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Neurogenic shock. Providing first aid in case of emergency conditions, accidents, anti-shock measures

Severe pain can cause painful shock due to overexcitation of the parasympathetic nervous system. This causes the heart rate to drop significantly (bradycardia), which in turn decreases the pulse and leads to a dangerous drop in blood pressure (shock).In terms of pathogenesis, pain shock corresponds to neurogenic shock.

Neurogenic shock is a distributive type of shock that results in low blood pressure, sometimes with a slow heart rate, due to disruption of the autonomic pathways in the spinal cord.
Exactly how excruciating pain causes neurogenic shock is not fully understood.

In textbooks, neurogenic shock refers to a condition in which, due to damage to the spinal cord or central nervous system, peripheral release of catecholamines does not occur. This causes loss of vasomotor tone and, as a consequence, accumulation of blood in the peripheral vessels and shock. This poor circulation causes muscles to process energy using a form of metabolism called anaerobic metabolism. Blood pressure drops. A drop in heart rate occurs if spinal cord damage affects areas above (proximal) the T-6 vertebrae. Below T-6, the heart rate will not be affected, but blood will pool in the lower extremities, causing warm, dry, and flushed skin.

Pain shock can be a dangerous complication, leading to organ dysfunction and death if not promptly recognized and treated. This condition should not be confused with spinal shock, which is not a circulatory disorder in nature.

Due to the lack of sympathetic tone, which plays a major role in other forms of shock, painful shock has a number of unique and atypical symptoms.

In other forms of shock, the sympathetic nervous system initiates various compensatory mechanisms, releasing adrenaline, norepinephrine and its main chemical mediators. These neurotransmitters cause increased heart rate, increased breathing, and sweating. They also cause blood vessels to narrow (vasoconstriction) to drain blood from the extremities to vital organs. During painful shock, the body loses the ability to activate the sympathetic nervous system and cannot initiate these compensatory mechanisms. All that remains is the parasympathetic tone.

Therefore, the unique presentation of neurogenic shock includes:

  • An immediate decrease in blood pressure (hypotension) due to sudden, massive relaxation of smooth muscle in the walls of blood vessels (vasodilation);
  • Warm, dry and red skin due to the formation of venous deposits due to loss of vascular tone
  • Priapism (also due to vasodilation);
  • The heart rate drops, which can lead to brachycardia.

In case of development of painful shock due to injuries of the upper spine:

  • If the injury is located below the fifth cervical vertebra, the patient will experience diaphragmatic breathing due to loss of neural control of the intercostal muscles (which are necessary for thoracic breathing);
  • When the injury is located above the third vertebra, breathing stops due to loss of nervous control over the diaphragm.


Causes

Painful shock can result from serious damage to the central nervous system (brain injury, cervical or upper thoracic spinal cord injury). Simply put: injury causes a sudden loss of background sympathetic stimulation of the blood vessels. This causes them to relax (vasodilation), which leads to a sudden decrease in blood pressure (secondary to a decrease in peripheral vascular resistance).

Neurogenic shock occurs as a result of damage to the spinal cord above the level of the 6th thoracic vertebra. It occurs in about half of people who suffer a spinal cord injury within the first 24 hours and usually does not go away within one to three weeks.

Treatment

Vasopressors are used to neutralize pain shock. They are used to maintain adequate blood pressure levels.An example of a commonly used vasopressor is dopamine, which acts primarily at alpha-1 receptors to cause vasoconstriction. This, in turn, increases blood pressure due to narrowing of the arteries. Dopamine is used alone or in combination with other inotropic agents.

Also widely used dobutamine, which acts on beta-1 receptors in the body, causing an increase in heart rate. This increase in heart rate increases blood pressure.

Phenylephrine may be used to treat victims with poor dopamine tolerance.

Atropine used to slow heart rate.

