinguished:

1. Shock 1 degree. A person retains consciousness, he makes contact, although the reactions are slightly inhibited. Pulse indicators - 90-100 beats, systolic pressure - 90 mm;

2. Shock 2 degrees. A person's reactions are also inhibited, but he is conscious, correctly answers the questions asked, and speaks in a muffled voice. There is rapid shallow breathing, frequent pulse (140 beats per minute), arterial pressure is reduced to 90-80 mm Hg. The prognosis for such a shock is serious, the condition requires urgent anti-shock procedures;

3. Shock 3 degrees. A person has inhibited reactions, he does not feel pain and is adynamic. The patient speaks slowly and in a whisper, may not answer questions at all, or in monosyllables. Consciousness may be completely absent. The skin is pale, with pronounced acrocyanosis, covered with sweat. The victim's pulse is barely noticeable, palpable only on the femoral and carotid arteries (usually 130-180 bpm). There is also shallow and frequent breathing. Venous central pressure may be below zero or zero, and systolic pressure may be below 70 mmHg.

4. Shock of the 4th degree is the terminal state of the body, often expressed in irreversible pathological changes - tissue hypoxia, acidosis, intoxication. The patient's condition with this form of shock is extremely severe and the prognosis is almost always negative. The victim does not listen to the heart, he is unconscious and breathes shallowly with sobs and convulsions. There is no reaction to pain, the pupils are dilated. In this case, blood pressure is 50 mm Hg, and may not be determined at all. The pulse is also hardly noticeable and is felt only on the main arteries. The skin of a person is gray, with a characteristic marble pattern and cadaver-like spots, indicating a general decrease in blood supply.

Types of shock

The state of shock is classified depending on the causes of shock. So, we can distinguish:

Vascular shock (septic, neurogenic, anaphylactic shock);

Hypovolemic (angidremic and hemorrhagic shock);

Cardiogenic shock;

Pain shock (burn, traumatic shock).

Vascular shock is a shock caused by a decrease in vascular tone. Its subspecies: septic, neurogenic, anaphylactic shock are conditions with different pathogenesis. Septic shock occurs as a result of human infection with a bacterial infection (sepsis, peritonitis, gangrenous process). Neurogenic shock most often occurs after injury to the spinal cord or medulla oblongata. Anaphylactic shock is a severe allergic reaction that occurs within the first 2-25 minutes. after the allergen enters the body. Substances that can cause anaphylactic shock are plasma preparations and plasma proteins, radiopaque and anesthetics, and other drugs.

Hypovolemic shock is caused by an acute deficiency of circulating blood, a secondary decrease in cardiac output, and a decrease in venous return to the heart. This shock condition occurs with dehydration, loss of plasma (angidremic shock) and loss of blood - hemorrhagic shock.

Cardiogenic shock is an extremely serious condition of the heart and blood vessels, characterized by high mortality (from 50 to 90%), and occurring as a result of a serious circulatory disorder. With cardiogenic shock, the brain experiences a sharp lack of oxygen due to a lack of blood supply (disturbed heart function, dilated vessels that are unable to hold blood). Therefore, a person in a state of cardiogenic shock loses consciousness and most often dies.

Pain shock, like cardiogenic, anaphylactic shock, is a common shock condition that occurs with an acute reaction to an injury (traumatic shock) or a burn. Moreover, it is important to understand that burn and traumatic shock are varieties of hypovolemic shock, because their cause is the loss of a large amount of plasma or blood (hemorrhagic shock). These can be internal and external bleeding, as well as exudation of plasma fluid through burned areas of the skin during burns.

Help with shock

When providing assistance in case of shock, it is important to understand that often the cause of belated shock conditions is improper transportation of the victim and first aid in case of shock, so it is very important to carry out elementary rescue procedures before the ambulance arrives.

Help with shock, is the following activities:

1. Eliminate the cause of shock, for example, stop bleeding, release pinched limbs, extinguish burning clothing on the victim;

2. Check for foreign objects in the mouth and nose of the victim, if necessary, remove them;

3. Check the presence of breathing, pulse, and if necessary, conduct a heart massage, artificial respiration;

4. Make sure that the victim lies with his head on his side, so he will not choke on his own vomit, his tongue will not sink;

5. Determine if the victim is conscious and give him an anesthetic. It is advisable to give the patient hot tea, but before that, exclude a wound in the abdomen;

6. Loosen clothes on the belt, chest, neck of the victim;

7. The patient must be warmed or cooled depending on the season;

8. The victim must not be left alone, he must not smoke. Also, you can not apply a heating pad to injured places - this can provoke an outflow of blood from vital organs.

Video from YouTube on the topic of the article:

Shock is a state of immediate threat to life, characterized by a general decrease in peripheral blood flow (hypoperfusion), which causes tissue hypoxia. It is most often accompanied by a decrease in blood pressure (hypotension), which, however, can be within normal limits (and even elevated) in the initial phase of shock (which is called compensated shock).

Causes and mechanisms of development

1. Decreased total blood volume (absolute hypovolemia) - hypovolemic shock:

1) blood loss(bleeding, or massive external or internal bleeding) - hemorrhagic shock;

2) decrease in plasma volume due to:

a) passage of plasma into crushed tissues (trauma) or loss from the surface of the skin (burns, Lyell's syndrome, Stevens-Johnson syndrome, exfoliative dermatitis);
b) decreased volume of extracellular fluid (states of dehydration) - insufficient water intake (more often in the elderly [for thirst disorders] and in self-dependent persons) or excessive loss of water and electrolytes through the gastrointestinal tract (diarrhea and vomiting), kidneys (osmotic diuresis in diabetic ketoacidosis and hyperosmolar non-ketoacidemic hyperglycemia), polyuria and excessive sodium removal with corticosteroid and mineralocorticoid deficiency, rarely hypothalamic or renal diabetes insipidus), skin (fever, hyperthermia);
c) fluid loss in the so-called. the third space - the intestinal lumen (paralytic or mechanical obstruction), rarely serous cavities (peritoneal - ascites);
d) an increase in the permeability of the walls of blood vessels in anaphylactic and septic shock.

2. Increased vascular capacity (relative hypovolemia, redistributive shock[vasogenic] - due to vasodilation) → decrease in effective volemia, i.e. filling with blood of blood circulation areas, volume and chemoreceptors (practically this applies to the arterial), while increasing the volume of blood in the venous and capillary vessels (the total blood volume can be unchanged and even increased):

1) septic shock- sepsis (sometimes toxic shock is released - caused by toxins of staphylococci or streptococci);

2) anaphylactic shock- anaphylaxis;

3) neurogenic shock- spinal cord injury (spinal shock); injuries, strokes and cerebral edema; orthostatic hypotension (long-term); vasodilation in response to pain (“pain shock”);

4) shock, (in addition to vasodilation, there may be a violation of the heart and other mechanisms) - acute adrenal insufficiency, thyrotoxic crisis, hypometabolic coma.

