Shock causes clinic treatment. What is shock in medicine? Shock types, causes and emergency care. Experimental shock models

Shock is a state of extreme depression of the circulatory system, as a result of which the blood flow becomes insufficient for normal oxygenation, nutrition and tissue metabolism.

5 types of shock:

1) hypovolemic shock

Reasons: blood, plasma loss; water and electrolyte disorders

If the loss does not exceed 500 ml, there is no clinic, only moderate tachycardia.

Losses from 501 to 1200 ml - moderate tachycardia, moderate hypotension, a sign of vasoconstriction (pallor)

Loss from 1201 to 1800 ml - pulse up to 120 beats / min, increasing hypotension, pallor, the patient is conscious, but restless

Losses from 1801 to 3000 ml - tachycardia above 170 beats / min, systolic pressure 60-70 mm Hg, pulse only on large vessels, the patient is unconscious, pale, cold, wet, anuria is observed. \

To assess the severity of the state of shock, the Algover index (shock index) is introduced:

SHI = heart rate \ syst.

Normally, SHI = 0.5 - 0.6 units.

Mild severity - 0.8 units

Average degree - 0.9 - 1.2 units

Severe degree - 1.3 or more units

2) cardiogenic shock

Causes: extensive infarction, ventricular aneurysm, rupture of the interventricular septum

Pat. mechanisms:

A) hyposystole - small cardiac output syndrome

B) deterioration of myocardial metabolism with extensive necrosis, a sharp decrease in SV, significant atherosclerotic occlusion of the coronary vessels.

Clinically similar to hypovolemic shock.

3) septic shock

Reasons: generalized infections - an increase in foreign lipopolysaccharides and bacteria, the object of which is microcirculation. Also, the appearance of bacterial toxins leads to overproduction of its own biologically active substances, hyperdynamic phase (1) septic shock: expansion of peripheral vessels, blood pressure is normal, frequent pulse, but good filling.

The patient is pink, the skin is warm, with time, the permeability of the vessels increases, so the liquid part of the blood goes into the tissue, the BCC decreases. The second stage begins - hypodynamic phase, clinically similar to hypovolemic shock.

4) neurogenic (spinal) shock

Causes: spinal injury, spinal anesthesia, acute expansion of the stomach.

Pathogenesis: the basis is the loss of sympathetic innervation by the heart and blood vessels. Clinic: the patient is always conscious, bradycardia, warm skin, moderate hypotension.

5) traumatic shock

Reasons: polytrauma, injuries, compression syndrome, burns, frostbite.

Mechanisms: pain, toxemia, blood loss, further cooling of the body

With crush syndrome and massive soft tissue injuries - toxemia - acute renal failure

In case of burns and frostbite - pain, toxemia and plasma loss - an increase in blood viscosity and ARF

In case of injuries and injuries - redistribution of blood - decrease in SV and venous return

Shock stages:

1) stage of excitement. Activation of all body functions, short-term: agitation, tachycardia, hypertension, shortness of breath

2) torpid stage. At the level of the central nervous system, diffuse inhibition occurs. No: reflexes, consciousness, pulse only on large vessels, blood pressure below 60, the patient is pale, cold, wet, anuria.

Any shock is accompanied by:

1) hyperactivation of the endocrine link

Baro- and volumoreceptors of all vessels are activated à the hypothalamic-pituitary-adrenal system is activated, SAS, vasopressin, aldosterone, RAAS work at a catabolic level

Aimed at: maintaining peripheral resistance, fluid retention to replenish the BCC, redistribution of blood flow in favor of vital organs, hyperglycemia to create an energy pool.

2) changes in the circulatory system

Primarily from the CCC side:

Reactions to compensate for hypovolemia

Tachycardia, aimed at maintaining the IOC

Peripheral vascular spasm and release of blood from the depot

Centralization of blood circulation

Hydremia - the flow of interstitial fluid into the bloodstream

Arterial tone changes under the influence of hormones

An increase in arterial tone leads to an increase in peripheral resistance à an increase in pressure load on the LN - gradually the force of contraction begins to fall

Cardiac output depends on the strength and speed of contraction, but if the pulse rate is higher than 170 beats, this leads to a sharp decrease in SV → blood practically does not enter the coronary vessels → metabolic disorders in the myocardium → toxic depression of the myocardium (irreversible factor of shock)

3) violations of the microvasculature

Associated with an increase in vascular tone and centralization of blood circulation. To the periphery, the blood flow rate begins to decrease → opening of arterio-venous anastomoses, through these anastomoses arterial blood, bypassing the capillaries, is discharged into the venous part → emptying of the capillary network → violation of tissue metabolism → increased formation of biologically active substances → vasodilation and blood entry begins, but the blood flow will be passive and dependent on the value of blood pressure.

BAS accumulation → vascular paralysis, capillaries are constantly open, do not respond to stimuli, microvasculature permeability increases, blood flow velocity decreases → disseminated intravascular coagulation → thrombus formation, venous return is sharply reduced, interstitial edema occurs, BCC decreases

4) metabolic disorders

Due to the action of hormones - hyperglycemia. Under the action of GCS and STH, hexokinase is blocked → glucose is used only for nutrition of vital organs

Under the influence of STH, ACTH, adrenaline, lipolysis is activated with the formation of free FA

Endorphins and enkephalins accumulate → hypotension and toxic depression of the myocardium. Decreased blood flow in the pancreas leads to the release of enzymes (trypsin and chemotrypsin), which coagulate endogenous proteins and damage small cell membranes.

5) cell hypoxia. Decreased blood flow in the thyroid gland → decreased secretion of thyroxine → cells stop using oxygen → cell hypoxia → increased permeability of cell membranes → cells stop using oxygen → decreased ATP → activation of glycolysis → increased osmolarity of cells → cellular edema and cell death

6) endotoxemia. Accumulation of own biologically active substances (lysosomes E) → spasm of coronary vessels → ischemia → changes in heart function

Multiple organ failure

1) initial functional state

2) resistance to hypoxia

Liver. Promotes endotoxemia (the liver itself does not suffer)

Lungs. Development of respiratory distress syndrome

Characterized by:

A) activation of the adhesive properties of the pulmonary vascular endothelium

B) increasing the permeability of the pulmonary vessels for water and B

C) the development of DIC syndrome

D) adhesion of activated neutrophils to the vascular endothelium, which leads to the development of inflammation

Clinically: refractory hypoxemia, the appearance of flocculent opacities of the lung fields, decreased lung compliance, impaired elasticity of the lung tissue, thickening of the alveolar membranes → chronic respiratory failure

Stomach - ulceration

Intestine - less affected (excl. Septic shock)

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General information

This is a serious condition where the cardiovascular system cannot keep up with the blood supply to the body, usually due to low blood pressure and damage to cells or tissues.

Shock reasons

Shock can be caused by a condition of the body when blood circulation is dangerously reduced, for example, with cardiovascular diseases (heart attack or heart failure), with a large loss of blood (heavy bleeding), with dehydration, with severe allergic reactions or blood poisoning (sepsis).

Shock classifications include:

• cardiogenic shock (associated with cardiovascular problems),
• hypovolemic shock (caused by low blood volume),
• anaphylactic shock (caused by allergic reactions),
• septic shock (caused by infections)
• neurogenic shock (disorders of the nervous system).

Shock is a life-threatening condition and requires immediate medical treatment, and emergency care is not excluded. The patient's condition in shock can quickly deteriorate, be prepared for primary resuscitation actions.

Shock symptoms

Symptoms of shock may include feelings of fear or excitement, bluish lips and nails, chest pain, confusion, cold, damp skin, reduction or cessation of urination, dizziness, fainting, low blood pressure, pallor, excessive sweating, rapid heart rate, shallow breathing, unconsciousness , weakness.

First aid for shock

Check the victim's respiratory tract, if necessary, artificial respiration should be performed.

If the patient is conscious and does not have injuries to the head, limbs, back, lay him on his back, while his legs should be raised by 30 cm; do not raise your head. If the patient is injured, in which the raised legs cause a feeling of pain, then they do not need to be lifted. If the patient has received severe damage to the spine, leave him in the position in which you found, without turning over, and provide first aid, treating wounds and cuts (if any).

The person should stay warm, loosen tight clothing, do not give the patient food or drink. If the patient is vomiting or drooling, turn his head to the side to ensure the outflow of vomit (only if there is no suspicion of a spinal cord injury). If, nevertheless, there is a suspicion of damage to the spine and the patient is vomiting, it is necessary to turn it over, fixing the neck and back.

Call an ambulance and continue monitoring vital signs (temperature, pulse, respiratory rate, blood pressure) until help arrives.

Preventive measures

Preventing shock is easier than treating it. Prompt and timely treatment of the underlying cause will reduce the risk of developing severe shock. First aid will help control the state of shock.

Shock is a pathological change in the functions of the vital systems of the body, in which there is a violation of breathing and blood circulation. This condition was first described by Hippocrates, but the medical term appeared only in the middle of the 18th century. Since various diseases can lead to the development of shock, for a long time scientists have proposed a large number of theories of its occurrence. However, none of them explained all the mechanisms. It has now been established that shock is based on arterial hypotension, which occurs when the volume of circulating blood decreases, cardiac output and total peripheral vascular resistance decrease, or when fluid is redistributed in the body.

Shock symptoms

The symptoms of shock are largely determined by the cause that led to its appearance, however, there are common features of this pathological condition:

• impaired consciousness, which can be manifested by excitement or depression;
• decrease in blood pressure from insignificant to critical;
• an increase in heart rate, which is a manifestation of a compensatory response;
• centralization of blood circulation, in which spasm of peripheral vessels occurs, with the exception of renal, cerebral and coronary vessels;
• pallor, marbling and cyanosis of the skin;
• rapid shallow breathing that occurs with an increase in metabolic acidosis;
• a change in body temperature, usually it is low, but with an infectious process it is increased;
• the pupils, as a rule, are dilated, the reaction to light is slow;
• in especially difficult situations, generalized convulsions, involuntary urination and defecation develop.

There are also specific manifestations of shock. For example, when exposed to an allergen, bronchospasm develops and the patient begins to choke, with blood loss, a person experiences a pronounced feeling of thirst, and with myocardial infarction, chest pain.

Shock degrees

Depending on the severity of the shock, four degrees of its manifestations are distinguished:

1. Compensated. At the same time, the patient's condition is relatively satisfactory, the function of the systems is preserved. He is conscious, systolic blood pressure is lowered, but exceeds 90 mm Hg, pulse is about 100 per minute.
2. Subcompensated. Violation of vital functions is noted. The patient's reactions are inhibited, he is sluggish. The skin is pale, moist. The heart rate reaches 140-150 per minute, breathing is shallow. The condition requires prompt medical attention.
3. Decompensated. The level of consciousness is reduced, the patient is severely inhibited and reacts poorly to external stimuli, does not answer questions or answers in one word. In addition to pallor, there is marbling of the skin due to impaired microcirculation, as well as cyanosis of the tips of the fingers and lips. The pulse can be determined only on the central vessels (carotid, femoral artery), it exceeds 150 per minute. Systolic blood pressure is often below 60 mm Hg. There is a malfunction of the internal organs (kidneys, intestines).
4. Terminal (irreversible). The patient, as a rule, is unconscious, breathing is shallow, the pulse cannot be felt. The pressure is often not determined by the usual method using a tonometer, heart sounds are muffled. But the skin appears blue spots in places of accumulation of venous blood, similar to cadaveric ones. Reflexes, including painful ones, are absent, the eyes are motionless, the pupil is dilated. The prognosis is extremely unfavorable.

To determine the severity of the condition, you can use the Algover shock index, which is obtained by dividing the heart rate by the systolic blood pressure. Normally, it is 0.5, with 1 degree -1, with the second -1.5.

Shock types

Depending on the immediate cause, there are several types of shock:

1. Traumatic shock resulting from external influences. In this case, there is a violation of the integrity of some tissues and the occurrence of pain.
2. Hypovolemic (hemorrhagic) shock develops when the volume of circulating blood decreases due to bleeding.
3. Cardiogenic shock is a complication of various heart diseases (tamponade, rupture of an aneurysm), in which the left ventricular ejection fraction is sharply reduced, as a result of which arterial hypotension develops.
4. Infectious-toxic (septic) shock is characterized by a pronounced decrease in the peripheral resistance of blood vessels and an increase in the permeability of their walls. As a result, there is a redistribution of the liquid part of the blood, which accumulates in the interstitial space.
5. develops as an allergic reaction in response to intravenous exposure to a substance (injection, insect bite). In this case, histamine is released into the blood and vasodilatation, which is accompanied by a decrease in pressure.

There are other types of shock that include various symptoms. For example, burn shock develops as a result of trauma and hypovolemia due to large losses of fluid through the wound surface.