Shock is a condition of immediate threat to life, characterized by a general decrease in peripheral blood flow (hypoperfusion), which causes tissue hypoxia. 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. Decrease in 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) transfer of plasma into crushed tissue (trauma) or its loss from the surface of the skin (burns, Lyell's syndrome, Stevens-Johnson syndrome, exfoliative dermatitis);
  • b) decrease in the volume of extracellular fluid (state of dehydration) - insufficient water intake (more often in elderly people [due to thirst disorders] and in people who are not independent in self-care) or excessive loss of water and electrolytes through the gastrointestinal tract (diarrhea and vomiting), kidneys (osmotic diuresis with diabetic ketoacidosis and hyperosmolar non-ketoacidemic hyperglycemia), polyuria and excessive sodium removal with deficiency of GCS and mineralocorticoids, rarely - hypothalamic or renal diabetes insipidus), skin (fever, hyperthermia);
  • c) fluid loss in the so-called. third space - intestinal lumen (paralytic or mechanical obstruction), less often serous cavities (peritoneal - ascites);
  • d) increased permeability of vascular walls during anaphylactic and septic shock.

2. Increased vascular capacity (relative hypovolemia, redistribution shock[vasogenic] - due to vasodilation) → decrease in effective volume, i.e. filling with blood of the circulatory areas, volumetric and chemoreceptors (in practice this applies to arterial), while simultaneously increasing the blood volume 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, disruption of the heart and other mechanisms is possible) - acute adrenal insufficiency, thyrotoxic crisis, hypometabolic coma.

3. Impaired heart function (acute heart failure) and changes in large vessels causing a decrease in cardiac output (cardiac output) - ​​ cardiogenicshock.

Consequences

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

1) excitation of the sympathetic nervous system and increased secretion 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 areas for life organs [heart and brain]); in case of hypovolemia, restoration of plasma volume by the transition of intercellular fluid into capillary vessels (due to spasm of precapillary vessels and a decrease in intracapillary hydrostatic pressure with 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 ejection volume); hyperventilation; hyperglycemia;

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

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

2.  Metabolic and electrolyte disturbances due to hypoxia:

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

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

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

CLINICAL PICTURE

1 .   Symptomswithsidessystemsblood circulation: (rarely, bradycardia, rather in the terminal phase, may precede circulatory arrest in the mechanism of asystole or pulseless electrical activity), hypotension (decrease in 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 in septic shock at the beginning the skin is usually dry and warm, and in states of dehydration it is dry and elastic), slowing of capillary refill (after stopping pressure on the nail, pallor disappears after > 2 s), cyanosis ;

2) muscles - weakening;

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

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

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

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

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

3 . Symptoms associated with 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 is usually not difficult, but it is often 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 causes other than shock of impaired oxygen supply to tissues and tissue hypoxia (anemia, respiratory failure, poisoning that disrupts the transport of oxygen in the blood and its use by cells).

Supporting research

1 . Examination of the circulatory system:

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

2) ECG with 12 leads and constant monitoring - rhythm disturbances, 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 regarding diagnosis and difficulties in treatment. To assess the status of flooding and preload (left ventricular filling), which is of basic importance in differential diagnosis and determining the pharmacological treatment strategy, PCWP assessment using a Swan-Hans catheter may be suitable. PCWP corresponds to left atrial pressure and directly informs left ventricular end-diastolic pressure; values ​​≈ 15-18 mm Hg. Art. indicate optimal filling of the left ventricle. The Swan-Hans catheter also allows you to assess CO using the thermodilution method (other methods for assessing CO are also currently available). In cardiogenic shock, CO is reduced, and in the initial phase of hypovolemic shock and in anaphylactic and septic shock, it is usually increased.

2 . Laboratory tests of venous blood:

1) general peripheral blood test:

a) hematocrit, hemoglobin concentration and number of red blood cells - 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 red blood cells;

2) coagulation study- increased MNI, prolonged aPTT and decreased fibrinogen concentration indicate disseminated intravascular coagulation syndrome or may be a consequence of post-hemorrhagic or post-transfusion coagulopathy; increased MNI and prolonged 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 syndrome;

3) biochemical studies of blood serum:

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

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

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

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

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

6 . Blood type: determine based on documentation or perform laboratory testing on each patient.