3. Violation of the heart (acute heart failure) and changes in large vessels, causing a decrease in cardiac output (cardiac output) - cardiogenicshock.

Consequences

1. Compensatory reactions(expire over time) - the most important are:

1) excitation of the sympathetic nervous system and an increase in the release of adrenaline by the adrenal medulla → tachycardia and centralization of blood circulation (narrowing of precapillary and venous vessels of the skin, then muscles, visceral and renal circulation → decrease in blood flow and filling of venous vessels in these areas → preservation of blood flow in the most important for life organs [heart and brain]); with hypovolemia, restoration of plasma volume by transferring intercellular fluid into capillary vessels (due to spasm of precapillary vessels and a decrease in intracapillary hydrostatic pressure with a constant oncotic pressure); in some cases of non-cardiogenic shock, an increase in the contractility of the heart muscle (as well as an increase in the volume of ejection); hyperventilation; hyperglycemia;

2) stimulation of the renin-angiotensin-aldosterone system and the release of vasopressin (ADH) and HA → leads to the centralization of blood circulation and promotes the retention of sodium and water in the body;

3) increased oxygen consumption by tissues in response to a decrease in its supply → a large deoxygenation of hemoglobin, a decrease in oxygen saturation of venous blood hemoglobin (SvO 2).

2. Metabolic and electrolyte disturbances due to hypoxia:

1) increased anaerobic metabolism and an increase in lactate production → metabolic lactic acidosis;

2) the transition of potassium, phosphates and some enzymes (LDH, CPK, AST, ALT) from cells and extracellular space, an increase in sodium intake into cells (due to impaired ATP synthesis) → hyponatremia, hyperkalemia and hyperphosphatemia are possible.

3. Consequences of organ ischemia: multiple organ failure (acute prerenal kidney injury, impaired consciousness [including comma] and other neurological disorders, acute respiratory failure, acute liver failure, DIC), bleeding from the gastrointestinal tract (due to acute hemorrhagic [erosive] gastropathy , stress ulcers of the stomach and duodenum or ischemic), paralytic ileus and penetration of microorganisms from the lumen of the gastrointestinal tract into the blood (may cause sepsis).

CLINICAL PICTURE

1 . Symptomscosidessystemsblood circulation: (rare, bradycardia, rather in the terminal phase, may precede circulatory arrest in the mechanism of asystole or pulseless electrical activity), hypotension (decreased systolic blood pressure<90 мм рт. ст. или его значительное снижение [напр. на>40 mmHg Art.], decrease in mean arterial pressure [sum of 1/3 systolic pressure and 2/3 diastolic pressure]<70 мм рт. ст. [снижение диастолического давления и, как следствие, среднего может опережать снижение систолического давления], в начале, нередко, только ортостатическая гипотензия или без гипотензии), снижение амплитуды и слабое наполнение пульса (при систолическом артериальном давлении <60 мм рт. ст. пульс на лучевой артерии обычно неосязаемый), уменьшение наполнения шейных вен (но при тампонаде сердца и напряженном пневмотораксе — увеличение), коронарный боль остановка кровообращения — особенно обращайте внимание на механизм электрической активности без пульса, который не обнаруживается мониторингом ЭКГ.

2 . Symptoms of organ hypoperfusion

1) skin - pallor, cooling and sweating (but with septic shock, the skin is usually dry and warm at the beginning, and in states of dehydration it is dry and elastic), slowing down of capillary filling (after stopping pressing the nail, blanching disappears after> 2 s), cyanosis ;

2) muscles - weakening;

3) digestive tract - nausea, vomiting, flatulence, weakening or absence of peristalsis, bleeding;

4) CNS - a feeling of fear, anxiety, confusion, psychomotor agitation, drowsiness, stupor, coma, focal neurological deficit;

5) kidneys - oliguria or anuria and other symptoms of acute insufficiency;

6) liver - jaundice is a symptom, appears rarely and late, or after withdrawal from shock;

7) - breathing at the beginning is superficial and rapid, then slow, residual or apnea; acute respiratory failure.

3 . Symptoms related to the cause of shock: symptoms of dehydration, bleeding, anaphylaxis, infection (sepsis), heart or large vessel disease, pulmonary embolism, tension pneumothorax, intestinal obstruction, etc.

The classic triad (hypotension, tachycardia, oliguria) may not be observed.

DIAGNOSTICS

Based on symptoms, it is generally not difficult, but it is not uncommon to be difficult to determine the cause, although it may be possible based on the history itself (eg, fluid or blood loss, symptoms of infection or anaphylaxis) and physical examination (eg, symptoms of active bleeding, dehydration , cardiac tamponade or tension pneumothorax). Consider other than shock causes of impaired oxygen supply to tissues and tissue hypoxia (anemia, respiratory failure, poisoning that disrupts oxygen transport in the blood and its use by cells).

Ancillary research

1 . Examination of the circulatory system:

1) blood pressure measurement(invasive with prolonged shock);

2) ECG with 12 leads and constant monitoring - rhythm disturbance, symptoms of ischemia or myocardial infarction or other heart disease;

3) echocardiography- can help in establishing the cause of cardiogenic shock (cardiac tamponade, valve dysfunction, impaired contractility of the heart muscle);

4) cardiac output assessment(CO) and wedge pressure in the capillary vessels of the lungs(PCWP) - in case of doubts about the diagnosis and difficulties in treatment. To assess the state of flooding and preload (left ventricular filling), which is of basic importance in the differential diagnosis and determining the strategy of pharmacological treatment, the assessment of PCWP using a Swan-Gans catheter may be suitable. PCWP corresponds to the pressure in the left atrium and directly informs the end-diastolic pressure in the left ventricle; values ≈ 15-18 mm Hg. Art. indicate optimal filling of the left ventricle. The Swan-Gans catheter also allows the assessment of CO by thermodilution (other methods for assessing CO are currently available). In cardiogenic shock, CO is reduced, and in the initial phase of hypovolemic and in anaphylactic and septic shock, as a rule, it is increased.

2 . Laboratory studies of venous blood:

1) general analysis of peripheral blood:

a) hematocrit, hemoglobin concentration and red blood cell count - decrease in hemorrhagic shock (but not in its initial phase), increase in other types of hypovolemic shock;

b) leukocytes - neutrophilic leukocytosis or leukopenia in septic shock; an increase in the number of leukocytes and the percentage of neutrophils is also possible with other types of shock (eg, hypovolemic); eosinophilia sometimes in case of anaphylaxis;

c) platelets - a decrease in the number is the first symptom of DIC (most often with septic shock or after massive injuries), it can also be a consequence of massive bleeding and transfusions of erythrocyte mass;

2) coagulation study- an increase in MNI, a prolongation of the APTT and a decrease in the concentration of fibrinogen indicate DIC or may be the result of post-hemorrhagic or post-transfusion coagulopathy; an increase in MNI and a prolongation of the APTT may be symptoms of liver failure; an increase in the concentration of D-dimers is not a specific symptom of pulmonary embolism, it is observed incl. with DIC;

3) biochemical studies of blood serum:

a) assessment of the consequences of shock - electrolyte disturbances (determine Na and K); increased concentration of lactate, creatinine, urea, bilirubin, glucose; increased activity of AST, ALT, CPK and LDH;

b) an increase in the activity of troponins, CPK-MB or myoglobin may indicate a recent myocardial infarction, and natriuretic peptides (BNP or NT-proBNP) - heart failure, as a cause or consequence of shock.