Shock help

Each person should be able to provide first aid in case of shock, since in most situations the count goes for minutes:

1. The most important thing that needs to be done is to try to eliminate the cause that caused the pathological condition. For example, if bleeding occurs, the arteries need to be clamped above the site of injury. And if bitten by an insect, try not to let the poison spread.
2. In all cases, with the exception of cardiogenic shock, it is advisable to raise the victim's legs above the head. This will help improve blood flow to the brain.
3. In cases of extensive injuries and suspicion of a spine, it is not recommended to move the patient before the arrival of an ambulance.
4. To replenish the loss of fluid, you can give the patient a drink, preferably warm water, as it is absorbed faster in the stomach.
5. If a person has severe pain, he can take an analgesic, but it is not advisable to use sedatives, since this will change the clinical picture of the disease.

Emergency doctors in cases of shock use either intravenous fluids or vasoconstrictor drugs (dopamine, adrenaline). The choice depends on the specific situation and is determined by a combination of various factors. The medical and surgical treatment of shock depends on the type of shock. So, in case of hemorrhagic shock, it is necessary to urgently replenish the volume of circulating blood, and in case of anaphylactic shock, administer antihistamines and vasoconstrictor drugs. The victim must be urgently taken to a specialized hospital, where treatment will be carried out under the control of vital signs.

The prognosis for shock depends on its type and degree, as well as the timeliness of assistance. With mild manifestations and adequate therapy, recovery almost always occurs, while with decompensated shock, there is a high probability of death, despite the efforts of doctors.

Shock(French choc; English shock) is a typical, phase-developing pathological process arising from disorders of neurohumoral regulation caused by extreme influences (mechanical injury, burns, electrical trauma, etc.) and characterized by a sharp decrease in the blood supply to tissues, a disproportionate level of metabolic processes, hypoxia and suppression of body functions. Shock is manifested by a clinical syndrome characterized in the most typical torpid phase for it by emotional inhibition, hypodynamia, hyporeflexia, hypothermia, arterial hypotension, tachycardia, dyspnea, oliguria, etc.

In the process of evolution, shock as a pathological process (see) is formed in the form of a series of reactions that can be regarded as adaptive, aimed at the survival of the species as a whole. From this point of view, shock seems to be such a response of the body to aggression, which can be classified as passive protection aimed at preserving life in conditions of extreme exposure.

The majority of Russian scientists adhere to the idea of ​​shock as a typical pathological process, but of an adaptive nature, which can arise under the action of various extreme factors and be a component of various diseases. Foreign researchers, for example, Weil and Shubin (M.N. Weil, N. Shubin, 1971), as a rule, do not discuss the general pathology of shock and pay main attention to its clinical manifestations, understanding by shock any syndrome that occurs in response to aggression and characterized by a significant suppression of the vital activity of the organism. Some researchers do not make significant distinctions between the concepts of "shock" and "collapse", while others, including domestic ones, distinguish between these concepts. Collapse (see) should be understood as an acutely developing vascular insufficiency, characterized, first of all, by a drop in vascular tone, as well as an acute decrease in the volume of circulating blood.

Story. The general severe changes that occur in the human body during trauma are described in the "Aphorisms" of Hippocrates. In 1575, A. Paré, referring to shock, described severe conditions that arise "when falling from a height on something hard or when hitting, causing bruises," and others.

The idea of ​​shock, close to modern, was first given by the French surgeon H. F. Le Dran in 1737 in the book "Traite ou reflexions tirees de la pratique sur les playes d'armes a feu". In 1795, the picture of traumatic shock was described in detail by D. J. Latta.

N.I. Pirogov, A.S. Tauber and others described the clinical picture of shock in detail and began to study the reasons causing it. N.I. Pirogov, V.V. Pashutin, K. Bernard and others attached importance to the development of shock, along with strong pain irritation, contributing to its development, to other factors, for example, blood loss, cooling, starvation, which reduce the body's resistance to injury. In the 19th century, theories of the pathogenesis of shock were put forward, the authors of which tried to explain the occurrence of shock by disorders of the functions of the sympathetic nervous system, cardiovascular system, etc.

An important stage in the development of the problem of shock was the study of its pathogenesis in the experiment. These studies have provided a lot of factual material. Shock is characterized by impaired blood circulation, respiration and metabolism, changes in blood biochemistry and morphology, etc. Initially, these studies were devoted to the shock that occurs during trauma. However, it soon turned out that trauma is not the only cause of shock. Due to the widespread use in the 20th century of methods of serotherapy of infectious diseases and their seroprophylaxis, and then blood transfusion, we had to face the development of processes that are largely similar to traumatic shock both in terms of the clinical picture and a number of other indicators. These processes, associated with anaphylaxis, hemolysis, toxemia, were later classified as collapse.

The development of the shock problem was intensified during the First World War. At this time, a large role of toxemia in the development of shock was revealed. During the Great Patriotic War, various groups of researchers led by the country's leading surgeons (N.N.Burdenko, P.A.Kupriyanov, M.N.

Since the 60s of the 20th century, research on the problem of shock has been intensively conducted in all developed countries of the world, which is due not only to the great theoretical significance of the problem, but also to its practical importance in connection with the more frequent exposure of a person to various extreme factors, which is due to the rapid development of industry and transport.

Classification

Until now, there is no single generally accepted classification of shock. The clearest is the classification by etiological, or rather, by etiopathogenetic characteristics. The following types of shock are distinguished: 1) shock due to the action of damaging environmental factors (painful exogenous): traumatic shock with mechanical injury, burn shock with thermal injury (see Burns), shock with electrical injury (see); 2) shock as a result of excessive afferent impulses in diseases of internal organs (painful endogenous): cardiogenic shock (see) with myocardial infarction, nephrogenic shock in kidney disease (see), abdominal shock with intestinal obstruction (see), hepatic colic ( see Cholelithiasis) and others; 3) shock caused by humoral factors (close in mechanism to collapse), sometimes called humoral: geotransfusion, or post-transfusion, shock (see Blood transfusion), anaphylactic shock (see), hemolytic, insulin, toxic (bacterial, infectious-toxic ) shock and shock with traumatic toxicosis (see). Some researchers distinguish psychogenic shock, which, apparently, should be attributed to reactive psychoses (see).

When creating classifications of shock, in addition to etiopathogenetic signs, its dynamics and severity should be assessed. The dynamics of shock (its phase development) is determined by the degree of impairment of the most important functions of the body. The most common is the classification of shock by severity (excluding terminal conditions), according to which shock I, II and III degrees are distinguished, or, respectively, mild shock, moderate shock and severe shock.

Etiology

The main factors cause damage, accompanied by intense afferent impulses, including painful impulses (see. Extreme stimulus). These include mechanical agents of considerable strength, high temperature, electric current, etc. These factors lead to the development of shock when they cause severe enough damage. The causes of endogenous pain shock include damage to the tissue elements of internal organs in various diseases, leading to intense afferent impulses. The causes of other types of shock, which are close in mechanism to collapse, are the ingress of toxic or other physiologically active substances into the bloodstream or excessive accumulation of toxic or other physiologically active substances that lower the vascular tone. Concomitant factors affect the likelihood of shock and its course. These include overheating, hypothermia, insufficient nutrition, emotional stress, etc. These factors, as a rule, change the body's reactivity and thereby contribute to the development of shock or, conversely, limit its manifestations. The role of the organism's reactivity in the occurrence of shock is extremely large: damaging factors identical in strength and time of action with the same localization of damage in one individual can cause a slight shock, and in another - a severe, even fatal. Changes in the reactivity of the body under the influence of overheating (see. makes the course of shock heavier. Currently, the problem of traumatic shock due to its widespread occurrence (damage as a result of transport, primarily road, injuries, falls from a height and other types of mechanical damage) is given the greatest attention.

Pathogenesis

Shock as a typical pathological process was formed in the process of evolutionary development. Its individual elements can be observed in various classes of vertebrates, but it is most pronounced in mammals and humans. According to Fine (J. Fine, 1965), there are no fundamental differences in the onset and course of shock in various mammalian species. This is the most important factor determining the possibility of its experimental study. Even N. N. Burdenko emphasized that shock should be considered not as a stage of dying, but as a reaction of an organism capable of living. In higher animals, the main ones are active forms of defense that have developed in the process of evolution and make it possible to avoid the action of unfavorable (damaging) environmental factors (avoidance of danger, struggle). When they fail, a set of reactions arises that are passive defensive in nature, ensuring, up to certain limits, the preservation of the individual's life - shock. The creature shock is the inhibition (see) of most functions, the development of hypothermia (see Cooling the body), reducing energy costs (see Metabolism and energy), that is, the most economical use of the body's remaining reserves.

The most common manifestations of various types of shock are suppression of motor activity, inhibition of specific functions, a decrease in the minute volume of blood, the development of hypoxia (see), the implementation of energy metabolism is predominantly anaerobic. These phenomena, if they are short-lived, ensure the preservation of the functions of vital organs and can contribute to a gradual release of shock, and in the future - recovery. If the dysfunctions deepen, the death of the organism occurs.

Along with these general mechanisms, various types of shock can have their own specific characteristics. So, with extensive crushing of soft tissues, the phenomena of severe toxicosis develop (see Traumatic toxicosis), with burns - the phenomenon of tissue dehydration (see Dehydration), with electrical trauma - intense afferent impulses, practically no blood loss, little expressed direct tissue damage. Currently, thanks to the development of anesthesiology (see), the so-called practically does not occur. operational shock is a type of traumatic shock previously observed during extensive surgical interventions.

During the shock, starting with the works of H. N. Burdenko, it is customary to distinguish between erectile and torpid phases. The erectile phase occurs immediately after extreme exposure and is characterized by generalized excitement of the central nervous system, intensification of metabolism, increased activity of some endocrine glands. This phase is rather short-lived and is rarely observed in; wedge, practice; however, its isolation as a phase in which the rudiments of the phenomena characteristic of the next phase - torpid are formed, is justified by the doctrine of the phasic development of nervous processes, the dominant (see), etc. The torpid phase is characterized by pronounced inhibition of the central nervous system, dysfunction of the cardiovascular system, the development of respiratory failure and hypoxia.

In the development of traumatic shock, the erectile and torpid phases differ more clearly than in other types of shock. However, a clear boundary cannot be drawn between the erectile and torpid phases, that is, circulatory disorders, oxygen deficiency and other phenomena typical of the torpid phase occur already in the erectile phase. Some researchers, for example D.M.Sherman (1972), distinguish the terminal phase of traumatic shock, distinguishing it from other terminal states.

Most researchers consider shock as a single process, however, determining the ratio of pathological and adaptive reactions in the dynamics of the torpid phase, they distinguish a number of periods in it: the period of disintegration of functions, the period of temporary adaptation, and the period of decompensation. V.K.Kulagin (1978) and other researchers, on the basis of the similarity of these periods, gave them somewhat different names - initial, stabilization period, final.

The majority of domestic researchers have come to the conclusion that it is advisable to consider traumatic shock as one of the pathological processes characteristic of a traumatic disease - the totality of all pathological and adaptive reactions that occur during severe mechanical damage to the body from the moment of injury (onset of the disease) to its outcome (complete or incomplete recovery, death). During the course of a traumatic illness, it is also customary to distinguish a number of periods: the period of acute reaction to trauma (lasts one to two days), the period of early manifestations, sometimes called post-shock (lasts up to 14 days), the period of late manifestations (after 14 days), the period of rehabilitation. With a severe course of traumatic illness in each of these periods, a lethal outcome can occur. Traumatic shock refers to one of the pathological processes typical of the period of acute reaction to trauma. Simultaneously with it, acute blood loss can develop (see), traumatic toxicosis, etc. Later periods of traumatic illness are manifested by the development of other pathological processes (severe dysfunctions of the central nervous system, respiratory disorders, etc.).

The main starting points of the pathogenesis of traumatic shock are: intense afferent impulses, blood loss, resorption of decay products of damaged tissues, and subsequently intoxication with products of impaired metabolism. Artificial isolation of one of these factors as the main one at one time gave rise to various kinds of unitary theories of shock (neurogenic, blood plasma loss, toxemic), which were replaced by an integrated approach to assessing its pathogenesis.

The development of traumatic shock in its early stages is due to disturbances in the activity of the nervous and endocrine systems. In case of severe mechanical injury in the damaged area, receptors are irritated, nerve fibers and nerve trunks are excited, the specificity of which in relation to the stimulus, in contrast to the receptors, is not expressed. Injuries with crushing and rupture of large nerve trunks lead to the development of a particularly severe shock. Typical traumatic shock usually occurs with multiple and associated injuries: injuries of the limbs, chest, abdomen, skull (see Polytrauma).

Irritation of the nerve elements that occurs during trauma, the nature of afferent impulses and the propagation of excitation are determined by the strength of the stimulus, the localization of damage, its vastness, and the intensity of the flow of impulses from organs with impaired functions. Irritation of nerve elements is maintained for a long time by compression of nerve fibers, by the action on receptors of toxic products of damaged tissues, impaired metabolism, etc.