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

TREATMENT OF SHOCK

1 .  Maintain a clear airway, if necessary, intubate and perform mechanical ventilation.

2 . Position the patient with legs elevated effective for hypotension, especially if no medical equipment is available, however, it can impair ventilation, and in cardiogenic shock with stagnation of blood in the pulmonary circulation, also heart function.

3 .  Putintravascular catheters:

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

4 . Apply etiological treatment→ see below and at the same time support the functioning of the circulatory system and oxygen saturation of tissues

  • 1) if the patient receives antihypertensive drugs → cancel them;
  • 2) with most types of shock, restoration of intravascular volume by IV infusion of solutions; the exception is cardiogenic shock with symptoms of blood stagnation in the pulmonary circulation. Colloidal solutions (6% or 10% hydroxyethyl starch [HES], 4% gelatin, dextran, albumin) 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, central venous pressure and diuresis, as well as side effects (symptoms of volume overload). For massive infusions, do not use 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 use 5% glucose to restore volume in shock. Colloidal solutions reproduce the intravascular volume - they remain almost completely in the vessels (plasma replacement agents - gelatin, 5% albumin solution), or remain in the vessels and lead to the transition of water from the extravascular space to the intravascular space [agents that increase plasma volume - hydroxyethyl starch [HES], 20% albumin solution, dextrans); crystalloid solutions level out the deficiency of extracellular fluid (extra- and intravascular); Glucose solutions increase the volume of total water in the body (external and intracellular fluid). Correction of significant volume deficiency can begin with the infusion of hypertonic solutions, for example, Special mixtures of crystalloids and colloids (the so-called Resuscitation in small volumes using between others. 7 .5% NaCl with 10% HES) as they are better at increasing plasma volume. In patients with severe sepsis or at increased risk of acute kidney injury, avoid the use of HES, especially those with molecular weight ≥ 200 kDa and/or molar substitution > 0.4; albumin solution may be used instead (but not in patients with head trauma);
  • 3) if hypotension cannot be eliminated, despite the infusion of solutions → start a constant intravenous infusion (preferably through a catheter into the vena cava) of catecholamines, constricting blood vessels, norepinephrine(adrenore, norepinephrine tartrate Agetan), usually 1-20 mcg/min (more 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, not currently the drug of choice for septic shock) 3-30 mcg/kg/min and use 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 a continuous i.v. infusion dobutamine(dobutamine Admeda, dobutamine-Health) 2-20 mcg/kg/min; if hypotension coexists, a vasoconstrictor can be used at the same time;
  • 5) simultaneously with the treatment described above, use oxygen therapy(by saturating hemoglobin with oxygen as much as possible, its supply to tissues increases; an absolute example is SaO 2<95%);
  • 6) if, despite the above actions, SvO 2<70%, а гематокрит <30% → примените трансфузию red blood cell mass.

5 .   The main method of correcting lactic acidosis is etiological treatment and treatment that supports the function of the circulatory system; evaluate the indications for the administration of NaHCO 3 IV 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, central venous pressure, gasometric parameters (and possibly lactate concentration), natremia and kalemia, parameters of renal and liver function; if necessary, cardiac output and pulmonary capillary wedge pressure.

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

8. If shock is contained:

  • 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 intravenous infusion of short-acting insulin, but avoid hypoglycemia; Aim for glycemic levels ranging from 6.7-7.8 mmol/L (120-140 mg/dL) to 10-11.1 mmol/L (180-200 mg/dL).

The circulatory disorder is based on direct damage to the spinal cord due to injury to the lower cervical and upper thoracic spine by intraneuronal 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.

