The role of Soviet and domestic scientists in the development of shock issues. traumatic shock

The classic description of shock by I.I. Pirogov, was included in almost all manuals on shock. For a long time, research on shock was performed by surgeons. The first experimental work in this area was carried out only in 1867. To date, there is no unambiguous definition of the concept of "shock" for pathophysiologists and clinicians. From the point of view of pathophysiology, the following is most accurate: traumatic shock is a typical pathological process resulting from damage to organs, irritation of receptors and nerves of injured tissue, blood loss and biologically active substances, that is, factors that collectively cause excessive and inadequate reactions of adaptive systems, especially sympathetic-adrenal systems, persistent disorders of neuroendocrine regulation of homeostasis, especially hemodynamics, disorders of specific functions of damaged organs, disorders of microcirculation, oxygen regime of the body and metabolism. It should be noted that the general etiology of traumatic shock in the form of a stable theory has not yet been developed. Nevertheless, there is no doubt that all the main factors of etiology take part in the development of shock: the traumatic factor, the conditions in which the injury was received, the body's response. For the development of traumatic shock great importance have environmental conditions. Traumatic shock is promoted by: overheating, hypothermia, malnutrition, mental trauma (it has long been noted that shock develops faster and is more severe in losers than in winners).

Significance of the state of the body for the occurrence of shock (data are still scarce): 1. Heredity - in humans, these data are difficult to obtain, but they are available in experimental animals. Thus, the resistance of dogs to injury depends on the breed. At the same time, dogs of pure lines are less resistant to injury than mongrels. 2. Type of nervous activity - animals with increased excitability are less resistant to injury and they develop shock after a small injury. 3. Age - in young animals (puppies), shock is easier to get, and more difficult to treat than adults. In the elderly and senile age, trauma affects a significantly weakened organism, characterized by the development of vascular sclerosis, hyporeactivity nervous system, endocrine system, so shock develops more easily and mortality is higher. 4. Pre-traumatic diseases. Contribute to the development of shock: hypertension; neuropsychic stress; hypodynamia; blood loss prior to injury. 5. Alcohol intoxication - on the one hand, it increases the likelihood of injury (disturbance of nervous activity), and at the same time it is used as an anti-shock liquid. But here, too, it should be remembered that in chronic alcoholism there are shifts in the nervous and endocrine systems, leading to a decrease in resistance to injury. Discussing the role of various pathogenetic factors in the origin of traumatic shock, most researchers note the difference in timing of their inclusion in the overall mechanism of the development of the process and far from the same significance in different periods shock. Thus, it is quite obvious that consideration of traumatic shock is unthinkable without taking into account its dynamics - its phase development.

There are two phases in the development of traumatic shock: erectile, following the injury and manifesting activation of functions, and torpid, expressed by inhibition of functions (both phases were described by N.I. Pirogov, and substantiated by N.N. Burdenko). The erectile phase of shock (from Latin erigo, erectum - to straighten, lift) is a phase of generalized excitation. AT last years it is called adaptive, compensatory, non-progressive, early. In this phase, activation of specific and nonspecific adaptive responses is observed. It is manifested by blanching of the integument and mucous membranes, increased arterial and venous pressure, tachycardia; sometimes urination and defecation. These reactions have an adaptive orientation. They provide, under the action of an extreme factor, the delivery of oxygen and metabolic substrates to tissues and organs, and the maintenance of perfusion pressure. As the degree of damage increases, these reactions become redundant, inadequate, and uncoordinated, which greatly reduces their effectiveness. This determines to a large extent a severe or even irreversible self-aggravating course of shock conditions. Consciousness is not lost during shock. Usually there is nervous, mental and motor excitement, manifested by excessive fussiness, agitated speech, increased responses to various stimuli (hyperreflexia), crying. In this phase, as a result of generalized excitation and stimulation of the endocrine apparatus, metabolic processes are activated, while their circulatory supply is insufficient. In this phase, prerequisites arise for the development of inhibition in the nervous system, circulation disorders, and oxygen deficiency occurs. The erectile phase is short and lasts usually minutes. If the adaptation processes are insufficient, the second stage of shock develops.