The erectile phase of shock is characterized by generalization of excitement, which is manifested by motor restlessness, increased sensitivity to additional stimuli. Excitation extends to the autonomic centers, which leads to the release of catecholamines (see), adaptive hormones (see Adaptation syndrome) into the bloodstream, as a result, the activity of the heart is stimulated. the tone of the small arteries and partly the veins increases, the metabolism increases.

The further development of shock (torpid phase) is due to the fact that prolonged afferent impulses from the site of injury and from organs with impaired functions, as well as changes in the lability (see) of nerve elements lead to the development of foci of inhibition, especially in those formations that are less liable and the flow of impulses to which is the most intense. Foci of inhibition are formed early in the mesencephalic region of the reticular formation, in some structures of the thalamus and spinal cord, which prevents the flow of impulses to the cerebral cortex and helps to limit corticofugal influences. Phase phenomena in the central nervous system are manifested by changes in the functions of other body systems, which, in turn, is reflected in the state of the nervous elements.

Some researchers, for example S.P. Matua (1981), note the suppression of the functions of the limbic structures of the brain (see Limbic system) and the release of activating systems of the brain from their influence, suppression of the function of the visual cortex, which is explained by the preservation of the activity of the reticular formations (see).

With the development of shock, a more rapid decrease in the lability of the reticular formation and the hypothalamus is revealed (see) in comparison with the cerebral cortex, that is, there is a functional blockade of the reticular formation from afferent impulses coming from the damaged area and organs with impaired functions. At the beginning of the development of shock, afferent impulses from the zone of damage increases. Spreading towards the cortical analyzer, nociceptive impulses causes desynchronization phenomena, but soon the processes that limit the conduction of impulses are turned on - hyperpolarization of intercalary neurons (see. Nerve cell) and iresynaptic inhibition.

Afferent impulses propagate along the ascending pathways of the spinal cord and subcortical regions to a greater extent on the side of the injury. There is a certain asymmetry in the content of neurotransmitters (see. Mediators) on the side of damage and contralateral.

After an injury that caused shock, the conduction of impulses in the thalamic, reticular-stem and spinal structures is significantly slowed down. In this case, the conduction function of axons is completely preserved. The inhibition arising in the reticular formation of the brainstem leads to a functional blockade of the cortical regions, ensuring the preservation of their activity. With the deepening of shock, disorders of the functions of the nervous system can be supported by disorders of cerebral blood flow (see. Cerebral circulation) and hypoxia. Despite the well-known autonomy of cerebral circulation, sufficient blood supply to the brain is achieved only with an average blood pressure (at least 40 mm Hg).

Changes in the reflex regulation of functions during the development of traumatic shock are combined with the reaction of the endocrine system, and especially those endocrine glands that are distinguished by the rapidity of the hormonal response. Initially, activation of the hypothalamic-pituitary-adrenal system is detected (increased synthesis of ACTH, increased production of gluco- and mineralocorticoids, release of catecholamines into the blood, etc.), and then a gradual inhibition of the peripheral link of endocrine regulation mechanisms, the development of extra-adrenal glucocorticoid insufficiency (see Glucocorticoid insufficiency) ... The functions of other endocrine glands also change, in particular, the synthesis of antidiuretic hormone increases (see Vasopressin), which is manifested by arterial hypotension, hypovolemia, increased osmotic pressure of the extracellular fluid, as well as renin (see) with kidney hypoxia, which leads to the release of angiotensin. There is an increase in the content of insulin (see) in the blood, however, with severe traumatic shock, insulin deficiency may also occur. In later periods, shock is revealed by interrenal insufficiency due to disorders of blood flow in the adrenal glands.

According to Yu. N. Tsibin (1974), with the development of shock, at first, the content of histamine (see) in the blood decreases, and then the content of histamine (see) in the blood decreases, the content of serotonin increases (see), the proteolytic activity of the blood increases. The content of acetylcholine (see) in the blood decreases with deep shock. In some cases, this is preceded by a sharp increase in its concentration.

Changes in reflex and humoral regulation primarily affect the activity of the circulatory system: in the erectile phase of shock, an increase in blood pressure is observed due to generalized spasm of resistive vessels of the arterial bed, resulting from the activation of the sympathoadrenal system and the release of catecholamines. An increase in the tone of resistive vessels is combined with the activation of arteriovenous anastomoses and the passage of part of the blood into the venous bed, bypassing the capillaries, which leads to an increase in venous pressure, impaired blood outflow from the capillaries and even their retrograde filling.

The restriction of capillary blood flow, combined with the stimulation of metabolic processes, leads already in the erectile phase to the development of hypoxia and oxygen debt (see Muscle work). Retention of blood in the capillaries and postcapillary venules, especially internal organs (its deposition), combined with blood loss, leads to the rapid onset of hypovolemia, the deepening of which is further promoted by the extravasation of fluid. Already in the erectile phase of shock, the exclusion of part of the blood from active circulation is detected. This is the main reason for a decrease in the minute blood volume, or cardiac output, which is facilitated by a slowdown in blood flow, especially in the venous part of the vascular bed, and, therefore, a decrease in venous return.

Changes in the total peripheral vascular resistance, which usually compensate for a decrease in the minute volume of blood, are inadequate in shock, the result of this is arterial hypotension typical for it (see. Arterial hypotension). Disturbances of circulation in severe shock are manifested by an increasing discrepancy between changes in the total peripheral resistance to the minute volume of blood. The most expedient adaptive reaction of blood circulation in case of impaired blood supply to tissues could be the restoration of heart performance, however, this reaction is limited, and in severe shock, adaptation is carried out by increasing the total peripheral resistance.

An increase in total peripheral resistance is determined not by a uniform total increase in the tone of resistive vessels, but by their peculiar dystonia, which finds expression in the centralization of blood circulation - a decrease in blood flow in the skin, muscles, and digestive organs while maintaining it in vital organs (see Blood loss). In accordance with the centralization of blood circulation, microcirculation also changes (see), whose disturbances in shock are characterized by a decrease in the number of functioning capillaries, a delay in blood cells in postcapillary venules, and bypassing of blood flow. This gives reason to believe that an increase in total peripheral resistance is determined not only by an increase in vascular tone, but also by blood retention in capillaries and venules, as well as by a change in its rheological properties. The latter is manifested by the tendency of the formed elements to aggregation, a decrease in the suspension stability of blood, an increase in the adhesive properties of erythrocytes (see Aggregation of erythrocytes), an increase in blood viscosity, especially at low shear stresses (see Viscosity).

The development of hypoxia is closely associated with circulatory disorders in shock, which is a consequence of the onset of oxygen debt already in the erectile phase and the concomitant restriction of oxygen transport as a result of circulatory disorders. In the genesis of hypoxia, a decrease in the oxygen capacity of the blood is also important (see. Blood, respiratory function).

Dyspnea observed during shock can be considered an adaptive response that ensures satisfactory oxygenation of arterial blood. Tissue hypoxia, which develops due to the limitation of oxygen utilization due to a decrease in tissue perfusion with blood, is compensated by additional extraction of oxygen from a unit volume of blood, which is manifested by a decrease in venous blood oxygenation and an increase in arteriovenous oxygen difference. Hypoxia in shock is combined with hypocapnia (see). Subsequently, with mild shock, the accumulation of carbon dioxide is detected, and with severe shock, a decrease in its content.

The oxygen regime of organs during shock varies unevenly and largely corresponds to circulatory disorders. Tissue elements retain the ability to utilize oxygen for a long time, that is, the respiratory enzyme system is not immediately damaged.

Changes in circulation and oxygen balance noticeably affect the course of metabolic processes, which also vary unequally in different organs. Stimulation of carbohydrate catabolism already in the erectile phase of shock leads to a decrease in glycogen stores in tissues and a change in the relationship between the glycolytic and oxidative phases of carbohydrate metabolism (see), resulting in hyperglycemia and hyperlactacidemia. The ratio of lactate-pyruvate in the torpid phase of shock increases, the content of creatine-phosphate and ATP in brain tissue, in muscles and liver decreases; simultaneously in the muscles and liver, the content of lactic acid (lactate) and inorganic phosphate increases. The stores of glycogen in the myocardium also decrease during shock, however, the ability to utilize lactic acid from the blood by it with a sufficient supply of oxygen ensures the functions of the heart for a long time. The potential ability of mitochondria of liver, kidney, and other organ cells to synthesize ATP during shock is preserved.

Disorders of lipid metabolism are closely associated with changes in carbohydrate metabolism (see Fat metabolism), which are detected in the torpid phase in the form of acetonemia and acetonuria. Changes in the utilization of free (non-esterified) fatty acids, their intensive assimilation at the onset of shock and insufficient later is one of the causes of energy deficiency. Reduced reserves of lipoproteins, phospholipids, total cholesterol.

Disorders of protein metabolism (see Nitrogen metabolism) in shock are manifested by an increase in the amount of non-protein nitrogen in the blood due to nitrogen of polypeptides, a decrease in the amount of serum protein due to albumin, and a slight increase in alpha-2-globulins in the blood. As a result of metabolic disorders in the body, acidic products of incomplete metabolism accumulate, which leads to the development of metabolic (metabolic) acidosis, then carbon dioxide accumulates and gas acidosis occurs (see).

Changes in metabolism and disorders of excretory processes cause deviations in the ionic composition of the plasma. For shock, hypokalemia is typical (see), as well as a gradual equalization of the concentration of ions in cells and extracellular fluid.

Changes in the internal environment of the body significantly affect the excitability of nerve elements, the permeability of cell membranes and the vascular wall. The latter, in combination with changes in oncotic and osmotic balance between tissues and blood plasma, as well as with a decrease in intravascular hydrostatic pressure, leads to extravasation of fluid and the development of tissue edema (see Edema).

Circulatory disorders, hypoxia and metabolic changes lead to dysfunctions of most organs. The functions of various organs in shock suffer to varying degrees, which is explained by the originality of circulatory disorders (its centralization) and different degrees of hypoxia. Long-term preservation in shock of a satisfactory blood supply to the brain and heart leads to the maintenance of their functions, which is manifested by the preservation of consciousness and speech with some inferiority.

The contractile function of the myocardium during the development of shock remains substantially intact for a long time; this is due to the fact that the supply of blood to it due to the centralization of blood circulation suffers little. The use of the myocardium as energy resources of lactic and pyruvic acids, which are formed in other organs in excess, provides its contractile ability. In the event of violations of the contractile function of the myocardium, shock phenomena progress rapidly. In the 70s of the 20th century, some researchers discovered in the blood of patients with severe shock a substance that inhibits the contractile function of the myocardium (a factor in myocardial depression), the physiological significance of which remains largely unclear. As for the changes in the bioelectric activity of the heart during shock, along with an increase in heart rate, the emergence of high teeth, a decrease in the ST segment and a deviation of the electrical axis of the heart to the right, is revealed. This can be regarded as a result of central regulation disorders and hyperkalemia.

Currently, much attention is paid to impaired lung function in shock. Previously, it was believed that in shock, circulatory hypoxia occurs, and shortness of breath should be considered as a reaction to hypoxia. In the lungs under conditions of a reduced minute volume of blood, even with severe shock, according to S. A. Seleznev (1973), there is a sufficient saturation of blood with oxygen, close to normal, - up to 95-98% of oxyhemoglobin. Only in the terminal phase of shock can pathological types of Cheyne-Stokes respiration (see Cheyne-Stokes respiration) or Kussmaul (see Kussmaul respiration) appear, but they already indicate a violation of the excitability of the respiratory center.

In traumatic shock, if there are no direct damage to the external respiration system and pathological processes in the respiratory organs, arterial hypoxechmia, which is the main indicator of respiratory failure (see rarely. More often, its development is characteristic of the post-shock period; it is manifested by an increase in the intensity of external respiration with a progressive decrease in it This is due to impaired alveolar ventilation as a result of a decrease in the compliance of lung tissue (edema), the development of atelectasis, changes in ventilation-perfusion relations, shunting blood flow. These phenomena of post-shock respiratory failure are currently defined as "respiratory distress", "congestive atelectasis", " shock lung ", etc. The immediate causes and mechanisms of post-shock respiratory failure have not yet been established. An important role in the development of this complication can be played by inhibition of respiratory regulation centers, hypoperfusion of the lungs with blood, stagnation and the release of physiologically active substances from them, inactivation of a surfactant (see), the consequences of metabolic acidosis, as well as aspiration of acidic gastric contents, secondary infection. An important role in the pathogenesis of post-shock respiratory failure can be played by such phenomena as overloading the body with fluids, colloidal-crystalloid blood imbalance, prolonged artificial ventilation of the lungs, high oxygen content in inhaled mixtures that occur during intensive shock therapy.