A relative deficit of blood volume occurs due to a discrepancy between the volume of circulating blood and the capacity of the vascular bed, and venous return decreases. Due to damage to the sympathetic centers, the sympathetic reaction is not realized, so 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 pale skin, no “white spot” symptom. Decreased sensitivity and motor activity complete the picture and correspond to the level of damage.

Burn shock

There are 3 degrees of OS:

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

Excitement gives way to adynamia, confusion, oliguria.

Subcompensated OS - develops when the burn area is from 20 to 45% of the body surface. Excitement gives way to adynamia, confusion, oliguria. Characterized by hemodynamic instability, hypotension of 90 mmHg, vomiting. Mortality up to 40% from burn disease.

Decompensated OS – develops when the burn surface is over 45%.

Hypothermia, vomiting “coffee grounds”, black urine with a burning smell, anuria, intestinal paresis, pulse pressure is sharply reduced, sometimes not detected. Mortality is approaching 100%.

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

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



The process severity index is determined using the Frank index.

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

Start anti-shock measures as early as possible.

Eliminate the cause of the shock.

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

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

5. Place a cold compress on the patient’s head

Ventilate the room or provide the patient with an oxygen-air mixture

Place a swab moistened with ammonia to the patient’s nose

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

9. Calm the patient and instill in him the idea of ​​​​quickly eliminating the problem.

10. Call a doctor or ambulance immediately


Pharmacotherapy at the prehospital stage

Rehydration and detoxification therapy for rapid restoration of blood volume

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

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

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

Colloidal solutions for detoxification of parenteral administration: Albumin, Poliglyukin, Reomacrodex, Reopoliglyukin, Plasmafusin, Gelatinol, Oxypolygelatin, Zhelifundol, Physiogel, Refortan, Stabizol and others.

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

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

Treatment of respiratory failure

Treatment objectives: to ensure airway patency, lung ventilation and tissue oxygenation.

In case of cardiogenic and neurogenic shock, oxygen inhalation is usually sufficient; in case of hypovolemic and septic shock, mechanical ventilation is often used.

Tracheal intubation is resorted to:

To ensure airway patency during depression of consciousness.

To prevent aspiration of gastric contents during depression of consciousness.

To clear the airways from mucus during pneumonia.

To stimulate the respiratory and vascular centers, inject : Caffeine; Cordiamine; Sulphocamphocaine.

Treatment of kidney failure

Restoring blood flow through the kidneys and stimulating diuresis is carried out by dopamine (increasing cardiac output and renal blood flow). For oliguria and anuria, the administration of diuretics is not effective. Eufillin slightly stimulates renal blood flow.

Treatment of heart failure

For cardiogenic, neurogenic and septic shock (not amenable to infusion therapy), Dopamine or Dobutamine and very rarely Adrenaline or Norepinephrine are administered parenterally. Isoprenaline, Amrinon, Ditoxin are used in the ICU as prescribed

(lat. n.vagus) begins to dominate. The leading clinical signs of neurogenic shock in spinal cord injury are arterial hypotension and bradycardia. In terms of the frequency of injuries to the spinal cord, the cervical region is in the lead, 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.

Neurogenic shock

Pathogenesis of cardiovascular disorders

To clearly understand 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 regulate the activity of the cardiovascular system.

Neuroanatomy

The center of regulation of the cardiovascular system is the 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.

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

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, loss of normal adaptability of the cardiovascular system and disruption of its reflex regulation.

Clinical picture

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

The clinical picture of neurogenic shock and the severity of the patient’s condition largely depends on the level of spinal cord damage. 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 spinal cord segments starting from the first thoracic and below only partially disrupts the activity of the sympathetic nervous system. The severity of the manifestations of neurogenic shock decreases along with a decrease in the localization of spinal cord pathology. For example, damage to the upper thoracic segments is accompanied by a more severe clinical picture than, for example, damage to the conus of the spinal cord (at the level of the thoracolumbar junction of the spine).

