Neurogenic shock. Anaphylaxis and anaphylactic shock. Providing first aid in case of emergencies, accidents, anti-shock measures Possible causes of neurogenic shock

Neurogenic shock

Neurogenic shock

Definition

Neurogenic shock- 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 unlimited tone of the vagus nerve (lat. n.vagus) begins to dominate. Leading clinical signs neurogenic shock in spinal cord injury are arterial hypotension and bradycardia. In terms of the frequency of injuries to the spinal cord, the leading level is the cervical one, then the level of the thoracolumbar junction of the spine, less often thoracic region and even less often the level lumbar region spine (damage to the cauda equina). Neurogenic shock must be differentiated from spinal shock, defined as areflexia below the level of spinal cord injury.

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 departments nervous system regulating the activity of the heart vascular system.

Neuroanatomy

Regulation Center of cardio-vascular system are the homonymous nuclei 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 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.

Regulation blood pressure 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 injury) and incomplete (partial impairment of spinal cord functions below the level of injury) neurological deficits due to injury.

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 to the previous ones, 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 occurs.

Differential diagnosis

The diagnosis of neurogenic shock should be made after excluding other critical conditions that have 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 neurogenic shock are hypotension, bradycardia, neurological dysfunction, 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; it is not a guide to action and is presented for additional education.

(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 leading level 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.

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 injury) and incomplete (partial impairment of spinal cord functions below the level of injury) neurological deficits due to injury.

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; it 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.

Write a review about the article "Neurogenic shock"

Notes and sources

An excerpt characterizing Neurogenic shock

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.

Neurogenic shock

Neurogenic shock is a condition of the human body that develops as a result of damage. 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).

Traumatic shock

Traumatic shock - pathological condition which occurs due to blood loss and pain syndrome in case of injury and poses a serious threat to the patient's life. Develops with injuries accompanied by large loss of blood or a decrease in the amount of plasma: traumatic brain injury, severe wounds of the neck, chest, abdomen or limbs, multiple fractures, frostbite, burns, etc. Regardless of the cause that caused it, traumatic shock always occurs “according to the same scenario,” that is, it manifests itself with the same symptoms. Urgent stoppage of bleeding, anesthesia and immediate delivery of the patient to the hospital are necessary. Treatment of traumatic shock is carried out in an intensive care unit and includes a set of measures to compensate for the resulting disorders. The prognosis depends on the severity and phase of shock, as well as the severity of the injury that caused it.

And yet the main thing here is the state of deep circulatory depression. As a result, blood flow becomes insufficient to properly supply tissues with oxygen, nourish them and cleanse them of metabolic products. If the development of shock does not stop spontaneously (which is practically unlikely) or is not interrupted by appropriate therapeutic measures, then death occurs. To prevent this from happening, you need to normalize blood circulation in the body as soon as possible. Currently, according to the reasons, it is customary to distinguish three categories of shock: hypovolemic, normovolemic, hypervolemic (cardiogenic).

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

Symptoms In the early stages of hypovolemic shock, blood loss is compensated by releasing a significant volume of blood from the skin, muscle vessels and subcutaneous fat in favor of the 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, blood circulation in the kidneys, heart, brain and liver also begins to deteriorate. At this stage of shock, thirst, decreased diuresis, and increased urine density are observed. Tachycardia (increased heart rate), instability of blood pressure, weakness, agitation, confusion, and sometimes even loss of consciousness may be observed. Blood pressure gradually decreases. The pulse quickens and becomes weak. The nature of breathing also changes, becoming deep and rapid.

If bleeding does not stop and 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 medication;

2) polyglucin and rheopolyglucin are administered, which occupy an important place in treatment. They remain in the circulatory system for quite a long time and are able to change the properties of the 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) begin a jet or drip (depending on the circumstances) transfusion of 500 ml of same-group, Rh-compatible blood, heated to 37 ° C, after which 500 ml of plasma, protein or albumin are poured in;

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

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

6) together with the beginning of blood replacement, 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 has great importance in the treatment of shock. With massive blood loss, oxygen transfer is significantly affected. 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 a lack of blood in the bloodstream and directly depends on it; only when late stages shock is possible due to damage to 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 blood output from the heart occurs when acute heart attack myocardium. Mortality from cardiogenic shock is high, reaching 90%.