Torpid phase of shock (from Latin torpidus - sluggish) - a phase of general inhibition, manifested by hypodynamia, hyporeflexia, significant circulatory disorders, in particular arterial hypotension, tachycardia, respiratory disorders (tachypnea at the beginning, bradypnea or periodic breathing at the end), oliguria, hypothermia etc. In the torpid phase of shock, metabolic disorders are aggravated due to disorders neurohumoral regulation and circulatory support. These violations in different organs are not the same. The torpid phase is the most typical and prolonged phase of shock, its duration can be from several minutes to many hours. Currently, the torpid phase is called the stage of disadaptation (decompensation). At this stage, two substages are distinguished: progressive (consisting in the depletion of compensatory reactions and tissue hypoperfusion) and irreversible (during which changes incompatible with life develop).

In addition to the erectile and torpid phases of traumatic shock in severe shock ending in death, it is advisable to distinguish the terminal phase of shock, thereby emphasizing its specificity and difference from the death stages of other pathological processes, usually united by the general term "terminal states". The terminal phase is characterized by certain dynamics: it begins to be detected by disorders of external respiration (Biot or Kussmaul respiration), instability and a sharp decrease in blood pressure slowing down the pulse. The terminal phase of shock is characterized by a relatively slow development and, consequently, a greater depletion of adaptation mechanisms, more significant than, for example, with blood loss, intoxication, and deeper dysfunctions of organs. Recovery of these functions during therapy is slower.

traumatic shock should be classified according to the time of development and the severity of the course. According to the time of development, primary shock and secondary shock are distinguished. Primary shock develops as a complication shortly after the injury and may resolve or lead to the death of the victim. Secondary shock usually occurs a few hours after the patient's recovery from primary shock. The reason for its development is most often additional trauma due to poor immobilization, heavy transportation, premature surgery, etc. The secondary shock is much more severe than the primary one, since it develops against the background of very low adaptive mechanisms of the body, which were exhausted in the fight against the primary shock, therefore, the mortality rate in secondary shock is much higher. By severity clinical course There are mild shock, moderate shock and severe shock. Along with this, shock is divided into four degrees. This division is based on the level of systolic blood pressure. I degree of shock is observed at a maximum arterial pressure above 90 mm Hg. Art. - slight stupor, tachycardia up to 100 beats / min, urination is not disturbed. Blood loss: 15-25% of the BCC. II degree - 90-70 mm Hg. Art., stupor, tachycardia up to 120 beats / min, oliguria. Blood loss: 25-30% of the BCC. III degree - 70-50 mm Hg. Art., stupor, tachycardia more than 130-140 beats / min, no urination. Blood loss: more than 30% of the BCC. IV degree - below 50 mm Hg. Art., coma, the pulse on the periphery is not determined, the appearance of pathological respiration, multiple organ failure, areflexia. Blood loss: more than 30% of the BCC. Should be regarded as a terminal state. On the clinical picture shock, a certain imprint is imposed by the type of nervous system, gender, age of the victim, comorbidities, infectious diseases history of trauma accompanied by shock. An important role is played by blood loss, dehydrating diseases and conditions that affect the BCC and lay the basis for hemodynamic disorders. About the degree of decrease in BCC and the depth of hypovolemic disorders, a certain idea allows you to get a shock index. It can be calculated using the following formula: shock index = pulse rate / systolic BP. Normally, the shock index is 0.5. In the case of an increase in the index to 1 (pulse and blood pressure are equal to 100), the decrease in BCC is approximately 30% of the due value, when it is increased to 1.5 (pulse is 120, blood pressure is 80), the BCC is 50% of the due value, and with the values ​​of the shock index 2.0 (pulse - 140, blood pressure - 70), the volume of circulating blood in active circulation is only 30% of the proper one, which, of course, cannot provide adequate perfusion of the body and leads to a high risk of death of the victim. The following can be distinguished as the main pathogenetic factors of traumatic shock: inadequate impulsation from damaged tissues; local blood and plasma loss; entry into the blood of biologically active substances resulting from cell destruction and oxygen starvation fabrics; prolapse or dysfunction of damaged organs. At the same time, the first three factors are nonspecific, that is, inherent in any injury, and the last characterizes the specifics of the injury and the shock that develops in this case.