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

According to S. Popa et al., all patients with complete neurological deficit due to spinal cord injury (ASIA A or B) have bradycardia, 68% of them have arterial hypotension, the correction of which in 35% of patients requires the introduction of vasopressors, and in 16%, severe bradycardia is observed, turning into asysitolia (cardiac arrest). In contrast, patients with incomplete neurological deficit due to spinal cord injury (ASIA C or D) have bradycardia in 35 - 71% of cases and only a few of them have arterial hypotension requiring vasopressor support, and cardiac arrest very rarely develops.

Differential diagnosis

The diagnosis of neurogenic shock should be made after excluding other critical conditions with a similar clinical picture. Neurogenic shock must be differentiated from other types of shock, in particular hypovolemic. In patients with severe trauma, low blood pressure may be due to ongoing bleeding. Thus, it is tactically correct to first exclude hemorrhagic shock in the patient. Key diagnostic criteria for neurogenic shock are hypotension, bradycardia, neurological dysfunction, and warm and dry skin of the patient.

Treatment

Treatment 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 for suspected neurogenic shock do not differ from those when providing care to injured patients and include emergency diagnosis and correction of life-threatening disorders.

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Notes and sources

An excerpt characterizing Neurogenic shock

From the hall, Berg ran into the living room with a floating, impatient step and hugged the count, kissed the hands of Natasha and Sonya and hurriedly asked about his mother’s health.
– How is your health now? Well, tell me,” said the count, “what about the troops?” Are they retreating or will there be another battle?
“One eternal god, dad,” 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, the truly ancient courage of the Russian troops, which they – it,” he corrected himself, “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 on the chest in the same way as one general who was talking in front of him hit himself, although a little late, because he should have hit himself on the chest at the word “Russian army”) - I’ll tell you frankly that we, the leaders, “Not only should we not have urged the soldiers or anything like that, but we could forcefully hold back these, these... yes, courageous and ancient feats,” he said quickly. – General Barclay, before Tolly, sacrificed his life everywhere in front of the army, I’ll tell you. Our corps was placed on the slope of the mountain. You can imagine! - And then Berg told everything that he remembered from the various stories he had heard during this time. Natasha, without lowering her gaze, which confused Berg, as if looking for a solution to some question on his face, looked at him.
– Such heroism in general, as shown by Russian soldiers, 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 persistent gaze... - “Russia is not in Moscow, it is in the hearts of her sons!” Right, dad? - said Berg.
At this time, the countess came out of the sofa room, looking tired and dissatisfied. Berg hastily jumped up, kissed the countess's hand, inquired about her health and, expressing his sympathy by shaking his head, stopped next to her.
– Yes, mother, I will truly tell you, difficult 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 needs to give orders. You'll regret Mitenka. Will this never end?
The Count wanted to say something, but apparently refrained. He stood up from his chair and walked towards the door.
Berg at this time, as if to blow his nose, took out a handkerchief and, looking at the bundle, thought, sadly and significantly shaking his head.
“And I have a big request to ask you, dad,” he said.
“Hm?..” said the count, stopping.
“I’m driving past Yusupov’s house now,” Berg said, laughing. “The manager, I know, ran out and asked if you would buy something.” I went in, you know, out of curiosity, and there was just a wardrobe and a toilet. You know how Veruschka wanted this and how we argued about it. (Berg involuntarily switched to a tone of joy about his well-being when he began talking about the wardrobe and toilet.) And such a delight! comes forward with an English secret, you know? But Verochka wanted it for a long time. So I want to surprise her. I saw so many of these guys in your yard. Give me one, please, I’ll pay him well and...
The Count frowned and gagged.
- Ask the countess, but I don’t give orders.
“If it’s difficult, please don’t,” said Berg. “I would really like it for Verushka.”
“Oh, go to hell, all of you, to hell, to hell, to hell!” shouted the old count. - My head is spinning. - And he left the room.
The Countess began to cry.
- Yes, yes, mummy, very difficult times! - said Berg.
Natasha went out with her father and, as if having difficulty understanding something, first followed him, and then ran downstairs.