3 . Pulse oximetry: possible decrease in SaO 2 ; monitoring is needed.

4 . Arterial blood gasometry: metabolic or mixed acidosis; sometimes, in the early phase of shock, respiratory alkalosis due to hyperventilation; possible hypoxemia.

5 . Imaging studies: chest x-ray- Evaluate if there are signs of heart failure (enlargement of the heart cavities, congestion in the pulmonary circulation, pulmonary edema) and causes of respiratory failure and sepsis. chest CT- with suspicion of pulmonary embolism (angio-CT), aortic dissection, rupture of an aortic aneurysm. Panoramic X-ray of the abdominal cavity- if you suspect a perforation of the gastrointestinal tract or mechanical intestinal obstruction. Ultrasound or CT scan of the abdomen— incl. detection of foci of infection in sepsis. Ultrasound of the veins- if pulmonary embolism is suspected. Head CT- if you suspect a stroke or cerebral edema or post-traumatic changes.

6 . Blood type: determine on the basis of documentation or perform a laboratory study in each patient.

7 . Other studies: microbiological (for septic shock), hormonal (TSH and free thyroxine for suspected hypometabolic coma or thyroid storm, cortisone for suspected adrenal crisis), toxicological (suspected poisoning), allergological (IgE and possibly skin tests after suffering anaphylactic shock) .

SHOCK TREATMENT

1 . Maintain airway patency intubate and mechanically ventilate if necessary.

2 . Lay the patient down with legs elevated effective in hypotension, especially if no medical equipment is available, but may impair ventilation, and in cardiogenic shock with pulmonary congestion, also cardiac function.

3 . Putintravascular catheters:

1) to peripheral veins 2 large diameter catheters (better ≥ 1.8 mm [≤ 16 G]), which will allow effective infusion therapy → see below;
2) if necessary, the introduction of many drugs (including catecholamines → see. Below) a catheter into the vena cava; also allows you to monitor central venous pressure (CVP);
3) an arterial catheter (usually a radiation catheter) makes invasive blood pressure monitoring in case of persistent shock or the need for long-term use of catecholamines. Catheterization of the vena cava and arteries should not delay treatment.

4 . Apply etiological treatment→ see below and at the same time support the work of the circulatory system and oxygenation of tissues

1) if the patient is receiving antihypertensive drugs → cancel them;
2) in most types of shock, restoration of intravascular volume by IV infusion solutions; the exception is cardiogenic shock with symptoms of blood stasis in the pulmonary circulation. Colloidal solutions (6% or 10% hydroxyethyl starch [HES], 4% gelatin solution, dextran, albumin solution) have not been shown to be more effective in reducing mortality than crystalloid solutions (Ringer's solution, polyelectrolyte solution, 0.9% NaCl), although to correct hypovolemia, a smaller volume of colloid is needed than crystalloids. Initially, 1000 ml of crystalloids or 300-500 ml of colloids are usually administered over 30 minutes, and this strategy is repeated depending on the effect on blood pressure, CVP and diuresis, as well as side effects (symptoms of volume overload). For massive infusions, do not apply 0.9% NaCl exclusively, as infusion of large volumes of this solution (incorrectly called saline) results in hyperchloremic acidosis, hypernatremia, and hyperosmolarity. Even with hypernatremia, do not apply 5% glucose to restore volemic shock. Colloidal solutions reproduce the intravascular volume - almost completely remain in the vessels (plasma substitutes - gelatin, 5% albumin solution), or remain in the vessels and lead to the transition of water from the extravascular space to the intravascular [plasma volume increasing agents - hydroxyethyl starch [HES], 20% albumin solution, dextrans); solutions of crystalloids equalize the deficit of extracellular fluid (outside and intravascular); glucose solutions increase the volume of total water in the body (external and intracellular fluid). Correction of a significant deficiency of volemia can begin with the infusion of hypertonic solutions, for example, Special mixtures of crystalloids and colloids (so-called. .5% NaCl with 10% HES) as they increase plasma volume better. In patients with severe sepsis or burdened with an increased risk of acute kidney injury, it is better not to use HES especially with a molecular weight ≥ 200 kD and/or a molar substitution > 0.4, an albumin solution can be used instead (however not in patients after a head injury);
3) if it is not possible to eliminate hypotension, despite the infusion of solutions → start a constant IV infusion (preferably through a catheter in the vena cava) of catecholamines, vasoconstriction, norepinephrine(adrenor, norepinephrine tartrate Agetane), usually 1-20 mcg/min (greater than 1-2 mcg/kg/min) or adrenaline 0.05-0.5 mcg/kg/min, or dopamine(dopamine Admeda, Dopamine-Darnitsa, Dopamine hydrochloride, dopamine-Health, Dopmin, currently not the drug of choice for septic shock) 3-30 mcg/kg/min and apply invasive blood pressure monitoring. For anaphylactic shock, start with an injection of epinephrine 0.5 mg IM into the outer thigh;
4) in patients with low cardiac output despite appropriate flooding (or in overhydration), administer as a continuous IV infusion dobutamine(Dobutamine Admeda, Dobutamine-Health) 2-20 mcg/kg/min; if hypotension coexists, a vasoconstrictor drug may be used concomitantly;
5) simultaneously with the treatment described above, use oxygen therapy(maximizing oxygenation of hemoglobin, its supply to tissues increases; the absolute display is SaO 2<95%);
6) if, despite the above actions, SvO 2<70%, а гематокрит <30% → примените трансфузию packed red blood cells.

5 . The main method of correction of lactic acidosis is etiological treatment and treatment that supports the function of the circulatory system; evaluate the indications for the administration of NaHCO 3 i.v. at pH<7,15 (7,20) или концентрации гидрокарбонатного иона <14 ммоль / л.

6 . Monitor vital signs (blood pressure, pulse, respiration), state of consciousness, ECG, SaO 2 , CVP, gasometric indicators (and possibly lactate concentration), natremia and potassium, parameters of kidney and liver function; if necessary, cardiac output and wedge pressure in the capillaries of the lungs.

7 . Protect the patient before heat loss And provide the patient with a calm environment .