Some researchers, for example Lillikhey (R. S. Lillehei, 1962), attached great importance to the pathogenesis of shock, especially its irreversibility, damage to the intestine (see), widespread hemorrhagic necrosis of its mucous membrane. In an experiment on dogs, the features of the reactivity of the intestinal vessels were revealed. In severe mechanical injuries, accompanied by the development of shock, distinct disorders of blood flow in the submucous layer of the intestine are found. The motor function of the gastrointestinal tract during shock is also impaired, but at the same time the absorption of a number of substances, including glucose, salts, water, is preserved.

With the development of shock, liver function is significantly impaired. Immediately after injury, the liver is freed from the deposited glycogen and loses the ability to synthesize it, protein-synthetic and barrier functions of the liver are disrupted. These changes are largely due to disorders of hepatic blood flow: a decrease in the total volume of liver perfusion with blood, shunting of blood flow at the level of the microvasculature, which leads to the development of severe hypoxia, despite the transition of the liver to a predominantly arterial blood supply. The share of arterial blood flow in the blood supply to the liver in the torpid phase of shock is, according to S. A. Seleznev (1971), about 60% (normally 20-25%), however, this does not prevent the development of hypoxia.

In shock, the excretory function of the kidneys is significantly impaired. Oliguria (see) is such a typical symptom of shock that some researchers consider it one of the main criteria in determining its severity. A decrease in urine production in the kidneys during shock is mainly due to a sharp restriction of the filtration of primary urine in the glomeruli and, to a lesser extent, changes in reabsorption. Filtration is impaired due to sharp disturbances of blood flow in the renal cortex. In the torpid phase of shock, the ratio between the blood supply to the cortical and medullary substance of the kidneys becomes approximately 1: 1 (instead of 9: 1 in the norm), which is due to both a decrease in the value of perfusion pressure as a result of arterial hypotension and an increase in the resistance of cortical vessels due to neuroendocrine influences.

When assessing the severity of shock, much attention is paid to the search for criteria for its irreversibility. "The irreversibility of shock" is a conditional concept. Two types of shock irreversibility can be distinguished: due to damage incompatible with life (absolute irreversibility) and due to insufficient effectiveness of modern therapeutic measures (relative irreversibility). At different times, the development of shock irreversibility was associated with dysfunction of one or another organ. So, I.R.Petrov, G.I. Vasadze (1972) attributed the main role in its development to dysfunctions of the central nervous system, although later it turned out that the brain and heart in shock for a long time do not suffer as a result of centralization of blood circulation. V.K.Kulagin (1978) identified the cerebral and somatic type of shock irreversibility: in the first case, irreversibility is due to severe dysfunctions of the brain, in the second - the functions of other organs. If in the development of irreversible phenomena in trauma accompanied by shock, the role of direct damage to organs is not taken into account, it can be assumed that prolonged ischemia leads to really irreversible changes in tissues (see), accompanied by the development of necrosis in those organs that are worse under conditions of centralized circulation supplied with oxygen (centrilobular necrosis of the liver, necrotic changes in the cortex of the kidneys, in the mucous and submucosa of the intestine).

In severe mechanical trauma, up to half of the victims, according to P.N.Petrov (1980), have injuries to the skull and brain of varying degrees. With a combination of traumatic brain injury (see) with extracranial shockogenic injury, accompanied by shock of the first degree, the symptoms of traumatic brain injury are regarded as symptoms of isolated traumatic brain injury. When a traumatic brain injury is combined with an extracranial shock-related injury, accompanied by shock of the II - III degree, the symptoms of brain damage are regarded as typical for a traumatic brain injury that is more severe than the actual one. Thus, damage to the diencephalic structures of the brain is manifested by the occurrence of reactions of a hyperergic nature, which masks the development of traumatic shock, and trauma to the structures of the middle and medulla oblongata is characterized by an aggravation of disorders typical of shock, which is caused by direct damage to the vasomotor center.

The clinical picture of traumatic brain injury against the background of traumatic shock is not clearly manifested, therefore, instrumental research methods, in particular electroencephalography, are of great importance for diagnosis (see). According to EEG data, damage to the diencephalic region of the brain is characterized by polyrhythmia with a predominance of theta waves, increased synchronizing influences from the frontal regions during functional loads, and damage to the structures of the midbrain and medulla oblongata is characterized by gross changes in bioelectric activity of a diffuse nature with high-amplitude delta rhythms.

With a combination of severe craniocerebral trauma with extracranial injuries, the erectile phase of shock is lengthened, and in the torpid phase, circulatory disorders rapidly progress, and the period of temporary adaptation of the torpid phase is significantly shortened.

Injury to the chest organs significantly affects the development of shock (pleuropulmonary shock). They are characterized by pronounced disorders of external respiration (its depth, frequency, volume). In these cases, and especially when a pneumothorax (see) and hemothorax (see) occurs, the relationship between alveolar ventilation and lung perfusion with blood is disrupted, as a result of which other types of circulatory hypoxia characteristic of shock are added, hypercapnia develops (see) ... In case of chest injuries, closed heart damage is possible; at the same time, the minute volume of blood decreases sharply, which aggravates hemodynamic disorders characteristic of shock.

With combined injuries, liver damage is not uncommon (see), as a result of which massive bleeding occurs, aggravating the hypovolemia typical for it with the development of shock and further reducing the minute blood volume. Damage to the pancreas (see) and the development of traumatic pancreatitis (see) also aggravate the course of shock. The reasons for this are the formation of physiologically active substances, disorders in the blood coagulation system (see), resulting from hyperenzymemia. If the intestine is damaged (see), both significant bleeding and blood flow disorders in the abdominal organs, accompanied by venous plethora and turning off part of the blood from active circulation, can occur. This leads to a decrease in the minute blood volume and aggravation of circulatory disorders characteristic of traumatic shock. Similarly, they affect the development of shock during the period of the body's primary reaction to injury, kidney damage (see), usually accompanied by significant hemorrhages in the peritoneal tissue.

The shock arising from electrical injury is quite close to traumatic shock in terms of development mechanisms (see). In those cases when under the action of the current there is no ventricular fibrillation of the heart, the shock is characterized by a pronounced, but short erectile phase followed by a long torpid phase. The starting pathogenetic factor of this type of shock is irritation by the current of receptors and nerve trunks, leading to an initial vasospasm and redistribution of blood flow. As a result, typical circulatory disorders appear - a decrease in the minute volume of blood, arterial hypotension, respiratory disorders and metabolic disorders that join them.

A burn shock that occurs with extensive thermal injuries - burns (see), is close to traumatic in terms of development mechanisms, since the leading role in its pathogenesis belongs to irritation of extensive receptor zones and damage to tissue elements. As a result of a burn injury, massive afferent impulses from the lesion occur, leading to the onset of excitation, and then the development of foci of inhibition into the central nervous system. This, in combination with changes in endocrine regulation, leads to hemodynamic and metabolic disorders characteristic of shock. Of great importance in circulatory and metabolic disorders in burns are tissue dehydration due to disorders of water metabolism, blood thickening and a change in its rheological properties towards an increase in dynamic viscosity, intoxication with decay products of damaged tissues, and renal dysfunction. Due to an increase in blood viscosity and a rather high tone of resistive blood pressure vessels in burn shock; does not decrease for a long time, which noticeably distinguishes it from other types of shock. These factors, typical of a burn disease, essentially determine its wedge, a picture at an early stage, which is characterized by the development of shock.

Cardiogenic shock (see), which occurs with extensive myocardial infarction. characterized by an initial significant decrease in the minute blood volume due to a weakening of the contractile function of the myocardium caused by a trophic disorder. In the development of cardiogenic shock, a well-known role is also played by intense afferent impulses from the damaged area. At the same time, venous return changes disproportionately, which can lead to circulatory disorders in a small circle and, in combination with other factors, to pulmonary edema.

Hemorrhagic shock caused by significant acute blood loss (see), as a separate type of shock, is not distinguished by all researchers. Domestic researchers, for example VB Koziner (1973), often describe not shock, but acute blood loss, considering it as an independent pathological process typical of the early period of traumatic illness. With long-term circulatory disorders as a result of hypovolemia caused by blood loss, tissue hypoxia and metabolic disorders, changes in the vascular tone of the micro-circulatory bed, typical of shock, may occur. This gives reason to regard the late stages of severe blood loss as a type of shock.

Anaphylactic shock (see), which occurs when antigens act on a sensitized organism, differs from other types of shock in that the triggering mechanism in its pathogenesis is the antigen-antibody reaction, as a result of which blood proteases are activated, histamine is released from mast cells, serotonin and others vasoactive substances that cause primary dilatation of resistive vessels, a decrease in total peripheral resistance and, as a consequence, arterial hypotension.

Anaphylactic shock is close to blood transfusion (post-transfusion) shock (see Blood transfusion), the main mechanism of which is the interaction of antigens of foreign erythrocytes incompatible in the A VO system with antibodies of blood serum, accompanied by agglutination of erythrocytes and hemolysis of substances in the release (see. leading to vascular dilatation, the development of circulatory disorders and hypoxia of the same type as in anaphylactic shock. The blockade of microvasculature vessels due to obturation of their lumen with agglutinated erythrocytes, as well as damage and irritation of the epithelium of some parenchymal organs (kidneys, liver) by hemolysis products, may be of some importance.

Close in pathogenesis to this type of shock is septic (toxic-infectious) shock, which is essentially a collapse. It occurs when bacterial toxins act on the body. As a result of dystonia of the vessels of the microcirculatory bed, under the influence of toxic factors, blood flow through the capillaries is disturbed, part of the blood is shunted through arteriovenular anastomoses, the resistance of the vascular bed decreases, arterial hypotension occurs, and tissue hypoxia develops. Toxins also have a direct effect on the assimilation of oxygen by cells of various tissues and on metabolic processes in them.

Similar phenomena are observed in severe exogenous poisoning (exotoxic shock) and endogenous intoxications that occur with extensive necrosis, metabolic disorders, impaired liver antitoxic function, etc. (endotoxic shock).

Experimental shock models

The main experimental shock models include traumatic shock reproduced by the Cannon method (application of a standard mechanical injury to the soft tissues of one or both thighs). A similar mechanism is the shock that occurs when the soft tissues of the thighs of animals are compressed by special vise with devices dosing the degree of compression. For some purposes, in particular for the primary analysis of the effectiveness of anti-shock agents, the shock according to Noble-Collip is reproduced, for which small animals (rats, mice) are placed in rotating drums with a given rotation speed. Depending on the speed and number of rotations, multiple mechanical trauma of varying severity occurs, accompanied by shock.

To analyze the role of afferent impulses in the pathogenesis of shock, stimulation of large nerve trunks or extensive receptor zones is used by non-damaging tissue with an electric current with specified parameters (strength, pulse repetition rate).

Hemorrhagic shock is reproduced by massive blood loss or blood loss up to a certain blood pressure value, followed by its maintenance by fractional bloodletting or reinfusion of released blood. For this purpose, sometimes special devices are used, which make it possible to automatically maintain a given value of blood pressure for a certain time. This shock model makes it possible to study the significance of circulatory disorders, the patterns of metabolic disorders in the pathogenesis of shock.

To identify the role of humoral factors in the development of shock, processes characterized by deep circulatory disorders are reproduced by introducing large doses of peptone, endotoxins, etc.

Pathological anatomy. The main pathological signs of shock are considered to be the liquid state of blood in the vessels of the corpse, disseminated intravascular coagulation (DIC) with hemorrhagic syndrome, blood deposition in the vessels of the microvasculature, shunting of blood flow, rapid mobilization of glycogen from tissue depots, and circulatory-hypoxic damage to organs.

The phenomenon of the liquid state of cadaveric blood due to postmortem fibrinolysis (see) is a sign of sudden death of any etiology. It is generally accepted that the liquid state of cadaveric blood in Sh. Is a consequence of consumption coagulopathy, that is, the use of all blood coagulation factors (see Blood coagulation system) in the process of DIC in the microvasculature. However, the detection of an insignificant number of microthrombi during dissection, especially in certain types of shock, suggests that fibrinolysis is observed in shock due to an extravaginal increase in the activity of the anticoagulant system. Therefore, the wedge, the phase of hyperfibrinogenemia may not be realized in microthrombosis, that is, in the internal combustion engine. This does not exclude the possibility that some of the microthrombi can be lysed during the patient's life and even posthumously. Currently, there are numerous data on internal combustion engines with various types of shock. This syndrome is indeed much more common in diseases complicated by shock. However, its magnitude and prevalence are not the same for different types of shock. More often it is found in bacterial shock, less often in cardiogenic shock.

Deposition of blood in the microvasculature is easily detected macroscopically by uneven blood filling of internal organs and signs of hypovolemia: an "empty" heart, a small amount of blood in large venous vessels, which corresponds to one of the leading clinical signs of shock - insufficient blood flow to the heart and low cardiac output. It is much more difficult to determine clinically and even at necropsy of selective blood deposition in a particular system, for example, portal. In shock, the weight of the liver and spleen never increases significantly, therefore, it is impossible to explain the loss of 2-3 liters of blood from the systemic circulation by depositing it in these organs. It also fails, as a rule, to detect the deposition of blood in any organ using microscopic examination.