Petya stood on the porch, arming the people who were traveling from Moscow. Pawned carts still stood in the yard. Two of them were untied, and an officer, supported by an orderly, climbed onto one of them.
- Do you know why? - Petya asked Natasha (Natasha understood that Petya understood why his father and mother quarreled). She didn't answer.
“Because daddy wanted to give all the carts to the wounded,” said Petya. - Vasilich told me. In my opinion…
“In my opinion,” Natasha suddenly almost screamed, turning her embittered face to Petya, “in my opinion, this is such disgusting, such an abomination, such... I don’t know!” Are we some kind of Germans?.. - Her throat trembled with convulsive sobs, and she, afraid to weaken and release the charge of her anger in vain, turned and quickly rushed up the stairs. Berg sat next to the Countess and comforted her with kindred respect. 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 walked up to her mother.
- This is disgusting! This is an abomination! - she screamed. - It can’t be that you ordered.
Berg and the Countess looked at her in bewilderment and fear. The Count stopped at the window, listening.
- Mama, this is impossible; look what's in the yard! - she screamed. - They remain!..
- What happened to you? Who are they? What do you want?
- The wounded, that's who! This is impossible, mamma; this doesn’t look like anything... No, Mama, darling, this is not it, please forgive me, darling... Mama, what do we care about what we’re taking away, just look at what’s in the yard... Mama!.. This can’t be !..
The Count stood at the window and, without turning his face, listened to Natasha’s words. Suddenly he sniffed and brought his face closer to the window.
The Countess looked at her daughter, saw her face ashamed of her mother, saw her excitement, understood why her husband was now not looking back at her, and looked around her with a confused look.
- Oh, do as you want! Am I disturbing anyone? – she said, not yet suddenly giving up.
- Mama, my dear, forgive me!
But the countess pushed her daughter away and approached the count.
“Mon cher, you do the right thing... I don’t know that,” she said, lowering her eyes guiltily.
“Eggs... eggs teach a hen...” the count said through happy tears and hugged his wife, who was glad to hide her ashamed face on his chest.
- Daddy, mummy! Can I make arrangements? Is it possible?.. – Natasha asked. “We’ll still take everything we need…” Natasha said.
The Count nodded his head affirmatively at her, and Natasha, with the same quick run as she used to run into the burners, ran across the hall to the hallway and up the stairs to the courtyard.
People gathered around Natasha and until then could not believe the strange order that she conveyed, until the count himself, in the name of his wife, confirmed the order that all carts should be given to the wounded, and chests should be taken to storerooms. Having understood the order, people happily and busily set about the new task. Now not only did it 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 that it couldn't be otherwise.
All the household, as if paying for the fact that they had not taken up this task earlier, busily began the new task of housing the wounded. The wounded crawled out of their rooms and surrounded the carts with joyful, pale faces. Rumors also spread in the neighboring houses that there were carts, and the wounded from other houses began to come to the Rostovs’ yard. Many of the wounded asked not to take off their things and only put them on top. But once the business of dumping things had begun, it could not stop. It didn't matter whether to leave everything or half. In the yard lay untidy chests with dishes, bronze, paintings, mirrors, which they had so carefully packed last night, and they kept looking for and finding 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 away my cart, otherwise where will they go?”
“Give me my dressing room,” said the countess. - Dunyasha will get into the carriage with me.
They also gave away a dressing cart and sent it to pick up the wounded two houses away. All the household and servants were cheerfully animated. Natasha was in an enthusiastically happy revival, which she had not experienced for a long time.
-Where should I tie him? - people said, adjusting the chest to the narrow back of the carriage, - we must leave at least one cart.
- What is he with? – Natasha asked.
- With the count's books.
- Leave it. Vasilich will clean it up. It is not necessary.
The chaise was full of people; doubted about where Pyotr Ilyich would sit.
- He's on the goat. Are you a jerk, Petya? – Natasha shouted.
Sonya kept busy too; but the goal of her efforts was the opposite of Natasha’s goal. She put away those things that were supposed to remain; I wrote them down, at the countess’s request, and tried to take with me as many as possible.