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

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

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

If shock continues, then fluid from the vessels goes into the cells, the volume of intravascular fluid decreases, and as an inevitable consequence, a 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 damp, the neck veins collapse, the pulse is rapid but weak, blood pressure decreases, and diuresis drops. 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 precisely established, the location 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 type of shock occurs as a result of various damage to 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 symptoms are a fairly low pulse and very mild hypotension. The skin is usually dry and warm, consciousness is preserved, respiratory function is not impaired, and the neck veins are collapsed. In some cases, it is quite enough to raise both lower limbs above the patient’s body in a horizontal position so that all symptoms of neurogenic shock are relieved. This technique is most effective for shock caused by high spinal anesthesia. In case of neurogenic shock caused by spinal cord injury, as a rule, there is a need to increase the volume of blood volume 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. For long-term crush syndrome and extensive soft tissue injuries, penetration large quantity toxins in 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) are associated with the redistribution of blood in the body: blood filling increases internal organs and muscle vessels. Central circulation (brain and heart), as well as peripheral circulation, 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 severe pain and blood poisoning with toxins, 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 there are two phases: erectile and torpid. In the erectile phase, processes of excitation of all body functions are observed. This is manifested by normal or even hypertension (increased blood pressure), tachycardia, and increased breathing. The patient is usually conscious, excited, worried, 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 and poorly responsive to light. Skin pale with an earthy tint, cold extremities, often the skin is covered with cold, sticky sweat, body temperature is reduced. The pulse is frequent, thread-like, sometimes not palpable in the limbs and is detected only in large vessels. Blood pressure, especially systolic, is significantly reduced. Cardiac output is reduced. Urine output is reduced or absent.

Treatment. In the accepted complex method of treating traumatic shock, the basis is fast and effective pain relief with analgesics or antipsychotics, compensation of blood loss and warming. When indicated for surgery, endotracheal anesthesia is used under mechanical ventilation; conduction, case anesthesia of the extremities; different kinds 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 administration of norepinephrine and adrenaline is indicated. The time factor is of decisive importance when providing assistance to a victim with mechanical damage who is in a state of shock: the sooner assistance is provided, the more favorable the outcome. Taking 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 of Emergency Medicine named after. 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 treatment of shock was carried out starting from the erectile phase. This treatment is mainly preventive measures: careful removal from the site of injury, creation of rest for both the injured and damaged organ (immobilization for fractures), administration of painkillers, drugs that support cardiac activity and vascular tone. In case of deep respiratory and cardiac disorders, artificial respiration and cardiac massage should be used. Antishock therapy should continue in the ambulance, where it is possible to temporarily stop bleeding, perform a novocaine blockade, administer intravenous blood and blood substitutes, administer oxygen therapy and give superficial anesthesia with nitrous oxide with artificial respiration.

Neurogenic shock

n.vagus

Neuroanatomy

Pathophysiological mechanisms

Clinical picture

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 % 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 capacitance, reducing venous return and cardiac output.

Neurogenic shock is usually a consequence of spinal cord injury due to fractures of the cervical or upper thoracic spine, when sympathetic regulation of peripheral vascular tone is interrupted.

Sometimes an injury such as an epidural hematoma extending into spinal cord, can cause neurogenic shock without vertebral fracture. Penetrating spinal cord injuries can also cause neurogenic shock.

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

Diagnosis of neurogenic shock

Classic symptoms of neurogenic shock include decreased blood pressure, bradycardia (absence of reflex tachycardia due to interruption of sympathetic impulses), warming of the extremities (loss of peripheral vasoconstriction), motor and sensory disturbances suggestive of spinal cord injury, and radiographic appearance of a vertebral fracture.

However, determining the presence of neurogenic shock can be difficult because patients with multiple injuries, including spinal cord injuries, often have traumatic brain injury, which can make it difficult to identify the cause of motor and sensory impairment. Moreover, combined injuries can cause hypovolemia and complicate the clinical picture.

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

Treatment of neurogenic shock

After ensuring patency respiratory tract and establishing adequate ventilation, fluid resuscitation, and intravascular volume restoration in neurogenic shock, systemic blood pressure and perfusion often improve. The introduction of vasoconstrictors can improve peripheral vascular tone, reduce vascular capacity and increase venous return, but only after hypovolemia has been excluded and a diagnosis of neurogenic shock has been established.

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

Restoration of normal hemodynamics should precede any surgical attempt to stabilize the 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) 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 leading level 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 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.

Preganglinal 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 exit the spinal cord segment as part of the ventral root and form a synapse with the postganglionic neuron located in the paravertebral sympathetic trunk. The fibers of postganglionic sympathetic neurons reach the vessels and heart as part of the peripheral nerves.

Pathophysiological mechanisms

In addition to the well-known motor and sensory deficits, autonomic impairments are often observed in spinal cord injury. The autonomic nervous system plays a very important role in regulating the activity 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 body. The parasympathetic nervous system reduces 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.

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 the 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 injury) and incomplete (partial impairment of spinal cord functions below the level of injury) neurological deficits due to injury.

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; it 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.