8. If shock is present:

1) allow bleeding from the gastrointestinal tract And thromboembolic complications(in patients with active bleeding or a high risk of its occurrence, do not use anticoagulant drugs, only mechanical methods);
2) correct hyperglycemia if > 10-11.1 mmol/l) continuous IV infusion of short-acting insulin, however avoid hypoglycemia; try to keep the glycemic level between 6.7-7.8 mmol/l (120-140 mg/dl) to 10-11.1 mmol/l (180-200 mg/dl).

Sometimes shock develops even in the absence of blood loss. If the capacity of the vascular system increases many times, even the normal volume of blood is insufficient to adequately fill it. The main reason for this is a sudden decrease in vascular tone, especially widespread varicose veins. The resulting condition is called neurogenic shock.

Role of vascular capacity in the regulation of hemodynamics is detailed in our article, where it was emphasized that both an increase in vascular capacity and a decrease in blood volume lead to a decrease in the mean systemic filling pressure and, consequently, to a decrease in venous return of blood to the heart. The decrease in venous return caused by vasodilation is called venous congestion.
Causes of neurogenic shock. The main neurogenic factors that cause a decrease in vascular tone are as follows.

1. Deep general anesthesia, which causes depression of the vasomotor center, leading to paralytic vasodilation and the development of neurogenic shock.
2. Spinal anesthesia (especially covering the entire spinal cord), which causes a blockade of the sympathetic nerves that go as part of the anterior roots, which can lead to the development of neurogenic shock.
3. Injuries to the brain, which often lead to paralytic vasodilation. Many patients with concussion or contusion of the basal parts of the brain develop deep neurogenic shock.

In addition, cerebral ischemia can cause shock. So, if in the first few minutes cerebral ischemia causes powerful stimulation of the vasomotor center and vasoconstriction, prolonged ischemia (lasting more than 5-10 minutes) leads to the opposite effect: complete inactivation of the stem vasomotor center with subsequent development of severe neurogenic shock.

Anaphylaxis and anaphylactic shock

Anaphylaxis is an allergic condition in which there is often a significant drop in cardiac output and blood pressure. It develops as a result of antigen-antibody reactions that occur immediately following the entry into the blood of an antigen to which a person is sensitive. The basis of anaphylactic shock is the release of histamine or histamine-like substances by blood basophils and mast cells of pericapillary tissues. Histamine causes: (1) an increase in the capacity of the vascular system due to the expansion of the veins, which leads to a decrease in the venous return of blood to the heart; (2) dilation of arterioles, leading to a drop in blood pressure; (3) a sharp increase in capillary permeability, which leads to a rapid transition of proteins and fluid from capillaries to tissues.

As a result, there is a significant decreased venous return and shock develops, sometimes so severe that the person dies in just a few minutes.

Intravenous administration of large doses of histamine causes the development of histamine shock, which is characterized by the same symptoms as anaphylactic shock.

And yet the main thing here is the state of deep oppression of blood circulation. As a result, the blood flow becomes insufficient for the normal provision of tissues with oxygen, their nutrition and purification from metabolic products. If the development of shock does not stop spontaneously (which is practically unlikely) or is not interrupted by appropriate medical measures, then death occurs. To prevent this from happening, you need to normalize blood circulation in the body as soon as possible. Currently, in accordance with the causes, it is customary to distinguish three categories of shock: hypovolemic, normovolemic, hypervolemic (cardiogenic).

Hypovolemic shock occurs when the BCC (volume of circulating blood) decreases due to bleeding, burns, loss of salts by the body, various forms of dehydration, etc. In healthy people, a decrease in BCC by 25% is compensated by the redistribution of blood flow. Early replacement of the lost volume of blood or plasma reliably prevents the development of shock.

Symptoms. In the early stages of hypovolemic shock, blood loss is compensated by releasing a significant amount of blood from the skin, muscle vessels and subcutaneous adipose tissue in favor of cardiac, cerebral, renal and hepatic blood flow. The skin becomes pale and cold, the blood supply to the cervical vessels decreases. If blood loss continues, then the circulation of the kidneys, heart, brain and liver also begins to deteriorate. At this stage of shock, thirst, decreased diuresis, and increased urine density are observed. There may be tachycardia (increased heart rate), instability of blood pressure, weakness, agitation, confusion, sometimes even loss of it. The blood pressure gradually decreases. The pulse quickens, becomes weak. The nature of breathing also changes, which becomes deep, rapid.

If the bleeding does not stop and the hypovolemia is not corrected immediately, cardiac arrest and death may occur.

Treatment of hypovolemic shock (main stages):

1) a plastic catheter of sufficient caliber is inserted into the vein to allow rapid administration of the drug;

2) polyglucin and reopoliglyukin are administered, which occupy an important place in the treatment. They remain in the circulatory system for quite a long time and are able to change the properties of blood: they reduce blood viscosity and significantly improve peripheral circulation. One of the most important properties of these drugs is to maintain normal renal blood flow;

3) start a jet or drip (depending on the circumstances) transfusion of 500 ml of one-group, Rh-compatible blood, heated to 37 ° C, after which 500 ml of plasma, protein or albumin are poured;

4) drugs are administered that normalize the acid-base balance of the body;

5) introduce large amounts (up to 1 l) of isotonic sodium chloride solution or Ringer's solution, which have a satisfactory effect;

6) together with the beginning of blood substitution, a large dose of hormones (prednisolone - 1–1.5 g) is administered intravenously. Hormones not only improve the contractile function of the heart muscle, but also relieve spasm of peripheral vessels;

7) use oxygen therapy, which is of great importance in the treatment of shock. With massive blood loss, oxygen transport is significantly affected. The lack of oxygen in the blood, along with spasm of small vessels, is the cause of oxygen starvation of tissues during shock.

It is important that urine output is normal, the optimal level is at least 50-60 ml / h. A small amount of urine discharge during shock primarily reflects the lack of blood in the bloodstream and directly depends on it; only in the later stages of shock is it possible due to damage to the kidney tissue.

Causes. It occurs as a result of a decrease in cardiac output and the development of the so-called low output syndrome. Insufficient output of blood by the heart occurs in acute myocardial infarction. Mortality from cardiogenic shock is high, reaching 90%.

Symptoms of cardiogenic shock resemble those of hypovolemic shock. The pulse is usually fast and weak, blood pressure is low, the skin is moist and cold, breathing is rapid, urination is reduced.

Causes. Most often, septic shock develops due to the occurrence of an acute infection, namely sepsis, in which a lot of foreign proteins (bacteria) enter the bloodstream. The work of capillaries is disrupted, in which the blood flow slows down until it stops completely. Immediately after this, oxygen starvation occurs in the tissues of the body.