Blood flow bypass surgery is an important symptom of shock, especially in the kidneys, liver and lungs. It is difficult to establish the shunting of blood flow in the internal organs during postmortem examination. Only in the kidneys with shock is the pallor of the cortex revealed with a sharp plethora of the juxtamedullary zone and pyramids. However, this macroscopic picture is not typical for all types of shock. It is possible that the signs of pulmonary blood flow shunting are numerous microatelectases and interstitial edema found in pulmonary shock.

Shock is characterized by rapid mobilization of the body's glycogen stores, in particular, the accelerated release of glycogen from the liver. On this basis, A.V. Rusakov (1946) suggested using a high-quality biochemical test for glycogen for the pathological diagnosis of shock. In subsequent years, methods for the quantitative determination of glycogen in liver tissue were used for these purposes. It turned out that the appearance of light (shock) hepatocytes, described by N.A.Kraevsky, is due to the rapid disappearance of glycogen from the cytoplasm with subsequent fatty degeneration of the cell. In the crust, it has been established that with the help of a biochemical study of cadaveric blood, it is possible to detect disorders of lipid and protein metabolism inherent in severe shock, manifested by acetonemia and azotemia.

Describing circulatory disorders in shock, pathologists use the concepts of "hyperemia", "sludge", "stasis", "thrombosis". With hyperemia (see), the enlarged lumen of the vessel is filled with erythrocytes freely located among the plasma, the walls of the vessels are not changed and retain the ability to diapedesis. Sludge - gluing erythrocytes into aggregates; in this case, between the dense aggregate of erythrocytes and the vessel wall, there remains a gap filled with plasma and freely located blood cells. When the lumen of the vessel is completely filled, it is almost impossible to distinguish sludge from stasis. Electron-microscopically, sludge is characterized by dense adhesion of erythrocytes, however, with the preservation of the membranes and boundaries between them. In a scanning microscope, a kind of bridge contacts can be found between individual erythrocytes. Stasis is an arrest of blood flow, in which the dilated lumen of the vessel is filled with deformed erythrocytes, there is little plasma, there is no diaedesis, and the endothelium is swollen. With prolonged stasis, as a rule, partial hemolysis of erythrocytes is observed. Due to the release of plasma coagulation factors into the interstitial tissue, thrombi are not formed, however, the loss of individual fibrin fibers is possible.

Traumatic shock is characterized by massive injuries of internal organs, skeleton, soft tissues, often in various combinations (see Polytrauma), liquid state of blood in vessels, moderate manifestations of DIC, lack of any selectivity in dystrophic changes in internal organs, general circulatory hypoxia, interstitial edema of parenchymal organs, etc. Severe shock-induced trauma, as a rule, is combined with more or less massive blood loss.

For hemorrhagic shock or a combination of traumatic shock with blood loss, an uneven plethora of internal organs is also characteristic - plethora of some organs, such as the lungs and liver, and anemia of others, such as the kidneys. At the same time, in the kidneys, there is a pallor of the cortical substance and a sharp hyperemia of the juxtamedullary zone and the medulla - shock kidney (see Renal failure). In uncompensated hemorrhagic shock, in cases where transfusion therapy was not performed for any reason, signs of hypovolemia are noted at autopsy.

Bacterial (endotoxic) shock is characterized by widespread disseminated intravascular coagulation with a predominant lesion of arterioles and capillaries of vital organs, and for some of its variants - predominant lesion of the gastrointestinal tract and lungs. Thrombosis of microvessels of the kidneys, adrenal glands and adenohypophysis, as a rule, manifests itself macroscopically in the form of foci of necrosis (see), which creates a specific picture of bacterial shock.

With anaphylactic shock (see), the lungs are mainly affected. They show interstitial and alveolar edema, as well as widespread hemorrhages in the parenchyma. Also known asphyxia variant of acute anaphylactic shock, manifested by a sharp edema of the mucous membrane of the larynx with stenosis of the airways and the morphological picture of asphyxia (see).

Burn shock is characterized by the presence of deep and widespread skin burns, thickening of the blood, manifestations of DIC, mainly in the microvessels of the gastrointestinal tract, pancreas and gallbladder.

Pathomorphological manifestations of cardiogenic shock are the most scarce and are detected, as a rule, in the torpid phase, with irreversible shock proceeding as hypovolemic. An autopsy reveals a uniform capillary and venous congestion, in other cases - signs of sudden death (see Sudden death): venous congestion of internal organs, liquid blood overflow of large venous trunks, pinpoint and spotted hemorrhages under the serous membranes, pulmonary edema.

With heterotransfusion (hemolytic) shock, kidney damage is noted with the development of acute renal failure (see).

Shock is a clinical and anatomical concept, therefore, its pathological diagnosis should not be based only on the results of a morphological study, and even more so on the basis of any one sign, for example, a shock lung (see Lungs, pathological anatomy). Only in rare cases of latent or clinically reduced surgical shock under anesthesia, for example, with latent transfusional conflict, can the diagnosis be made on the basis of morphological signs of hemoglobinuric nephrosis (see Kidney, pathological anatomy) and acute renal failure.

The pathological picture of shock can be significantly changed as a result of intensive care. However, the resulting diagnostic difficulties should not be exaggerated. Shock is most often the phase of the underlying disease. Therefore, if death occurs from shock, that is, in the most acute period of the disease, then the autopsy reveals almost all signs of hemodynamic disorder. In irreversible forms of hemorrhagic shock, despite massive blood transfusions, microscopic signs of blood bypass in the kidneys remain. In those cases when death occurs on the 3-4th day or later, after the elimination of the shock state, then its cause, obviously, is not the shock itself, but its consequences, which are superimposed on the complications of the underlying disease and inadequate therapy. In such a situation, an attempt to detect pathological changes characteristic of shock is usually unsuccessful.

Currently, the concept of "shock organ" has been established in the medical literature. Basically, it involves shock lung and shock kidney. Initially, this concept was based on some morphological (clinical and anatomical) features or selectivity of organ damage in shock of a certain etiology, as well as on the primary organ damage that caused the shock. Many researchers, not taking into account the morphological specifics of shock, use the concept of "shock organ" for any organ damage, accompanied by its acute and sometimes irreversible functional failure, including shock genesis. Thus, the term "shock organ" has practically acquired an independent meaning, not always equivalent to the concept of "shock".

Some researchers use the term "shock cell", implying structural and biochemical disorders of the cell during shock. The essence of these changes in crust, time is well known: rapid utilization of glycogen, a decrease in the activity of enzymes of the Krebs cycle (see. Tricarboxylic acid cycle) with simultaneous activation of enzymes of the cycle of anaerobic glycolysis, dystrophic-necrotic changes. However, it should be borne in mind that as one approaches the subcellular and molecular level, the specificity of shock, and, consequently, the diagnostic value of the detected changes is increasingly lost.

Clinical presentation, diagnosis and complications

The clinical picture of shock is determined by its phase and degree of development. The erectile phase, which occurs immediately after the injury, is characterized by speech and motor excitement while maintaining consciousness, lack of a critical attitude to one's condition and to the environment, increased heart rate and respiration, and increased blood pressure. In patients with severe mechanical injuries accompanied by Sh., Upon admission to the hospital, a developed torpid phase of shock is usually observed. The classical description of this phase belongs to NI Pirogov: “With a torn off leg or arm, such a numb person lies motionless on the dressing station; he does not shout, does not yell, does not complain, does not take part in anything and does not demand anything; his body is cold, his face is pale as that of a corpse; the gaze is motionless and directed into the distance; pulse - like a thread, barely noticeable under the finger and with frequent dashes. The numb one either does not answer at all, or only in a barely audible whisper to himself; breathing is also barely perceptible. The wound and skin are almost not sensitive at all; but if the diseased nerve hanging from the wound is irritated by something, then the patient with one slight contraction of his personal muscles reveals a sign of feelings. Sometimes this condition disappears after a few hours from the use of stimulants; sometimes it continues unchanged until his death ... The stiff one has not completely lost consciousness, he is not at all unaware of his suffering, he seemed to be completely immersed in it, as if he had calmed down and was numb in it. "

Diagnosis of shock at the prehospital stage is reduced to an approximate assessment of the nature and severity of injuries, the general condition of the patient and the degree of dysfunctions of the most important body systems in terms of blood pressure, pulse rate, nature and frequency of respiration, pupil response, etc. its severity in relation to the torpid phase. Currently, the most accepted is the three-degree classification (excluding terminal states) of Kit, which is based on one sign - the value of systolic blood pressure. According to this classification, grade I shock (mild) is distinguished, when the general condition of the victim does not inspire fear for his life. Consciousness is preserved, but the patient has little contact. The skin and mucous membranes are pale. The body temperature is slightly lowered. Pupils react to light. The pulse is rhythmic, somewhat quickened. Systolic blood pressure 100-90 mm Hg. Art., diastolic - about 60 mm Hg. Art. Breathing is quickened. Reflexes are weakened.

With shock of the II degree (moderate severity), consciousness is preserved, but clouded. The skin is cold, the face is pale, the gaze is motionless, the pupils react poorly to light. The pulse is fast, weak filling. Systolic blood pressure 85 - 75 mm Hg. Art., diastolic - about 50 mm Hg. Art. Breathing quickened, weakened. Reflexes are inhibited.

With shock of the III degree (severe), the consciousness is confused. The skin is pale or bluish, covered with clammy sweat. Pupils do not respond to light. The pulse is fast and threadlike. Systolic blood pressure 70 mm Hg. Art. and below, diastolic - about 30 mm Hg. Art. Breathing is weakened or intermittent.

The unreliability of one criterion for assessing the severity of shock prompted researchers to look for other parameters. The Allgever principle turned out to be quite successful - determining the severity of shock in relation to the ratio of the pulse rate to the value of systolic blood pressure. Normally, it is 0.5-0.6, with grade I shock - about 0.8, with grade II shock - 0.9 - 1.2, with grade III shock - 1.3 and higher.

In the late 60s and 70s of the 20th century, there was a tendency to search for methods of parametric multifactorial assessment of the severity of shock and predicting its course and outcomes. In the USSR, a number of formulas and nomograms have been developed for assessing the severity of injuries and predicting the duration and outcome of shock with optimal treatment.

As additional criteria for the severity of shock and for assessing the disruption of the body's vital functions, criteria that reflect the state of function of the most affected systems, primarily the blood circulation, can be used. It is important to determine the volume of circulating blood (see. Blood circulation), which can be carried out by the isotopic method with a separate assessment of the globular volume and the volume of circulating plasma. Other methods for determining the volume of circulating blood (by hematocrit and other indicators) give unreliable results due to the impossibility of establishing the time elapsed after blood loss, and due to changes in indicators under the influence of rapidly initiated infusion therapy. Determination of the minute volume of blood (see. Blood circulation) in victims allows us to identify different types of circulatory disorders: hyperperfusion, when the minute volume of blood exceeds normal values ​​(about 5 l / min), and gioperfusion. These types, apparently, depend not only on circulatory disorders, but also on the nature of the ratio of transfusion and vasoactive therapy. An important indicator is the value of the central venous pressure (see. Blood pressure). Its increase over 15-20 cm of water. Art. indicates redundancy of transfusions or the development of heart weakness.

In connection with the assessment of circulatory disorders, the diagnosis of bleeding is important (see). Failure of transfusion therapy should be suggestive of ongoing bleeding. The diagnosis of bleeding into the pleural cavity with chest injuries is established on the basis of physical examination, radiography, or by puncture of the pleural cavity. If you suspect bleeding into the abdominal cavity, they resort to a puncture of the abdomen and the introduction of a "groping" catheter (see. Laparocentesis). The presence of blood in the abdominal cavity is an indication for emergency laparotomy (see).

Respiratory failure of the body is closely associated with circulatory disorders in shock. Indicators of impaired ventilation-perfusion relations are a decrease in oxygen tension in arterial blood below 70 mm Hg. Art. or saturation of hemoglobin with oxygen is less than 80% and an increase in carbon dioxide tension in arterial blood over 50-60 mm Hg. Art .; reducing it to 32-28 mm Hg. Art. serves as a sign of hyperventilation (see Respiratory Failure). Hypocapnia can lead to cardiac arrhythmias due to disturbances in the ratio of extracellular and intracellular potassium, the development of cerebral hypoxia due to vasospasm (see Hypoxia), and deepening of arterial hypotension. Particular attention should be paid to the diagnosis of respiratory disorders in chest injuries (multiple rib fractures, development of pneumothorax, primarily valvular).