In the very general view the scheme of the pathogenesis of shock is presented in the following form. The traumatic factor acts on organs and tissues, causing their damage. As a result of this, cell destruction occurs and the release of their contents into the intercellular environment; other cells are exposed to concussion, as a result of which their metabolism and their inherent functions are disturbed. Primarily (due to the action of a traumatic factor) and secondarily (due to changes in the tissue environment), numerous receptors in the wound are irritated, which is subjectively perceived as pain, and objectively characterized by numerous reactions of organs and systems. Inadequate impulses from damaged tissues have a number of consequences. 1. As a result of inadequate impulses from damaged tissues, a pain dominant is formed in the nervous system, which suppresses other functions of the nervous system. Along with this, a typical defensive reaction occurs with stereotypical vegetative accompaniment, since pain is a signal to escape or fight. At the heart of this vegetative reaction, the most important components are: the release of catecholamines, increased pressure and tachycardia, increased respiration, activation of the hypothalamic-pituitary-adrenal system. 2. The effects of pain stimulation depend on its intensity. Weak and moderate irritation causes stimulation of many adaptive mechanisms (leukocytosis, phagocytosis, increased SPS function, etc.); strong irritations inhibit adaptive mechanisms. 3. Reflex tissue ischemia plays an important role in the development of shock. At the same time, incompletely oxidized products accumulate, and the pH decreases to values ​​that are borderline with those acceptable for life. On this basis, there are disorders of microcirculation, pathological deposition of blood, arterial hypotension. 4. Pain and the whole situation at the time of injury, of course, cause emotional stress, mental stress, a sense of anxiety about danger, which further enhances the neurovegetative reaction.

The role of the nervous system. When exposed to the body of a damaging mechanical agent in the area of ​​damage, various nerve elements are irritated, and not only receptors, but also other elements - nerve fibers passing through the tissues that make up nerve trunks. While the receptors have a known specificity in relation to the stimulus, characterized by differences in the threshold value for different stimuli, the nerve fibers in relation to mechanical stimulation do not differ so sharply from each other, therefore mechanical stimulation causes excitation in the conductors of various kinds of sensitivity, and not only painful or tactile. This explains the fact that injuries accompanied by crushing or rupture of large nerve trunks are characterized by more severe traumatic shock. The erectile phase of shock is characterized by generalization of excitation, which is externally manifested in motor restlessness, speech excitement, screaming, increased sensitivity to various stimuli. Excitation also covers vegetative nerve centers, which is manifested by an increase in the functional activity of the endocrine apparatus and the release of catecholamines, adaptive and other hormones into the blood, stimulation of the activity of the heart and an increase in the tone of resistance vessels, activation of metabolic processes. Prolonged and intense impulses from the site of damage, and then from organs with impaired functions, changes in the lability of nerve elements due to circulatory disorders and oxygen regime determine the subsequent development inhibitory process. Irradiation of excitation - its generalization - is a necessary prerequisite for the onset of inhibition. Of particular importance is the fact that inhibition in the zone of the reticular formation protects the cerebral cortex from the flow of impulses from the periphery, which ensures the safety of its functions. At the same time, the elements of the reticular formation that facilitate the conduction of impulses (RF+) are more sensitive to circulation disorders than those that inhibit the conduction of impulses (RF–). From this it follows that circulatory disturbances in this zone should contribute to the functional blockade of the conduction of impulses. Gradual inhibition extends to other levels of the nervous system. It tends to deepen due to impulses from the area of ​​injury.

The role of the endocrine system.
Traumatic shock is also accompanied by changes in the endocrine system (in particular, the hypothalamic-pituitary-adrenal system). During the erectile phase of shock, the content of corticosteroids in the blood increases, and in the torpid phase, their amount is reduced. However, the cortical layer of the adrenal glands retains a reaction to ACTH introduced from the outside. Consequently, the inhibition of the cortical layer is largely due to insufficiency of the pituitary gland. For traumatic shock, hyperadrenalemia is very typical. Hyperadrenalemia, on the one hand, is a consequence of intense afferent impulses caused by damage, on the other hand, a reaction to the gradual development of arterial hypotension.