Symptoms. In the first phase of septic shock, called "hyperdynamic shock", there is an activation of blood circulation, which is characterized by an increase in cardiac output. During this period, the body temperature rises moderately. The pulse is frequent, tense with normal blood pressure and satisfactory filling of the jugular veins. Often there is some increase in breathing. Since peripheral blood flow is increased during the hyperdynamic phase, the skin remains warm, sometimes pink, and urine output is normal.

If the shock continues, then the fluid from the vessels goes into the cells, the volume of the intravascular fluid decreases, as an inevitable consequence, the hypodynamic phase of shock develops. From this point on, septic shock is more similar to hypovolemic shock. As a result, the patient's skin becomes gray, cold and wet, the neck veins subside, the pulse is rapid but weak, blood pressure decreases, diuresis falls. If septic shock is not treated immediately, coma develops and death soon follows.

Successful treatment of the described form of shock is possible when the cause of its occurrence is accurately established, the site of inflammation and the type of pathogen are determined. It is quite obvious that until the cause of septic shock is eliminated (before drainage of abscesses, operations for peritonitis, pancreatic necrosis, etc.), treatment can only be supportive and symptomatic.

Causes. Usually it is a consequence of a decrease in vascular tone, which, in turn, develops as a result of a violation of the innervation of the vascular wall. This variant of shock occurs as a result of various injuries of the central nervous system, most often as a result of spinal cord injury, and can also be observed in patients subjected to high spinal anesthesia.

Symptoms. In some cases, tachycardia and hypotension (low blood pressure) may occur, but the most common are a fairly rare pulse and very mild hypotension. The skin, as a rule, is dry and warm, consciousness is preserved, the respiratory function is not disturbed, the cervical veins are collapsed. In some cases, it is quite enough to raise both lower limbs above the patient's body, which is in a horizontal position, so that all the symptoms of neurogenic shock are removed. This technique is most effective in shock caused by high spinal anesthesia. In neurogenic shock caused by spinal cord injury, as a rule, it becomes necessary to increase the BCC by intravenous administration of a plasma substitute and a drug to maintain vascular tone.

Causes. The main causes of this shock are pain, blood loss and subsequent cooling. With prolonged crush syndrome and extensive soft tissue damage, the penetration of a large amount of toxins into the blood is one of the main causes of shock. Circulatory disorders in typical traumatic shock (with the exception of burn, chemical, electrical and cold shock) are associated with the redistribution of blood in the body: the filling of internal organs and muscle vessels with blood increases. The central circulation (of the brain and heart), as well as the peripheral one, suffers significantly under these conditions. Due to blood loss and the movement of large volumes of blood to the periphery, venous return and, consequently, cardiac output are reduced.

In case of burn shock, in addition to the occurrence of severe pain and blood poisoning with toxins, an important point is the loss of blood plasma from the surface of the burn, on which protein and potassium deficiency subsequently largely depends. There is also a pronounced concentration of blood in the vessels, and because of this, kidney function is impaired.

Symptoms. During traumatic shock, two phases are distinguished: erectile and torpid. In the erectile phase, the processes of excitation of all body functions are observed. This is manifested by normal or even hypertension (increased blood pressure), tachycardia, increased respiration. The patient is usually conscious, agitated, anxious, reacts to any touch (increased reflex excitability), the skin is pale, the pupils are dilated.

The torpid phase is characterized by indifference and prostration, absence or weak reaction to external stimuli. The pupils are dilated, poorly responsive to light. The skin is pale with an earthy tint, the limbs are cold, often the skin is covered with cold, sticky sweat, the body temperature is reduced. The pulse is frequent, threadlike, sometimes not palpable on the limbs and is determined only on large vessels. Arterial pressure, especially systolic, is significantly reduced. Cardiac output is reduced. Urine output is reduced or absent.

Treatment. In the accepted complex method of treatment of traumatic shock, the basis is fast and effective pain relief with analgesics or neuroleptics, compensation for blood loss and warming. With indications for surgery, endotracheal anesthesia is used under mechanical ventilation; conduction, case anesthesia of the extremities; various types of blockades. Antihistamines (diphenhydramine, pipolfen), large doses of corticosteroids (up to 10-15 mg/kg hydrocortisone), plasma, plasma-substituting solutions (albumin, protein), rheopolyglucin, polyglucin, bicarbonate solutions to normalize acid-base balance, diuretics should be used .

The most important measure in the treatment of traumatic shock is the transfusion of fresh donor blood. With a deep decrease in blood pressure (irreversible shock), the introduction of norepinephrine, adrenaline is indicated. Of decisive importance in assisting a victim with mechanical injuries in a state of shock is the time factor: the sooner assistance is provided, the more favorable the outcome. The adoption of anti-shock measures at the scene is of great importance because it is carried out during the erectile phase of shock, which reduces the severity of the torpid phase. According to the Institute for Emergency Medicine. N. V. Sklifosovsky, treatment in the torpid phase requires a longer time and mortality is 10 times higher compared to the group of victims, where shock treatment was carried out starting from the erectile phase. This treatment is mainly in the nature of preventive measures: careful removal from the site of injury, creating rest for both the injured and damaged organ (immobilization in case of fractures), the introduction of painkillers, agents that support cardiac activity and vascular tone. With deep disorders of breathing and cardiac activity, artificial respiration and heart massage should be used. Anti-shock therapy should continue in an ambulance, where it is possible to temporarily stop bleeding, produce novocaine blockade, inject blood and blood substitutes intravenously, carry out oxygen therapy and give surface anesthesia with nitrous oxide with artificial respiration.

neurogenic shock

n.vagus

neuroanatomy

Pathophysiological mechanisms

Clinical picture

According to C. Popa and co-authors, all patients with complete neurological deficit due to spinal cord injury (ASIA A or B) have bradycardia, 68% of them have arterial hypotension, for the correction of which in 35% of patients the introduction of vasopressors is required, and 16% have severe bradycardia, turning into asicitolia (cardiac arrest). In contrast to the previous ones, patients with incomplete neurological deficit due to spinal cord injury (ASIA C or D) have bradycardia in % of cases and only a few of them have arterial hypotension requiring vasopressor support, and cardiac arrest very rarely develops.

Differential Diagnosis

Treatment

Neurogenic shock is

Neurogenic shock is defined as a decrease in tissue perfusion as a result of loss of vasomotor tone in the peripheral arterial bed. The loss of vasoconstrictor impulses leads to an increase in vascular capacity, decreasing venous return and cardiac output.

Neurogenic shock is usually the result of damage to the spinal cord in fractures of the cervical or upper thoracic spine, when the sympathetic regulation of peripheral vascular tone is interrupted.

Occasionally, an injury such as an epidural hematoma that extends into the spinal cord can cause neurogenic shock without vertebral fracture. Penetrating injuries of the spinal cord can also cause neurogenic shock.