In the second hour, the four Rostov carriages, loaded and stowed, stood at the entrance. The carts with the wounded rolled out of the yard one after another.
The carriage in which Prince Andrei was 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 stood at the entrance.
– Whose stroller is this? – Sonya asked, leaning out of the carriage window.
“Didn’t you know, young lady?” - answered the maid. - The prince is wounded: he spent the night with us and is also coming with us.
- Who is this? What's the last name?
– Our very former groom, Prince Bolkonsky! – sighing, answered the maid. - They say he is dying.
Sonya jumped out of the carriage and ran to the Countess. The countess, already dressed for the trip, in a shawl and hat, tired, walked around the living room, waiting for her family in order to sit with the doors closed and pray before leaving. Natasha was not in the room.

General information

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

There are the following causes of shock:

1. Injuries received as a result of mechanical or chemical influence: burns, ruptures, tissue damage, separation of limbs, exposure to current (traumatic shock);

2. Loss of blood in large quantities accompanying the injury (hemorrhagic shock);

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

4. Allergens entering a sensitized environment (anaphylactic shock);

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

Shock can be diagnosed in a person who has suffered shock or trauma based on the following signs:

  • anxiety;
  • foggy consciousness with tachycardia;
  • reduced blood pressure;
  • impaired breathing
  • decreased volume of urine excreted;
  • the skin is cold and moist, marbled or pale cyanotic in color

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 suffered shock and provide assistance with shock, several stages of this condition should be distinguished:

1. Shock 1st degree. The person retains consciousness and makes contact, although his reactions are slightly inhibited. Pulse indicators – 90-100 beats, systolic pressure – 90mm;

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

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

4. Stage 4 shock is a 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’s heart cannot be heard, 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 inconspicuous and is felt only in the main arteries. Human skin is gray, with a characteristic marble pattern and spots similar to those of a corpse, 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 highlight:

Vascular shock (septic, neurogenic, anaphylactic shock);

Hypovolemic (anhydremic and hemorrhagic shock);

Cardiogenic shock;

Painful shock (burn, traumatic shock).

Vascular shock is shock caused by a decrease in vascular tone. Its subtypes: septic, neurogenic, anaphylactic shock are conditions with different pathogenesis. Septic shock occurs as a result of a person becoming infected 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 and plasma protein preparations, X-ray contrast agents 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 (anhydremic 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 occurs as a result of serious circulatory disorders. In cardiogenic shock, the brain, due to lack of blood supply (impaired heart function, dilated vessels unable to hold blood), experiences a sharp lack of oxygen. Therefore, a person in a state of cardiogenic shock loses consciousness and most often dies.

Painful shock, like cardiogenic shock, anaphylactic shock is a common shock condition that occurs during an acute reaction to an injury (traumatic shock) or burn. Moreover, it is important to understand that burn and traumatic shock are types of hypovolemic shock, because they are caused by the loss of a large amount of plasma or blood (hemorrhagic shock). This may include 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 delayed shock conditions is improper transportation of the victim and provision of first aid for shock, therefore, carrying out basic rescue procedures before the arrival of the ambulance team is very important.

Help with shock consists of the following:

1. Eliminate the cause of shock, for example, stop bleeding, free trapped limbs, extinguish clothes that are burning on the victim;

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

3. Check for breathing, pulse, and, if necessary, perform cardiac massage and artificial respiration;

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

5. Determine whether the victim is conscious and give him an anesthetic. It is advisable to give the patient hot tea, but rule out any abdominal injury before doing so;

6. Loosen clothing on the victim’s belt, chest, and neck;

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

8. The victim must not be left alone; he must not smoke. You should also not apply a heating pad to injured areas - this can cause blood to flow away from vital organs.

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