Local blood and plasma loss.
With any mechanical injury, there is a loss of blood and plasma, the dimensions of which are very variable and depend on the degree of tissue trauma, as well as on the nature of vascular damage. Even with a small injury, exudation is observed in the injured tissues due to the development of an inflammatory reaction, and hence the loss of fluid. However, the specificity of traumatic shock is still determined by neuro-pain trauma. Nerve pain injury and blood loss are synergistic in action on cardiovascular system. With pain irritation and with loss of blood, vasospasm and the release of catecholamines first occur. With blood loss immediately, and with pain irritation later, the volume of circulating blood decreases: in the first case due to exit from the vascular bed, and in the second - as a result of pathological deposition. It should be noted that even a small bloodletting (1% of body weight) sensitizes (increases the body's sensitivity) to mechanical damage.

Circulatory disorders.
The very concept of "shock" includes mandatory and severe violations hemodynamics. Hemodynamic disorders in shock are characterized by sharp deviations of many parameters of the systemic circulation. Disorders of systemic hemodynamics are characterized by three cardinal signs - hypovolemia, a decrease in cardiac output and arterial hypotension. Hypovolemia has always been given importance in the pathogenesis of traumatic shock. On the one hand, it is due to blood loss, and on the other hand, blood retention in capacitive vessels (venules, small veins), capillaries - its deposition. The exclusion of part of the blood from the circulation can be clearly detected already at the end of the erectile phase of shock. By the beginning of the development of the torpid phase, hypovolemia is even more pronounced than in subsequent periods. One of the most typical symptoms of traumatic shock is phase changes in blood pressure - its increase in the erectile phase of traumatic shock (the tone of resistive and capacitive vessels increases, as evidenced by arterial and venous hypertension), as well as a short-term increase in circulating blood volume, combined with a decrease in the capacity of a functioning vascular bed of organs. An increase in blood pressure, typical for the erectile phase of traumatic shock, is the result of an increase in the total peripheral vascular resistance due to the activation of the sympathoadrenal system. An increase in the tone of resistive vessels is combined with the activation of arteriovenous anastomoses and the ejection of blood from the system of high pressure vessels (arterial bed) into the system of low pressure vessels (venous bed), which leads to an increase in venous pressure and prevents the outflow of blood from the capillaries. If we take into account the fact that most of the capillaries are devoid of sphincters at their venous end, then it is not difficult to imagine that under such conditions, not only direct, but also retrograde filling of the capillaries is possible. Numerous researchers have shown that hypovolemia limits afferent impulses from baroreceptors (stretch receptors) of the aortic arch and carotid sinus zone, resulting in excitation (disinhibition) of the pressor formations of the vasomotor center and spasm of arterioles in many organs and tissues. The sympathetic efferent impulse to the vessels and the heart is enhanced. As blood pressure decreases, tissue blood flow decreases, hypoxia increases, which causes impulses from tissue chemoreceptors and further activates the sympathetic effect on blood vessels. The heart is more fully emptied (residual volume decreases), and tachycardia also occurs. A reflex also arises from the baroreceptors of the vessels, leading to an increased release of adrenaline and norepinephrine by the adrenal medulla, the concentration of which in the blood increases by 10-15 times. In a later period, when renal hypoxia develops, vasospasm is maintained not only by increased secretion of catecholamines and vasopressin, but also by the release of renin by the kidneys, which is the initiator of the renin-angiotensin system. It is believed that the vessels of the brain, heart and liver do not participate in this generalized vasoconstriction. Therefore, this reaction is called the centralization of blood circulation. Peripheral organs suffer more and more from hypoxia, as a result of which metabolism is disturbed and under-oxidized products and biologically active metabolites appear in the tissues. Their entry into the blood leads to acidosis of the blood, as well as the appearance in it of factors that specifically inhibit the contractility of the heart muscle. Another mechanism is also possible here. The development of tachycardia leads to a reduction in the time of diastole - the period during which the coronary blood flow is carried out. All this leads to a violation of myocardial metabolism. With the development of an irreversible stage of shock, endotoxins, lysosomal enzymes and other biologically active substances specific for this period can also affect the heart. Thus, blood and plasma loss, pathological deposition of blood, extravasation of fluid lead to a decrease in the volume of circulating blood, a decrease in venous blood return. This, in turn, along with metabolic disorders in the myocardium and a decrease in the performance of the heart muscle, leads to hypotension, which is characteristic of the torpid phase of traumatic shock. Vasoactive metabolites accumulating during tissue hypoxia disrupt the function of vascular smooth muscles, which leads to a decrease in vascular tone, which means a decrease in the total resistance of the vascular bed and, again, to hypotension.
Disorders of capillary blood flow deepen as a result of a violation of the rheological properties of blood, aggregation of red blood cells, which occurs as a result of an increase in the activity of the coagulation system and thickening of the blood due to the release of fluid into the tissues. Respiratory disorders. In the erectile stage of traumatic shock, frequent and deep breathing is observed. The main stimulating factor is irritation of the receptors of injured tissues, which causes excitation of the cerebral cortex and subcortical centers, the respiratory center is also excited medulla oblongata.
In the torpid phase of shock, breathing becomes more rare and superficial, which is associated with depression of the respiratory center. In some cases, as a result of progressive hypoxia of the brain, periodic breathing of the Cheyne-Stokes or Biot type appears. In addition to hypoxia, various humoral factors have an inhibitory effect on the respiratory center - hypocapnia (due to hyperventilation - but CO2 accumulates later), low pH. The development of hypoxia, one of the most important moments in the pathogenesis of traumatic shock, is closely related to circulatory and respiratory disorders. In the genesis of shock hypoxia, the hemic component also occupies a certain place, due to a decrease in the oxygen capacity of the blood due to its dilution and aggregation of erythrocytes, as well as disorders of external respiration, but tissue perfusion and redistribution of blood flow between the terminal vessels still play a major role.