Sympathetic signals to the heart, which normally increase heart rate and contractility, and signals to the adrenal medulla, which increase catecholamine release, may be interrupted in high spinal cord injury, preventing the typical reflex tachycardia that occurs with relative hypovolemia due to increased venous capacity. channels and loss of vasomotor tone.

Diagnosis of neurogenic shock

The classic symptoms of neurogenic shock are low blood pressure, bradycardia (absence of reflex tachycardia due to interruption of sympathetic impulses), warm extremities (loss of peripheral vasoconstriction), motor and sensory disturbances indicative of spinal cord injury, and x-ray evidence of spinal fracture.

However, establishing the presence of neurogenic shock can be difficult, as patients with multiple injuries, including spinal cord injuries, often have brain trauma that can make it difficult to identify the cause of motor and sensory impairments. Moreover, combined injuries can cause hypovolemia and complicate the clinical picture.

In the subgroup of patients with spinal cord injuries due to penetrating injuries, the majority of patients with hypotension have blood loss (74%) rather than a neurogenic cause, and only a few (7%) have all the classic features of neurogenic shock. Hypovolemia should be ruled out before a diagnosis of neurogenic shock is made.

Treatment of neurogenic shock

After securing the airway and establishing adequate ventilation, fluid infusion, and restoration of intravascular volume in neurogenic shock, systemic blood pressure and perfusion often improve. Administration of vasoconstrictors may improve peripheral vascular tone, reduce vascular capacity, and increase venous return, but only after hypovolemia has been ruled out and a diagnosis of neurogenic shock has been established.

Specific treatment for shock is often short-lived, and the need for vasoconstrictor drugs usually lasts only hours. The duration of vasopressor support in neurogenic shock may correlate with the overall prognosis of improvement in neurological function. Appropriate rapid restoration of blood pressure and perfusion may also improve blood supply to the spinal cord, prevent the progression of spinal cord ischemia, and minimize secondary cord injury.

Restoration of normal hemodynamics should precede any surgical attempt to stabilize a vertebral fracture.

neurogenic shock

R 57.8.

Neurogenic shock is a condition of the human body that develops as a result of damage to the spinal cord, during which the conduction of impulses of the sympathetic nervous system is disrupted, and the unrestricted tone of the vagus nerve (lat. n.vagus) starts to dominate. The leading clinical signs of neurogenic shock in spinal cord injury are arterial hypotension and bradycardia. According to the frequency of injuries of the spinal cord, the leader is the cervical, then the level of the thoracolumbar junction of the spine, less often the thoracic region, and even less often the level of the lumbar spine (damage to the cauda equina). Neurogenic shock must be differentiated from spinal shock, defined as areflexia below the level of spinal cord injury.

neuroanatomy

The centers of regulation of the cardiovascular system are nuclei of the same name in the medulla oblongata. This center, in turn, is influenced by impulses from the cerebral cortex and subcortical nuclei. Parasympathetic impulses from the cardiovascular nuclei of the medulla oblongata reach their targets through the fibers of the vagus nerve (n. vagus). Preganglionic fibers form synapses with postganglionic parasympathetic neurons near the myocardium. Peripheral vessels do not have parasympathetic innervation.

Preganglial sympathetic neurons are located in the intermediolateral nuclei of the lateral horns of the Th1-L2 segments of the spinal cord. The axons of these cells leave the segment of the spinal cord as part of the ventral root and form a synapse with a postganglionic neuron located in the paravertebral sympathetic trunk. The fibers of the postganglionic sympathetic neurons reach the vessels and the heart as part of the peripheral nerves.

Pathophysiological mechanisms

In addition to the well-known motor and sensory deficits, autonomic disorders are often observed in spinal cord injury. The autonomic nervous system plays a very important role in the regulation of the cardiovascular system and controls parameters such as blood pressure and heart rate (HR). The autonomic nervous system consists of the sympathetic and parasympathetic systems. They interact with each other antagonistically depending on certain adaptive reactions of the organism. The parasympathetic nervous system reduces the heart rate. In turn, the sympathetic nervous system increases heart rate, myocardial contractility, and through vasoconstriction also increases total peripheral vascular resistance and blood pressure.

The regulation of blood pressure is modulated by the activity of the supraspinal centers (located in the brain), which, through descending pathways, send stimulatory impulses to the spinal sympathetic preganglionic neurons. As a result of a spinal cord injury, the descending pathways of the spinal cord are interrupted and the sympathetic neurons located here lose their ability to generate signals from the sympathetic nervous system.

Thus, a break in the descending pathways of the spinal cord leads to a decrease in the activity of the sympathetic nervous system and the elimination of its antagonistic effect on the parasympathetic part, the impulses of which reach their targets through the intact vagus nerve. A decrease in the activity of the sympathetic nervous system leads to a decrease in blood pressure, to the loss of the normal adaptability of the cardiovascular system and a violation of its reflex regulation.

Clinical picture

More often, patients with neurogenic shock have low blood pressure, the patients' skin is warm and dry. These symptoms appear as a result of inhibition of the sympathetic innervation of the cardiovascular system, leading to a decrease in blood return from the peripheral vascular bed, to a decrease in total peripheral vascular resistance (OPVR) and to a violation of the centralization of blood flow. Patients may experience hyperthermia. In this case, there is a pronounced loss of heat.

The clinical picture of neurogenic shock and the severity of the patient's condition largely depend on the level of spinal cord injury. Damage localized above the first thoracic segment of the spinal cord (Th1) leads to the destruction of the spinal cord pathways that control the activity of the entire sympathetic nervous system (regulating the normal functioning of many organ systems, including vital ones - cardiovascular, respiratory, and others).

Damage localized in the segments of the spinal cord from the first thoracic and below, only partially disrupt the activity of the sympathetic nervous system. The severity of manifestations of neurogenic shock decreases along with a decrease in the localization of the pathology of the spinal cord. So, for example, injuries of the upper thoracic segments are accompanied by a more severe clinical picture than, for example, damage to the cone of the spinal cord (at the level of the thoracolumbar junction of the spine).

Neurogenic shock can accompany both complete (absence of motor and sensory functions below the level of damage) and incomplete (partial dysfunction of the spinal cord below the level of damage) neurological deficits due to damage.

Differential Diagnosis

The diagnosis of neurogenic shock should be made after the exclusion of other critical conditions that have a similar clinical picture. Neurogenic shock must be differentiated from other types of shock, in particular hypovolemic ones. In severely injured patients, low blood pressure may be due to continued bleeding. Thus, it is tactically correct to rule out hemorrhagic shock in the patient in the first place. The key diagnostic criteria for neurogenic shock are arterial hypotension, bradycardia, neurological dysfunction, warm and dry skin of the patient.

Treatment

Therapeutic tactics in the emergency department

Attention! The information is intended for students and current professionals in the field of medicine, is not a guide to action and is presented for additional education.

The initial examination and treatment tactics in case of suspected neurogenic shock does not differ from that in providing care to injured patients and includes urgent diagnosis and correction of life-threatening disorders.