1. Parameter control respiratory system and airway patency.
2. Immobilization (external fixation) of the injured spine.
3. Intravenous infusion of crystalloid solutions to maintain mean arterial pressure above 70 mmHg. rt. Art. To prevent excessive infusions, a catheter may be placed in the pulmonary artery, allowing you to monitor the hemodynamic response. If intravenous administration solutions are ineffective, to maintain adequate perfusion of body tissues, inotropic agents can be additionally administered, such as dopamine at a dose of 2.5 to 20.0 mcg/kg/min and dobutamine at a dose of 2.0 to 20.0 mcg/kg/ min.
4. If necessary, intravenous administration of 0.5–1.0 mg of atropine every 5 minutes up to a total dose of 3.0 mg can be used to relieve severe bradycardia.
5. If there is a neurological deficit, in the first 8 hours from the moment of injury, hormonal decongestant therapy with glucocorticoids should be carried out according to the following 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.
6. Patients with neurogenic shock urgently should be consulted by an orthopedic traumatologist and a neurosurgeon to identify spinal injuries complicated by contusion and compression of the spinal cord in order to provide emergency surgical care.

Write a review of the article “Neurogenic shock”

Notes and sources

1. 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.
2. Spinal cord injury: progress, promise, and priorities / Committee on Spine Cord Injury, Bard of Neuroscience and Behavioral Health C T Liverman. The National Academies Press, Washington, 2005.

An excerpt characterizing Neurogenic shock

– 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, to hell, to hell, to hell, all of you. - shouted the old count. - My head is spinning. - And he left the room.

- 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, my dear, this is not the same, please forgive me, my dear... Mama, what do we care about what we’re taking away, just look at what’s in the yard... Mama. It 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? Can. – 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.

MED24INfO

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

Neurogenic shock

Neurogenic shock, including spinal shock, develops with traumatic brain or spinal injury when sympathetic innervation is disrupted blood vessels and hearts. Neurogenic shock is usually caused by trauma cervical spine spine, but neurogenic shock can also develop with traumatic brain injury or with 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 elevated pulse pressure
• Normal heart rate or bradycardia

Additional signs include increased breathing rate, diaphragmatic breathing (using the diaphragm rather than the chest wall muscles to breathe), and other signs of spinal cord injury in 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, resulting in bradycardia.

Neurogenic shock

Neurogenic shock

Definition

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 unlimited tone of the vagus nerve (lat. n.vagus) begins to dominate.

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.

Preganglinal 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 exit the spinal cord segment as part of the ventral root and form a synapse with the postganglionic neuron located in the paravertebral sympathetic trunk. The fibers of postganglionic sympathetic neurons reach the vessels and heart as part of the peripheral nerves.

Pathophysiological mechanisms

In addition to the well-known motor and sensory deficits, autonomic impairments are often observed in spinal cord injury. The autonomic nervous system plays a very important role in regulating the activity 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 body. The parasympathetic nervous system reduces 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.

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 the 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 injury) and incomplete (partial impairment of spinal cord functions below the level of injury) neurological deficits due to injury.

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 % 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; it 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.

1. Monitoring the parameters of the respiratory system and airway patency.
2. Immobilization (external fixation) of the injured spine.
3. Intravenous infusion of crystalloid solutions to maintain mean arterial pressure above 70 mmHg. rt. Art. To prevent excessive infusions, a pulmonary artery catheter may be placed to monitor the hemodynamic response. If intravenous administration of solutions is ineffective, inotropic agents such as dopamine at a dose of 2.5 to 20.0 mcg/kg/min and dobutamine at a dose of 2.0 to 20.0 mcg/min can be additionally administered to maintain adequate perfusion of body tissues. kg/min.
4. If necessary, intravenous administration of 0.5–1.0 mg of atropine every 5 minutes up to a total dose of 3.0 mg can be used to relieve severe bradycardia.
5. If there is a neurological deficit, in the first 8 hours from the moment of 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.
6. Patients with neurogenic shock should urgently be consulted by an orthopedic traumatologist and neurosurgeon to identify spinal injuries complicated by contusion and compression of the spinal cord to provide emergency surgical care.

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 expansion of the veins. The condition that develops as a result of this is called neurogenic shock.

The role of vascular capacity in the regulation of hemodynamics is described in detail in our article, which emphasized that both an increase in vascular capacity and a decrease in blood volume lead to a decrease in the average systemic filling pressure and, consequently, to a decrease in venous return of blood to the heart. A decrease in venous return caused by vasodilation is called venous stasis.
Causes of neurogenic shock. The main neurogenic factors causing 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 running as part of the anterior roots, which can lead to the development of neurogenic shock.
3. Brain injuries, which often lead to paralytic vasodilation. Many patients with a concussion or contusion of the basal parts of the brain develop deep neurogenic shock.

In addition, cerebral ischemia can cause shock. Thus, 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 the 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 after the entry into the blood of an antigen to which a person is sensitive. Anaphylactic shock is based on 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 dilation of the veins, which leads to a decrease in venous return of blood to the heart; (2) dilation of arterioles, which leads to a drop in blood pressure; (3) a sharp increase in capillary permeability, which leads to the rapid transfer of proteins and fluid from the capillaries to the tissues.

As a result, there is a significant decreased venous return and shock develops, sometimes so severe that the person dies literally within 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.