Disturbances in the lungs and the effects they cause are combined into a symptom complex called respiratory distress syndrome. This is an acute disorder of pulmonary gas exchange with life threatening severe hypoxemia as a result of a decrease to a critical level and below the number of normal respirons (respiron is a terminal or final respiratory unit), which is caused by negative neurohumoral influences (neurogenic spasm of pulmonary microvessels in pathological pain), damage to the pulmonary capillary endothelium with cytolysis and destruction of intercellular connections, migration of blood cells (primarily leukocytes), plasma proteins into the lung membrane, and then into the lumen of the alveoli, the development of hypercoagulability and thrombosis of the pulmonary vessels.

Metabolic disorders. Energy exchange.
Shock of various etiologies through microcirculation disorders and destruction of the histohematic barrier (exchange capillary - interstitium - cell cytosol) critically reduces oxygen delivery to mitochondria. As a result, rapidly progressive disorders of aerobic metabolism occur. The links in the pathogenesis of dysfunctions at the level of mitochondria in shock are: - edema of mitochondria; - disorders of mitochondrial enzyme systems due to deficiency of essential cofactors; - a decrease in the content of magnesium in the mitochondria; - an increase in the content of calcium in mitochondria; - pathological changes content in mitochondria of sodium and potassium; - disorders of mitochondrial functions due to the action of endogenous toxins (free fatty acids, etc.); - free radical oxidation of phospholipids of mitochondrial membranes. Thus, during shock, the accumulation of energy in the form of high-energy phosphorus compounds is limited. A large amount of inorganic phosphorus accumulates, which enters the plasma. Lack of energy disrupts the function of the sodium-potassium pump, as a result of which an excess amount of sodium and water enters the cell, and potassium leaves it. Sodium and water cause mitochondrial swelling, further uncoupling respiration and phosphorylation. As a result of a decrease in energy production in the Krebs cycle, the activation of amino acids is limited, and as a result, protein synthesis is inhibited. A decrease in the concentration of ATP slows down the connection of amino acids with ribonucleic acids (RNA), the function of ribosomes is disrupted, resulting in the production of abnormal, incomplete peptides, some of which may be biologically active. Severe acidosis in the cell causes rupture of lysosome membranes, as a result of which hydrolytic enzymes enter the protoplasm, causing the digestion of proteins, carbohydrates, and fats. The cell dies. As a result of cell energy deficiency and metabolic disorders, amino acids, fatty acids, phosphates, and lactic acid enter the blood plasma. Apparently, mitochondrial dysfunctions (like any pathological processes) develop in different organs and tissues asynchronously, mosaically. Especially damage to mitochondria and disorders of their functions are expressed in hepatocytes, while in neurons of the brain they remain minimal even in decompensated shock.
It should be noted that mitochondrial damage and dysfunction are reversible in compensated and decompensated shock and are reversed by rational analgesia, infusions, oxygen therapy, and hemorrhage control. carbohydrate metabolism. In the erectile phase of traumatic shock, the concentration of catecholamine insulin antagonists increases in the blood, stimulating the breakdown of glycogen, glucocorticoids, which enhance the processes of gluconeogenesis, thyroxine and glucagon as a result of increased activity of the endocrine glands. In addition, the excitability of the sympathetic nervous system (hypothalamic centers) is increased, which also contributes to the development of hyperglycemia. In many tissues, glucose uptake is inhibited. In this case, in general, a false diabetic picture is found. In the later stages of shock, hypoglycemia develops. Its origin is associated with the full use of liver glycogen reserves available for consumption, as well as a decrease in the intensity of gluconeogenesis due to the use of the substrates necessary for this and relative (peripheral) corticosteroid deficiency.