Control of parameters of the respiratory system and airway patency.
Immobilization (external fixation) of the damaged spine.
Intravenous infusion of crystalloid solutions to maintain mean arterial pressure above 70 mm. rt. Art. To prevent over-infusion, a pulmonary artery catheter may be placed to monitor the hemodynamic response. If intravenous fluids are not effective, inotropic agents such as dopamine at a dose of 2.5 to 20.0 µg/kg/min and dobutamine at a dose of 2.0 to 20.0 µg can be additionally administered to maintain adequate perfusion of body tissues. /kg/min.
If necessary, intravenous administration of 0.5-1.0 mg of atropine every 5 minutes to a total dose of 3.0 mg can be used to stop severe bradycardia.
In the presence of a neurological deficit in the first 8 hours after the injury, hormonal decongestant therapy with glucocorticoids should be carried out according to the scheme: during the first 15 minutes, methylprednisolone is administered as a bolus at a dose of 30 mg/kg, after which the administration of the drug continues for the next 23 hours at a rate of 5, 4 mg/kg/h.
Patients with neurogenic shock should urgently be consulted by an orthopedic traumatologist and a neurosurgeon to identify spinal injuries complicated by contusion and spinal cord compression for emergency surgical care.

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Notes and sources

Constantin Popa, Florian Popa, Valentin Titus Grigorean et al. Vascular dysfunctions following spinal cord injury / Journal of Medicine and Life Vol. 3, No.3, July - September 2010, pp.
Spinal cord injury: progress, promise, and priorities / Committee on Spinal Cord Injury, Bard of Neuroscience and Behavioral Health C T Liverman. The National Academies Press, Washington, 2005.

An excerpt characterizing Neurogenic shock

What is your health now? Well, tell me, - said the count, - what about the troops? Are they retreating or will there be more fighting?

“One eternal god, father,” said Berg, “can decide the fate of the fatherland. The army is burning with the spirit of heroism, and now the leaders, so to speak, have gathered for a meeting. What will happen is unknown. But I’ll tell you in general, dad, such a heroic spirit, truly ancient courage of the Russian troops, which they - it, - he corrected, - showed or showed in this battle on the 26th, there are no words worthy to describe them ... I’ll tell you, dad (he hit himself in the chest in the same way as one general who spoke in front of him hit himself, although a little late, because it was necessary to hit himself in the chest at the word "Russian army") - I will tell you frankly that we, the bosses, not only did we not have to urge the soldiers or anything like that, but we could hardly hold on to these, these ... yes, courageous and ancient feats, ”he said quickly. “General Barclay before Tolly sacrificed his life everywhere in front of the troops, I'll tell you. Our body was placed on the slope of the mountain. Can you imagine! - And then Berg told everything that he remembered from the various stories he had heard during this time. Natasha, not lowering her gaze, which confused Berg, as if looking for the solution of some question on his face, looked at him.

- Such heroism in general, which Russian soldiers showed, cannot be imagined and deservedly praised! - Berg said, looking back at Natasha and as if wanting to appease her, smiling at her in response to her stubborn look ... - "Russia is not in Moscow, it is in the hearts of all sons!" So, papa? Berg said.

At that moment, the Countess came out of the sofa-room, looking tired and displeased. Berg hastily jumped up, kissed the countess's hand, inquired about her health, and, expressing his sympathy by shaking his head, stopped beside her.

- Yes, mother, I will tell you truly, hard and sad times for every Russian. But why worry so much? You still have time to leave...

“I don’t understand what people are doing,” said the countess, turning to her husband, “they just told me that nothing is ready yet. After all, someone has to take care of it. So you will regret Mitenka. Will this end?

The count wanted to say something, but apparently refrained. He got up from his chair and walked to the door.

Berg at this time, as if to blow his nose, took out a handkerchief and, looking at the bundle, fell into thought, shaking his head sadly and significantly.

“And I have a big request for you, dad,” he said.

- Hm. said the Count, stopping.

“I’m driving past Yusupov’s house right now,” Berg said, laughing. - The manager is familiar to me, ran out and asked if you could buy something. I came in, you know, out of curiosity, and there was only a wardrobe and a toilet. You know how much Verushka wanted this and how we argued about it. (Berg involuntarily turned into a tone of joy about his well-being when he began to talk about a chiffonier and a toilet.) And such a charm! comes forward with the English secret, you know? And Verochka has long wanted to. So I want to surprise her. I saw so many of these men in your yard. Give me one, please, I'll pay him well and...

The Count winced and sighed.

“Ask the countess, but I don’t order.

“If it’s difficult, please don’t,” Berg said. - I would only really like for Verushka.

“Ah, go to hell, to hell, to hell, to hell. cried the old count. - My head is spinning. And he left the room.

- Yes, yes, mama, very hard times! Berg said.

Natasha went out with her father and, as if thinking something with difficulty, first followed him, and then ran downstairs.

On the porch stood Petya, engaged in arming people who were traveling from Moscow. In the yard, the laid wagons were still standing. Two of them were untied, and an officer, supported by a batman, climbed onto one of them.

- Do you know why? - Petya asked Natasha (Natasha realized that Petya understood: why father and mother quarreled). She didn't answer.

“Because papa wanted to give all the carts to the wounded,” said Petya. “Vassilyitch told me. In my opinion…

“In my opinion,” Natasha almost suddenly screamed, turning her embittered face to Petya, “in my opinion, this is such disgusting, such an abomination, such ... I don’t know!” Are we Germans? - Her throat trembled with convulsive sobs, and she, afraid of weakening and releasing a charge of her anger for nothing, turned and quickly rushed up the stairs. Berg sat beside the Countess and kindly comforted her. The count, pipe in hand, was walking around the room when Natasha, with a face disfigured by anger, burst into the room like a storm and quickly approached her mother.

- This is disgusting! This is an abomination! she screamed. “It can't be what you ordered.

Berg and the countess looked at her in bewilderment and fear. The count stopped at the window, listening.

- Mom, this is impossible; look what's in the yard! she screamed. - They stay.

- What happened to you? Who are they? What do you want?

- The wounded, that's who! It's impossible, mother; it doesn’t look like anything ... No, mother, dear, this is not it, please forgive me, dear ... Mother, well, what do we take away, you just look at what is in the yard ... Mother. It can't be.

The count stood at the window and, without turning his face, listened to Natasha's words. Suddenly he sniffled and put his face close to the window.

The countess looked at her daughter, saw her face, ashamed of her mother, saw her excitement, understood why her husband now did not look back at her, and looked around her with a bewildered look.

“Oh, do as you please! Am I bothering anyone! she said, not yet suddenly giving up.

- Mommy, my dear, forgive me!

But the countess pushed her daughter away and went up to the count.

- Mon cher, you dispose of it as it should ... I don’t know this, - she said, lowering her eyes guiltily.