Of great importance in the diagnosis of shock is the assessment of renal function, which can be significantly impaired as a result of filtration disorders in the glomerular apparatus due to arterial hypotension. Decrease in blood pressure to 70-60 mm Hg. Art. and less leads to cessation of filtration. The development of renal failure can be suspected in those cases when, when the value of systemic blood pressure is restored, a proportional increase in diuresis is not observed (see). An increase in the amount of non-protein nitrogen in the blood, a decrease in the specific gravity of urine is also a confirmation of renal dysfunction. To control diuresis in victims in a state of shock, an hourly measurement of the amount of urine is carried out. The critical level of urine output is 50 ml per hour.

When assessing the severity of the course of shock, the degree of metabolic disorders that arise immediately after injury due to circulatory disorders, changes in the oxygen regime, and disorders of neuroendocrine regulation are determined. Disorders of carbohydrate metabolism, manifested by excessive formation of lactate, play an especially important role. The lactate content in the blood can reach 24.3-30.6 mg% (2.7-3.4 mmol / l), normally 9-16 mg% (0.99-1.77 mmol / l). Some researchers, for example Weil, Shubin (MN Weil, N. Shubin, 1971), believe that it is not necessary to determine the value of the lactate / pyruvate ratio if the saturation of arterial blood with oxygen is stable enough. Since shock is manifested by an increase in catabolic processes, including protein catabolism, it may be important to determine the creatine-creatinine index in shock: creatine -f- creatinine -1-. According to creatinine Yu, N. Tsibin and GD Shushkov (1974), with mild shock, it reaches 1.5, and with severe shock - 2.0 and higher (normal - 1.0).

Due to the limitation of heat production, the introduction of a large number of solutions, the temperature of the mixed venous blood in the victims is reduced to 31-30 °. Its determination, for example, with the help of a thermoprobe inserted into the venous bed or in another way, can have diagnostic and prognostic value.

A number of researchers recommend using various tests to assess the severity of shock and determine the functional state of vital systems. Thus, the absence of a pressor reaction to intra-arterial blood injection or to intravenous administration of a norepinephrine solution can be considered as evidence of irreversible changes in the circulatory system.

The severity of shock can vary significantly depending on the reactivity of the body (see). So, alcoholic intoxication, leading to a change in the functions of the central nervous system, can mask the course of shock and even contribute to the removal of shock victims in severe injuries, however, in the post-shock period of traumatic illness, these victims die much more often from various complications.

The course of shock depends significantly on the age of the victim. So, in newborns, even minor injuries can lead to the development of severe shock. A higher metabolic rate in children, imperfect adaptive responses lead to a more rapid development of oxygen debt. The shock becomes more severe in a short time. Hemodynamic disorders in children with shock are more difficult to eliminate, blood pressure may remain unstable for a long time. Children easily develop hypocapnia and metabolic acidosis.

In elderly and senile people, shock is also severe, especially if it is combined with massive blood loss. Often, due to hypertension, arterial hypotension characteristic of shock is not detected in them. In the elderly, renal excretory function is significantly impaired - anuria occurs more often. The functions of other organs are also impaired.

The course of shock is undoubtedly influenced by the conditions in which the injury was received. Shock during natural disasters (see) can be more severe.

After removing from shock - in the post-shock period - pathological processes may develop, the frequency and nature of which depend on the severity of the shock suffered (they occur 2 times more often after a severe shock than after a light shock). The most frequent complications of the post-shock period are various kinds of inflammatory processes: pneumonia (see), peritonitis (see), wound suppuration (see Wounds, injuries), etc.; many of them are caused by opportunistic flora. One of the factors predisposing to the development of infectious complications in the post-shock period is transient immunosuppression (see Immunosuppressive states): inhibition of the system of mononuclear phagocytes (see) and polymorphonuclear leukocytes (the development of complications is preceded by a weakening of the chemotaxis of these leukocytes, a decrease in the content of cationic protein in their lysosomes). The degree of suppression of the immune response depends on the severity of the injury.

From complications in the post-shock period, according to M.P. Gvozdev et al. (1979), 2-5% of victims who have suffered a slight shock and over 40% who have suffered a severe shock die.

Treatment and prognosis

Shock therapy begins with assistance at the scene, usually by ambulance teams (see Ambulance). In order to achieve maximum continuity in providing assistance to victims at the prehospital and hospital stages, in 1958 in Leningrad, and then in other large cities of the USSR, specialized resuscitation (anti-shock) teams were created, providing the required amount of medical care at a high professional level. Further anti-shock care is carried out in a specialized intensive care unit (see).

The main tasks of providing medical care at the prehospital stage are: prevention of the development of shock in severe injuries; elimination of the phenomena that threaten the life of the victim with already developed shock; fast and safe transportation of the victim to the hospital.

The therapeutic measures carried out at the prehospital stage include: 1) anesthesia of fracture sites by introducing novocaine (see. Local anesthesia) and immobilization with transport tires (see. Splinting]); 2) the introduction of analgesics, and in severe shock - anesthesia (see) nitrous oxide or retylanum; 3) in severe condition, intravenous infusion of 250-1000 ml of plasma-substituting solutions, the introduction of cardiovascular (cordiamine, korglucon) and antihistamines; 4) the introduction of glucocorticoids in large doses; 5) carrying out oxygen therapy. If necessary, make a temporary stop of external bleeding (see), restore the patency of the upper airways, carry out intubation (see) or tracheostomy (see), apply aseptic dressings on wounds and occlusive dressings with open pneumothorax. With asystole, an external heart massage is performed (see) or electrical defibrillation (see) in combination with artificial ventilation (see Artificial respiration). After completing these urgent measures to ensure the possibility of transporting the victim, he is taken to a specialized hospital. On the way, he continues to provide the necessary assistance.

Prevention of shock at the scene and during transportation of the victim consists in preventing the occurrence of additional damage and limiting afferent impulses. For this purpose, the victim, who has received a serious injury, is placed on a special shield (re-placement should be excluded), the damaged parts of the body are immobilized (see Immobilization), proper anesthesia is carried out, as well as other anti-shock measures before the onset of shock symptoms.

In the hospital, the provision of assistance to victims provides for the fastest possible assessment of the severity of his condition, for example, based on the results of determining the most informative indicators of blood circulation and respiration, as well as reflexes. In case of shock of the 1st degree, the main thing is to prevent its deepening. To do this, the victim is provided with maximum rest, blockade of the pathways for conducting afferent impulses (see Novocaine blockade), set the proper oxygen regime, eliminate hypovolemia by introducing 200-500 ml of plasma-substituting solutions (until the blood pressure is normalized). At the same time, glucocorticoid hormones are administered, as well as cardiotropic drugs and vitamins.

An important anti-shock measure is an urgent surgical intervention carried out for health reasons (ongoing internal bleeding, severe breathing disorders that do not respond to conservative therapy, intracranial hematomas, ruptures of internal organs, etc.). It is advisable to refrain from operations that are not related to vital indications until the victim is removed from shock (for example, surgery on a blood vessel should be postponed if a reliable temporary stop of bleeding is possible). The exception is short-term and less traumatic interventions, for example, incisions for anaerobic infection, removal of the non-viable part of the limb held on to soft tissue flaps (the so-called transport amputation).

Treatment for shock of II and III degrees is aimed at restoring the functions of the nervous system, eliminating circulatory and respiratory disorders, correcting metabolic disorders, ionic balance and acid-base balance. Activities usually begin with the introduction of crystalloid solutions and, as quickly as possible, massive infusions of blood and blood-substituting fluids into one or more veins (see Infusion therapy, Blood transfusion). If at the same time blood pressure does not rise above 70 mm Hg. Art., the pumping of blood into the artery is shown. In case of shock of the first degree, the total volume of infusions is 1000 - 1500 ml (liquids), in shock of the second degree - 2000-2500 ml (of which up to 30% of blood), and in shock of the third degree - 3500-5000 ml (of which up to 35% blood). Transfusion-infusion therapy, depending on the degree of shock, is carried out with different intensities. So, for the first 3 hours with shock of I degree, 200 ml of liquids are injected in 1 hour, then more slowly; with shock of the II degree - 350 ml in 1 hour; in case of shock of the III degree - 500-GOO ml per 1 hour.

For transfusion, single-group donor blood, erythrocyte mass, dry plasma, albumin are used, sometimes reinfusion of previously filtered blood that has poured into the pleural or abdominal cavity (with internal bleeding) is possible. It is useful to supplement infusion therapy with the administration of isogenic blood serum. When using colloidal plasma-substituting solutions (polyglyukin, reopolyglyukin, etc.), their amount, according to Yu.N. Tsibin et al. (1977), should not exceed V4 of the total volume of infusions, the rest falls on crystalloids. To improve the rheological properties of blood, it is advisable to use hemodilution (see), while the hematocrit number should not be less than 30%. Transfusions and infusions are carried out under the control of hemodynamic parameters and, first of all, the values ​​of blood pressure and central venous pressure (an increase in central venous pressure over 15 cm of water column indicates redundancy of infusions).

When recovering from severe shock, vasoactive drugs are used. However, the use of drugs such as norepinephrine and mezatone should be considered as a last resort to prevent life-threatening circulatory disorders. Currently, vasodilators (alpha-blockers or beta-stimulants) are more commonly used in shock therapy to expand resistive vessels; arterial hypotension is controlled by an increase in the minute blood volume due to additional transfusions.

The elimination of respiratory failure involves, first of all, the restoration of the patency of the upper respiratory tract, inhalation of an air-oxygen mixture with a sufficient ventilation volume (6-8 l / min). With a sharp depression of respiration, accompanied by a decrease in its minute volume, as well as in the presence of obstacles in the lower parts of the upper respiratory tract, intubation and transfer of the victim to artificial respiration in conditions of muscle relaxation is necessary (see. Muscle relaxants). Long-term artificial respiration is carried out with volumetric respirators in the mode of moderate hyperventilation. To reduce the volume of dead space, prevent possible aspiration of mucus from the oral cavity or stomach contents, limit the influence of reflexes from the upper respiratory tract during artificial respiration, intubation is used, and for special indications, tracheostomy. Artificial respiration is carried out with an oxygen-air mixture (2: 3) under the control of oxygen and carbon dioxide tension in the blood.

An essential point of anti-shock therapy is the correction of the functions of the nervous system and anesthesia, which is carried out by the use of drugs of local and resorptive action. Local anesthesia is achieved by immobilization and novocaine blockades. In a hospital, transport immobilization is replaced with a permanent one only after determining the severity of the shock, preventing its deepening and conducting effective anesthesia. To ensure constant immobilization, extrafocal osteosynthesis is used (see), carried out with the help of special devices (see. Distraction-compression devices). For anesthesia, novocaine blockade, promedol (intravenously 0.5-1 ml of a 2% solution), fentanyl, nitrous oxide mixed with oxygen in a 1: 1 or 2: 1 ratio are usually used. In case of mild shock or after recovery from severe shock, sodium oxybutyrate and viadryl are injected intravenously for anesthesia (in severe forms of shock or in diagnostically unclear cases, the use of these drugs can be dangerous due to the duration of their action). In addition, neuroleptanalgesia is used (see). However, the danger of lowering blood pressure with the introduction of, for example, droperidol limits its use.

For emergency pain relief and during surgical interventions in patients with traumatic shock, especially against the background of unreplenished blood loss and arterial hypotension, ketamine (ketalar), a short-acting anesthetic with a pronounced analgesic effect, is widely used. It is administered at a dose of up to 2 mg / kg intravenously, for children - 5-10 mg / kg intramuscularly (in rare cases, the drug causes respiratory depression, but the pharyngeal and laryngeal reflexes, the tone of the striated muscles remain). Since ketamine increases blood pressure, it is used if an urgent operation is necessary against the background of unreplenished blood loss (including to stop bleeding). This property of the drug allows you to start anesthesia, transfer the victim to artificial ventilation of the lungs and then carry out full-fledged infusion therapy. Ketamine is used for both induction and main anesthesia. Ketamine is contraindicated in severe traumatic brain injury, when a significant increase in intracranial and spinal pressure is possible.

To restore the regulatory function of the hypothalamic-pituitary-adrenal system, large doses of corticosteroids are usually prescribed.

In order to correct metabolic disorders, especially energy metabolism, glucose is injected (60-100 ml of a 40% solution, 1 U of insulin is added for every 4 g of glucose). Hormonal (glucocorticoid) therapy also has a positive metabolic effect - it leads to stimulation of the formation of carbohydrates due to gluconeogenesis (see Glycolysis). It is also advisable to prescribe vitamins C and B due to their positive effect on metabolism and regenerative processes.

An important place in shock therapy is occupied by the correction of acid-base balance (see) and ionic balance (see.Water-salt metabolism). The elimination of metabolic acidosis (see) is facilitated by intravenous drip administration of a 3% sodium bicarbonate solution under the control of acid-base equilibrium indicators. Impaired electrolyte metabolism, mainly sodium-potassium balance, is compensated by the administration of a solution of calcium chloride (potassium antagonist) and sodium chloride. Correction of the ionic balance is carried out under the control of the content of potassium, sodium and blood chlorides.

In case of massive damage to soft tissues, detoxification measures are carried out (see.Detoxification therapy), which is achieved by stimulating diuresis, by infusing large amounts of isotonic sodium chloride solution, Ringer-Locke's solution, 5% glucose solution (up to 2-3 liters per day). To stimulate diuresis, mannitol (300 ml of 15% solution) can be used under the control of hourly diuresis and central venous pressure. With changes in these indicators, the development of edema can be suspected; in such cases, furosemide is used, which limits reabsorption in the tubular apparatus of the kidneys and stimulates renal blood flow.

In severe shock, despite the entire complex of the described therapy, cardiac arrest and cessation of breathing (clinical death) may occur, requiring immediate resuscitation (see Resuscitation). Recovery of cardiac activity (in case of cardiac arrest) in shock is a more difficult task than in case of cardiac arrest during operations, with acute blood loss or even acute asphyxia; this is due to the prolonged tension of the adaptive responses during the development of shock and their depletion.

The prognosis for the patient's life depends on the reasons that caused the shock, the severity of the shock, the degree of suppression of the vital functions of the body, the timeliness and effectiveness of the measures taken.

Features of traumatic shock in military field conditions

Traumatic shock in the wounded is characterized by a number of features, which gave reason to some researchers to call it wound, military wound or military traumatic shock.

Emotional and mental overstrain during the conduct of hostilities, lack of sleep and irregular nutrition, prolonged overheating, thirst and dehydration during the hot season, hypothermia and high consumption of energy resources in winter cause extreme stress of all functional systems, especially the apparatus of their regulation and, above all, the central nervous system ... Bleeding and blood loss arising after injury, respiratory disorders or the functions of vital organs further increase the tension of regulatory systems and life support systems, which, against the background of unfavorable effects of a combat situation, leads to a rapid depletion of energy resources and a breakdown in compensation - a torpid phase of traumatic shock develops.

Inadequate or untimely provision of first aid, long, sometimes inconvenient removal from the battlefield, prolonged transportation of the wounded to the advanced stages of medical treatment. evacuations along military roads contribute to the rapid progression and deepening of the arising disorders of hemostasis, a more severe course of traumatic shock.

The frequency and severity of traumatic shock in military field conditions is influenced by numerous factors, among which the timing of removal from the battlefield and the provision of assistance, the nature of combat trauma are important; the quality, content and timing of the provision of first aid; delivery times and conditions for the evacuation of the wounded (see. Medical evacuation) to the stages of medical evacuation (see); working conditions of medical centers, terms and quality of first aid (see) and qualified medical care (see). According to S.I.Banaitis (1948), during the Great Patriotic War in the regimental medical center (see) shock was recorded in 2 - 7% of the wounded, and in the divisional medical center (see Medical and sanitary battalion) - already in 5 -11% wounded.

Significant fluctuations in the frequency of traumatic shock could not be made dependent on the nature of combat pathology, since during the research conducted, the enemy's firearms practically did not change. According to S.I.Banaitis (1948), a lower frequency of traumatic shock was recorded in those areas of the front where the first medical aid was the most complete, and the time for carrying out and delivering the wounded to the stages of medical aid was shorter. The frequency of traumatic shock depended mainly on the magnitude of sanitary losses (see) and the associated terms of delivery of the wounded to the regimental and divisional medical centers. Increase dignity. losses steadily entailed lengthening delivery times. So, according to N.A. Eremin (1943), shock of the I-II degree accounted for 68% of all cases of shock in the wounded, delivered to the divisional first-aid post within 6 hours from the moment of injury, 62.3% - in the wounded, delivered up to 12 hours, and 40.4% - in the wounded, delivered before 24 hours, and, accordingly, the shock of the III degree was 32% in the wounded, delivered before 6 hours, 37.7% - up to 12 hours and 59.6% - in the wounded delivered before 24 hours. That is, the severity of the shock, depending on the delivery time, increased proportionally.

The incidence of shock in wounds of different localization varies significantly, depending on the nature of the injuries and their early complications. When cranial injuries are combined with injuries of other localizations, the frequency and severity of shock depend mainly on the nature of the injuries of extracranial localization. During the Great Patriotic War, shock was noted in 1.9% of cases with injuries of the upper extremities, and in 7.8% of cases with injuries of the lower extremities. Timely stopping of bleeding and immobilization by the simplest techniques contributed to the elimination or weakening of the effect of the main shockogenic factors, therefore, the course of shock in case of wounds of the extremities was more favorable. With penetrating chest wounds, not accompanied by open pneumothorax and hemothorax, shock was observed in 20-25% of the wounded. In chest injuries accompanied by open or valvular pneumothorax, pronounced hemothorax, the frequency of shock reached 50% of cases. This was due not only to the extent of tissue damage and blood loss, but also to a sharp disturbance in breathing due to collapse of the lung on the side of the injury and a more rapid increase in hypoxia. With penetrating wounds of the abdomen (see), traumatic shock was observed in 23.3 - 65% of the wounded. The main shockogenic factors in abdominal injuries are pain and blood loss. In addition, if the hollow organs are damaged, the outpouring of gastric or intestinal contents into the free abdominal cavity causes a sharp irritation of the interoreceptors of the peritoneum, and then intoxication of the body as peritonitis develops (see). As a result, traumatic shock with injuries to the abdomen is especially difficult. With multiple and associated injuries, traumatic shock is characterized by the most severe manifestations and rapid depletion of regulatory systems and life support organs. This is due to the simultaneous damage to several anatomical areas of the body, damage to vital organs, massive blood loss (external and internal bleeding), excessive pain impulses.

With the use of new types of weapons, sanitary losses will be characterized by a significant increase in the proportion of severe injuries and, consequently, an increase in the frequency of traumatic shock. So. according to some researchers, for example Pickkart (K.-N. Pi-ckart, 1979), in modern wars the frequency of shock can reach 20-30% of the total number of wounded. Moreover, it is possible to change the pathogenesis and clinical picture of traumatic shock. This is due to the fact that the impact of pathogenetic factors of traumatic shock characteristic of mechanical trauma (neurogenic, blood loss, respiratory distress, intoxication) can be combined with contusion (see) of internal organs, ionizing radiation (see), burns (see) or with a combination of these lesions (see Combined lesions). Therefore, the clinical manifestations of traumatic shock can vary due to the predominance of symptoms, such as radiation sickness (see) or poisoning (see). In a war with the use of modern weapons, the role of first aid on the battlefield, the removal of the wounded and their timely delivery to medical institutions, full-fledged first medical and qualified assistance will become especially important.

Prevention and treatment of shock on the battlefield and in the regimental medical center include the following measures: early use of analgesics, blockade of the damaged area with anesthetic, reliable transport immobilization, the imposition of a protective primary dressing; combating bleeding and blood loss, which is achieved by temporarily stopping bleeding, infusing plasma-substituting solutions, as quickly as possible evacuating the wounded to the stages of providing qualified medical care; elimination of impaired external respiration (cleansing the oral cavity and nasopharynx from mucus and foreign bodies, eliminating tense valvular pneumothorax, closing open pneumothorax wound with an occlusive dressing, preventing tongue retraction in case of skull injury or mandibular fractures); the use of hormonal drugs that contribute to the elimination of endocrine disorders.

In a medical-sanitary battalion (a separate medical detachment), anti-shock therapy should be carried out in full, ensuring a stable removal of the victim from a state of shock and creating conditions for his possible evacuation to subsequent stages of medical evacuation. Such anti-shock measures include: maintaining active pulmonary ventilation; effective pain relief; the fight against hemodynamic disorders and hypovolemia by stopping bleeding, replenishing the deficit of circulating blood, body fluids and electrolytes, normalizing the water-salt balance; maintaining or restoring blood circulation using direct or indirect heart massage; surgical interventions; fight against cerebral edema and hyperthermia, restoration of urine output.

Infectious toxic shock

Infectious-toxic (toxic-infectious) shock is most often caused by gram-negative bacteria - meningococci (see Meningococcal infection), Salmonella (see Salmonella), Shigella (see), Escherichia coli (see), Yersinia (see, Yersiniosis, Plague ); in about 1/3 of cases, the cause of infectious toxic (exotoxic) shock is gram-positive microbes - staphylococci (see), streptococci (see), pneumococci (see). Currently, infectious-toxic shock, especially in children and persons in old and old age, against the background of chronic inflammatory processes is more often caused by Proteus (see Proteus), Klebsiella (see Klebsiella), Pseudomonas aeruginosa (see), aerobacter, bacteroids (see v. 20, additional materials). It can develop with bacterial, viral, rickettsial (see Epidemic typhus), spirochetous and even fungal diseases. Infectious-toxic shock accounts for more than 1/3 of all cases of shock, yielding in frequency to cardiogenic and hypovolemic shock, but the mortality rate is higher; it usually exceeds 50%.

The decisive role in the pathogenesis of infectious toxic shock is assigned to bacterial toxins (see), mainly endotoxin (endotoxic shock). Endotoxins in clinical practice and on the model of experimental endotoxin shock can directly affect the tone of regional vessels, causing the opening of short arteriovenous shunts and significantly slowing down capillary blood flow, which leads to microcirculation disorders (see). At the same time, they stimulate the release of catecholamines (see), which increase the spasm of arterioles and venules, slow down blood flow and lead to the deposition and sequestration of blood in the capillary network. The progressive, often lightning-fast development of infectious-toxic shock is explained by the immune mechanism of specific hypersensitivity to endotoxin with activation of the complement system (see). Complement activation leads to the accumulation of vasoactive substances that increase vascular permeability and cause lysis of cells, including leukocytes and platelets. Endotoxins increase blood coagulation, acting mainly on the vascular-platelet mechanisms of hemostasis (see. Blood coagulation system). Disseminated intravascular blood coagulation is an essential pathophysiological mechanism of infectious toxic shock. An essential role in its progression is played by the activation of the kinin-kallikrein system (see Kinins / as well as a decrease in oxygen consumption by cells under the influence of bacterial toxins. In the future, with an increasing deficit of blood volume and heart failure, a hypodynamic phase sets in. With a continuing violation of microcirculation, a decrease in venous blood return and cardiac output, blood pressure falls, hypoxia, acidosis increase, irreversible changes in metabolism, cell and tissue death are observed.

The clinical picture of infectious toxic shock is characterized by a combination of symptoms of acute vascular insufficiency and generalized infectious process. In infectious diseases (see), infectious-toxic shock most often develops in 1-2 days of the disease. Its early and constant signs are pronounced chills, an increase in body temperature up to 40 °. In cases of later development, it is preceded by a hectic or remitting type of temperature reaction (see. Fever), repeated chills, profuse sweating. At the same time, headache intensifies, confusion, vomiting, convulsions, hyperesthesia, and motor excitement appear. With a pronounced hyperdynamic phase (compensated shock), the limbs of patients remain warm, there is hyperemia of the face and upper half of the body, breathing becomes more frequent, tachycardia up to 110-120 beats per minute is combined with good filling of the pulse and a slight change in blood pressure. With the progression of an infectious-toxic shock and its transition to a subcompensated degree, there is a darkening of consciousness up to the development of a coma (see Coma), pallor of the skin, acrocyanosis, marble color of the skin. Chills and hyperemia are replaced by a decrease in body temperature, often with a critical drop to subnormal numbers, the hands and feet become pale cyanotic, cold, moist. The pulse reaches 160 beats per minute, becomes weak, arrhythmic, blood pressure drops rapidly, hemorrhages often appear on the skin and mucous membranes, gastric bleeding is possible (decompensated shock). With infectious toxic shock, the lungs and kidneys are most affected. With a "shock" lung, acute respiratory failure, shunting in the pulmonary circulation are noted, with an X-ray examination - decreased transparency of the lung tissue and the presence of mosaic shadows. The picture of the "shock" kidney is characterized by progressive acute renal failure (see).

The characteristic features of infectious-toxic shock in children are a high severity of general intoxication, lesions of the central nervous system, dyspeptic disorders (repeated vomiting, diarrhea, increased intestinal motility, the appearance of pain in the upper abdomen), the presence of a hemorrhagic rash.

Infectious-toxic shock caused by gram-negative bacteria is more severe and gives a higher mortality rate than infectious-toxic shock caused by gram-positive bacteria, in which adequate vascular perfusion is maintained for a longer time.

Diagnosis of infectious toxic shock is based on characteristic clinical and laboratory changes. In children and elderly and senile people with a severe course of generalized infectious processes, diagnosis causes significant difficulties.

In laboratory studies in patients with infectious toxic shock, hypoxemia, metabolic acidosis, an increase in the concentration of lactate in the blood, azotemia (see), hyponatremia (see), hypoalbuminemia, signs of disseminated intravascular coagulation (see Hemorrhagic diathesis) are determined.