“Eggs ... eggs teach a chicken ...” the count said through happy tears and hugged his wife, who was glad to hide her ashamed face on his chest.

- Daddy, mommy! Can you arrange? Can. Natasha asked. “We will still take everything we need,” Natasha said.

The count nodded his head in the affirmative, and Natasha, with the quick run with which she ran into the burners, ran down the hall into the hall and up the stairs to the courtyard.

People gathered near Natasha and until then they could not believe the strange order that she transmitted, until the count himself, in the name of his wife, confirmed the orders to give all the carts under the wounded, and carry the chests to the pantries. Understanding the order, people with joy and trouble set to a new business. Now it not only did not seem strange to the servants, but, on the contrary, it seemed that it could not be otherwise, just as a quarter of an hour before it not only did not seem strange to anyone that they were leaving the wounded and taking things, but it seemed which could not be otherwise.

All the households, as if paying for the fact that they had not taken up this earlier, set about with troublesome new business of accommodating the wounded. The wounded crawled out of their rooms and surrounded the wagons with joyful pale faces. A rumor also spread in the neighboring houses that there were carts, and the wounded from other houses began to come to the Rostovs' courtyard. Many of the wounded asked not to take things off and only to put them on top. But once the business of dumping things had begun, it could no longer stop. It was all the same to leave all or half. In the yard lay uncleaned chests with dishes, with bronze, with paintings, mirrors, which they had so carefully packed the previous night, and everyone was looking for and found an opportunity to put this and that and give away more and more carts.

“You can still take four,” said the manager, “I’m giving my wagon, otherwise where are they?

“Yes, give me my dressing room,” said the countess. Dunyasha will sit in the carriage with me.

They also gave a dressing wagon and sent it for the wounded through two houses. All the household and servants were merrily animated. Natasha was in an enthusiastically happy animation, which she had not experienced for a long time.

- Where can I tie it? - people said, fitting the chest to the narrow back of the carriage, - you must leave at least one cart.

- Yes, what is he with? Natasha asked.

- With count books.

- Leave it. Vasilyich will remove it. It is not necessary.

The cart was full of people; doubted where Pyotr Ilyich would sit.

- He's on the goats. After all, you are on the goats, Petya? Natasha screamed.

Sonya busied herself without ceasing, too; but the aim of her troubles was the opposite of Natasha's. She put away those things that should have been left; wrote them down, at the request of the countess, and tried to take with her as much as possible.

At two o'clock, the four Rostovs' crews, laid down and laid down, stood at the entrance. Carts with the wounded, one after another, drove out of the yard.

The carriage in which Prince Andrei was being carried, passing by the porch, attracted the attention of Sonya, who, together with the girl, was arranging seats for the countess in her huge tall carriage, which was standing at the entrance.

Whose wheelchair is this? Sonya asked, leaning out the carriage window.

"Don't you know, young lady?" the maid replied. - The prince is wounded: he spent the night with us and they are also coming with us.

- Yes, who is it? What's the last name?

- Our very former fiance, Prince Bolkonsky! - Sighing, answered the maid. They say dying.

Sonya jumped out of the carriage and ran to the countess. The countess, already dressed for the road, in a shawl and hat, tired, walked around the living room, waiting for her family, in order to sit with closed doors and pray before leaving. Natasha was not in the room.

MED24INFO

Unknown, Pediatric Advanced Life Support (PALS) Provider manual. Qualified resuscitation in pediatrics, 2006

neurogenic shock

Neurogenic shock, including spinal shock, develops with a traumatic brain or spinal injury, when the sympathetic innervation of blood vessels and the heart is disturbed. Usually the cause of neurogenic shock is trauma to the cervical spine, but neurogenic shock can also develop with a traumatic brain injury or damage to the spinal cord above the level of the sixth thoracic segment (T6).

Physiology of neurogenic shock

The sudden loss of sympathetic innervation to the smooth muscles of the blood vessel walls leads to uncontrolled vasodilation.

Signs of neurogenic shock

The main signs of neurogenic shock:

Hypotension with increased pulse pressure
Normal heart rate or bradycardia

Additional signs include an increase in respiratory rate, diaphragmatic breathing (using the diaphragm to breathe rather than the muscles of the chest wall), and other signs of spinal cord injury at the level of the cervical or upper thoracic segments.

Neurogenic shock should be differentiated from hypovolemic shock. Hypovolemic shock typically occurs with hypotension, decreased pulse pressure due to compensatory vasoconstriction, and compensatory tachycardia. In neurogenic shock, hypotension is not accompanied by compensatory tachycardia or peripheral vasoconstriction because the sympathetic innervation of the heart is also impaired, leading to bradycardia.

neurogenic shock

Definition

Pathogenesis of cardiovascular disorders

For a clear understanding of the pathogenetic mechanisms of the development of cardiovascular disorders, it is necessary to dwell on the neuroanatomy of the parts of the nervous system that regulates the activity of the cardiovascular system.

neuroanatomy

Pathophysiological mechanisms

Thus, interruption of the descending pathways of the spinal cord leads to a decrease in the activity of the sympathetic nervous system and the elimination of its antagonistic effect on the parasympathetic part, the impulses of which reach their targets through the intact vagus nerve. A decrease in the activity of the sympathetic nervous system leads to a decrease in blood pressure, to the loss of the normal adaptability of the cardiovascular system and a violation of its reflex regulation.

Clinical picture

Differential Diagnosis

Treatment

Therapeutic tactics in the emergency department

Attention! The information is intended for students and current professionals in the field of medicine, is not a guide to action and is presented for additional education.

Control of parameters of the respiratory system and airway patency.
Immobilization (external fixation) of the damaged spine.
Intravenous infusion of crystalloid solutions to maintain mean arterial pressure above 70 mm. rt. Art. To prevent over-infusion, a pulmonary artery catheter may be placed to monitor the hemodynamic response. If intravenous administration of solutions is ineffective, inotropic agents such as dofamim at a dose of 2.5 to 20.0 µg/kg/min and dobutamine at a dose of 2.0 to 20.0 µg/min can be additionally administered to maintain adequate perfusion of body tissues. kg/min.
If necessary, intravenous administration of 0.5-1.0 mg of atropine every 5 minutes to a total dose of 3.0 mg can be used to stop severe bradycardia.
In the presence of a neurological deficit in the first 8 hours after the injury, hormonal decongestant therapy with glucocorticoids should be carried out according to the scheme: during the first 15 minutes, methylprednisolone is administered as a bolus at a dose of 30 mg/kg, after which the administration of the drug continues for the next 23 hours at a rate of 5, 4 mg/kg/h.
Patients with neurogenic shock should urgently be consulted by an orthopedic traumatologist and a neurosurgeon to identify spinal injuries complicated by contusion and spinal cord compression for emergency surgical care.