Treatment should be comprehensive and aimed at both etiological and pathogenetic factors. In order to restore hemodynamics, treatment should begin with intravenous administration of crystalloid and colloidal solutions (preference is given to rheopolyglucin and hemodez). Intravenous infusion of 5% albumin solution is shown, which improves the rheological properties of blood and helps to restore capillary permeability. Of crystalloid drugs, preference is given to polyionic solutions, which must be infused with extreme caution under the control of central venous pressure in cerebral edema (see Edema and swelling of the brain), "shock" lung, acute renal failure. Broad-spectrum antibiotics are used. It should be borne in mind that therapy with massive doses of antibiotics can contribute to the death of a large number of bacteria, which is accompanied by an increase in the amount of endotoxin circulating in the blood and the progression of infectious-toxic shock. Shows the appointment of corticosteroids in a daily dose of up to 30 mg / kg (in terms of prednisolone), which have a pharmacodynamic effect. In addition, protease inhibitors (counterkal, gordox, trashgol) are administered. With the ineffectiveness of blood-substituting fluids, patients are given sympathomnmetics (dopamine, isoproterenol). In infectious toxic shock caused by staphylococci, specific immunoglobulin (see) and blood plasma are widely used. Severe respiratory failure against the background of a "shock" lung requires artificial ventilation; with the development of disseminated intravascular coagulation, heparin, frozen blood plasma is used; in acute renal failure - forced diuresis, hemodialysis.

The prognosis is especially unfavorable in case of subcompensated and decompensated shock, in cases when it is caused by gram-negative bacteria, in children of the first year of life, people over 60 years of age with concomitant diseases of the cardiovascular system, kidneys, liver, impaired immune status of the body.

Prevention of infectious-toxic shock consists in early diagnosis and timely intensive care for severe infectious diseases.

See also Anaphylactic shock; Cardiogenic shock; Burns; Blood transfusion, reactions and complications.

Bibliography: Azhibaev KA Physiological and pathophysiological mechanisms of damage to the body by electric current, Frunze, 1978; Alipov G.V. Traumatic shock, Shurn. modern hir., v. 5, v. 5-6, p. 841, v, 7-8, p. 1072, 1930, vol. 6, c. 1-2, p. 17, 1931; Akhunbaev IK and Frenkel GL Essays on shock and collapse, Frunze, 19o7; Banaytis SI Military field surgery, M., 1946; he, Traumatic shock in experiment, clinic and practice of military field surgery, Kaunas, 1948; Barkagan 3. S. Hemorrhagic diseases and syndromes, M., 1980 ;, Bunin K. V. and Sor and neon C, N. Emergency therapy for infectious diseases, D., 1983; Burdenko H., N. Collected works, t. 3, M., 1951; Weil MG and Shubin G. Diagnostics and treatment of shock, the lane with from English, M., 1971; Vishnevsky AA and Shreiber MI Military field surgery, M., 1975; Davydovsky I.V. 7, M., 1954; Zeropno DD and Lukasevich LL Syndrome of disseminated intravascular coagulation as the main morphological manifestation of shock, Arkh. patol., t. 45, No. 12, p. 13, 1983; Zorkin AA and Nigulyanu V.Y. Pituitary-adrenal system and metabolism in shock, Chisinau, 1977; Kennon V. The problem of shock, trans. from English., M. - L., 1943; Kochetygov N.I. Burn disease. (Essays on pathological physiology), L., 1973; Kulagin VK Pathological physiology of injury and shock, L., 1978; Lemus VB Central regulation of blood circulation in trauma and blood loss, L., 1983; Luzhnikov EA, Dagaev VN and Firsov H. N. Fundamentals of resuscitation in acute poisoning, M., 1977; Lytkin M., etc. Septic shock, L., 1980; Nasonkin OS and Pashkovsky EV Neurophysiology of shock, L., 1984; Emergency surgical care for injuries, ed. B. D. Komarova, M., 1984; General human pathology, ed. A.I. Strukov and others, p. 246, M., 1982; The experience of Soviet medicine in the Great Patriotic War 1941-1945, v. 3, p. 342, 391, M., 1953; Fundamentals of resuscitation, ed. By V. A. Negovsky, Tashkent, 1977; Parenteral nutrition for severe injuries, ed. R. M. Glantsa, M., 1985; Pathological physiology of extreme states, ed. PD Gorizontov and H. N. Sirotinina, M., 1973; Permyakov NK Fundamentals of resuscitation pathology, M., 1979; he, Nodal questions of general pathology and pathological anatomy of shock, Arkh. patol., t. 45, No. 12, p. 3, 1983; Petrov IR and Vasadze G. Sh. Irreversible changes in shock and blood loss, L., 1972; Pokrovsky V.I., Favorova L. A. and Kostyukova H. N. Meningococcal infection, M. , 1976; Rabi K. Localized and diffuse intravascular coagulation, trans. from French., M., 1974; Rozhinsky MM, Zhizhin VN and Katkovsky GB Basics of traumatological resuscitation, M., 1979; Seleznev S. A. Liver in the dynamics of traumatic shock, L., 1971; Seleznev S. A. and Khudayberenov G. S. Traumatic illness, Ashgabat, 1984; Seleznev SA, Vashetina SM and Mazurkevich GS Complex assessment of blood circulation in experimental pathology, L., 1976; Smetnev A. S. Cardiogenic shock with myocardial infarction, M., 1971; Traumatic Shock, ed. I.R.Petrova, M., 1962; Traumatic shock, Bibliography of Russian and foreign literature, 1961 -1970, comp. RB Zhigulina, etc., L., 1972; Traumatic shock, Bibliography of domestic and foreign literature, 1971-1975, comp. RB Zhigulina, etc., L., 1978; VP Tumanov and MD Malamud. Changes in the central nervous system during thermal, radiation and combined trauma, Electron-microscopic and hemodynamic research, Chisinau, 1977; Sherman D. M. Problem of traumatic shock, M., 1972; Schuster X. P., Schönborn X. and Lauer H. Shock. (Emergence, Recognition, Control, Treatment), trans. from it., M., 1981; Shuteu Y. et al. Shock, Terminology and classifications, Shock cell, Pathophysiology and treatment, trans. from Romanians., Bucharest, 1981; Shushkov GD Traumatic shock, L., 1967; Hershey S. G. Current theories of shock, Anesthesiology, v. 21, p. 303, 1960, bibliogr .; Schock und hypotone Kreislaufsto-rungen, Pathophysiologie, Diagnostik, The-rapie, hrsg. v. E. F. Gersmeyer u. E. C. Ya-sargil, Stuttgart, 1978; Shoemaker W. C. Shock, chemistry, physiology and therapy, Springfield, 1967.

M. P. Gvozdev, S. A. Seleznev; I.I.Derya bin, Yu.N. Shanin (features of traumatic shock in military field conditions); V. V. Maleev (infectious toxic shock); N. K. Permyakov, M. N. Lanzman (pat.an.).

Shock- this is an acutely emerging critical state of the body with progressive failure of the life support system, caused by acute insufficiency of blood circulation, microcirculation and tissue hypoxia.

In shock, the functions of the cardiovascular system, respiration, kidneys change, the processes of microcirculation and metabolism are disrupted. Shock is a polyetiological disease.

Shock types:

Depending on the cause of the occurrence, the following types of shock are distinguished.

Traumatic shock:

as a result of mechanical injury (wounds, bone fractures, tissue compression, etc.);
as a result of burn injury (thermal and chemical burns);
as a result of exposure to low temperatures - cold shock;
as a result of electrical injury - electrical shock.

Hemorrhagic, or hypovolemic, shock:

bleeding, acute blood loss;
acute water imbalance - dehydration.

Septic (bacterial toxic) shock:

common purulent processes caused by gram-negative or gram-positive microflora.

Cardiogenic shock:

myocardial infarction,
acute heart failure.

Shock reasons:

Despite various reasons and some features of pathogenesis (starting points), the main in the development of shock is vasodilation and, as a result, an increase in the capacity of the vascular bed, hypovolemia - a decrease in the volume of circulating blood (BCC) due to various reasons: blood loss, redistribution of fluid between blood and tissues, or mismatch normal blood volume, increasing vascular capacity as a result of vasodilation.

The resulting discrepancy between the BCC and the capacity of the vascular bed leads to a decrease in the minute blood volume of the heart and a disorder of microcirculation.

The main pathophysiological process caused by microcirculation disorders develops at the cellular level.
Disorders of microcirculation, which unite the system of arterioles - capillaries - venules, lead to serious changes in the body, since it is here that the main function of blood circulation is performed - the exchange of substances between the cell and the blood.

Capillaries are the direct site of this exchange, and capillary blood flow, in turn, depends on the level of blood pressure, arteriole tone and blood viscosity. Slowing down of blood flow in the capillaries leads to the aggregation of formed elements, stagnation of blood in the capillaries, an increase in intracapillary pressure and the transition of plasma from the capillaries to the interstitial fluid.

Blood thickens, which, along with the formation of erythrocyte coin columns, platelet aggregation, leads to an increase in its viscosity and intracapillary coagulation with the formation of microthrombi, and as a result, capillary blood flow completely stops. Violation of microcirculation threatens to disrupt the function of cells and even their death.

A feature of the causes of septic shock is that impaired blood circulation under the influence of bacterial toxins leads to the opening of arteriovenous shunts and the blood bypasses the capillary bed, rushing from the arterioles to the venules. Cell nutrition is disrupted due to a decrease in capillary blood flow and the action of bacterial toxins directly on the cell, and the supply of oxygen to cells decreases.

The cause of anaphylactic shock - under the action of histamine and other biologically active substances, capillaries and veins lose their tone, the peripheral vascular bed expands, its capacity increases, which leads to redistribution of blood - its accumulation (stagnation) in the capillaries and veins, causing disruption of the heart. The existing BCC does not correspond to the capacity of the vascular bed, the cardiac output decreases. Stagnation of blood in the microvasculature causes a metabolic disorder between the cell and blood at the level of the capillary bed.

Disorder of microcirculation, regardless of the mechanism of its occurrence, leads to cell hypoxia and disruption of redox processes in it. In tissues, anaerobic processes begin to prevail over aerobic processes, metabolic acidosis develops. The accumulation of acidic metabolic products, primarily lactic acid, increases acidosis.

In the development of cardiogenic shock, the cause is a decrease in the productive function of the heart, followed by a violation of microcirculation.

The mechanism of shock development:

The main mechanisms for the development of shock are.
a decrease in the volume of circulating blood - hemorrhagic, hypovolemic shock;
vasodilation, an increase in the capacity of the vascular bed, redistribution of blood - anaphylactic, septic, shock;
violation of the productive function of the heart - cardiogenic shock.

All types of hemodynamic disturbances in any type of shock lead to microcirculation disturbances. Regardless of the starting points that determine the development of acute vascular insufficiency, the main ones are the disorder of capillary perfusion and the development of hypoxia and metabolic disorders in various organs.

Inadequate blood circulation at the capillary level in shock leads to changes in metabolism in all organs and systems, which is manifested by dysfunction of the heart, lungs, liver, kidneys, and nervous system. The degree of inadequate organ function depends on the severity of the shock, and this determines its outcome.

The developed circulatory disorder, primarily microcirculation disorder, leads to ischemia of the liver and disruption of its functions, which aggravates hypoxia in severe stages of shock. Detoxification, protein-forming, glycogen-forming and other functions of the liver are impaired. Disorder of the main, regional blood flow, impaired microcirculation in the kidneys causes impairment of both filtration and concentration functions of the kidneys with the development of oliguria, up to anuria. This leads to the accumulation of nitrogenous toxins in the body - urea, creatinine and other toxic metabolic products.

Violation of microcirculation, hypoxia cause dysfunction of the adrenal cortex and a decrease in the synthesis of corticosteroids (glucocorticoids, mineralocorticoids, androgenic hormones), which aggravates circulatory and metabolic disorders.

Disorder of blood circulation in the lungs causes a violation of external respiration, a decrease in alveolar metabolism, blood shunting, microthrombosis, as a result of which respiratory failure develops, aggravating tissue hypoxia.

Hemorrhagic shock:

Hemorrhagic shock is the body's response to blood loss. Acute loss of 25-30% of the BCC leads to severe shock. The development of shock and its severity are determined by the volume and rate of blood loss, and, depending on this, the following stages of hemorrhagic shock are distinguished: compensated hemorrhagic shock, decompensated reversible shock and decompensated irreversible shock.

With compensated shock, pallor of the skin, cold sweat, a small and frequent pulse, blood pressure within normal limits or slightly reduced, and urine output are reduced. With decompensated reversible shock, the skin and mucous membranes are cyanotic, the patient is inhibited, the pulse is small, frequent, the arterial and central venous pressure decreases, oliguria develops, the Algover index is increased, the ECG shows a malnutrition of the myocardium. In case of irreversible shock, consciousness is absent, blood pressure is not determined, the skin is marbled, anuria is noted - the cessation of urination. Algover's index is high. To assess the severity of hemorrhagic shock, it is important to determine the BCC, the volume of blood loss.