lipid metabolism. Changes in carbohydrate metabolism are closely associated with lipid metabolism disorders, which are manifested in the torpid phase of shock by ketonemia and ketonuria. This is explained by the fact that fats (as one of the main energy sources) are mobilized from the depot during shock (their concentration in the blood increases), and oxidation does not go to the end.
Protein metabolism. A manifestation of its violation is an increase in the content of non-protein nitrogen in the blood, mainly due to the nitrogen of polypeptides and, to a lesser extent, urea nitrogen, the synthesis of which is disturbed with the development of shock. Changes in the composition of serum proteins in traumatic shock are expressed by a decrease in their total amount, mainly due to albumins. The latter may be associated with both metabolic disorders and changes in vascular permeability. It should be noted that with the development of shock, the content of -globulins in the serum, which, as is known, is directly related to the vasoactive properties of blood, increases. The accumulation of nitrogenous products and changes in the ionic composition of the plasma contribute to impaired renal function. Oliguria, and in severe cases of shock - anuria are constant in this process. Renal dysfunction usually corresponds to the severity of shock. It is known that with a decrease in blood pressure to 70-50 mm Hg. Art. the kidneys completely stop filtration in the glomerular apparatus of the kidney due to changes in the relationship between hydrostatic, colloid osmotic and capsular pressure. However, in traumatic shock, renal dysfunction is not exclusively a consequence of arterial hypotension: shock is characterized by restriction of cortical circulation due to increased vascular resistance and shunting through the juxtaglomerular pathways. This is determined not only by a decrease in the productivity of the heart, but also by an increase in the vascular tone of the cortical layer.
ion exchange. Significant shifts are found in the ionic composition of the plasma. With traumatic shock, a gradual convergence occurs, the concentration of ions in the cells and extracellular fluid, while normally K+, Mg2+, Ca2+, HPO42-, PO43- ions predominate in cells, and Na+, C1-, HCO3- ions in the extracellular fluid. Entry into the blood of biologically active substances. For the subsequent course of the process, the release of active amines from cells, which are chemical mediators of inflammation, is of great importance. Over 25 such mediators have been described so far. The most important of them, appearing immediately after damage, are histamine and serotonin. With extensive tissue damage, histamine can enter the general circulation, and since histamine causes expansion of the precapillaries and spasm of the veins without directly affecting the capillary bed, this leads to a decrease in peripheral vascular resistance and a drop in blood pressure. Under the influence of histamine, channels and gaps are formed in the endothelium, through which blood constituents, including cellular elements (leukocytes and erythrocytes), penetrate into the tissues. As a result of this, exudation and intercellular edema occur. Under the influence of trauma, the permeability of vascular and tissue membranes increases, but nevertheless, due to circulatory disorders, the absorption of various substances from injured tissues slows down. An important role in the development of secondary alteration is played by enzymes of lysosomes of tissue cells and neutrophils. These enzymes (hydrolases) have a pronounced proteolytic activity. Along with these factors, plasma kinins (bradykinin), as well as prostaglandins, play a certain role in circulation disorders. These factors also affect the microcirculation system, causing the expansion of arterioles, capillaries and an increase in their permeability, which occurs initially (mainly in venules) due to the formation of intercellular gaps and transendothelial channels. Later, the permeability of the capillary and precapillary sections of the vascular bed changes.

A few words about wound toxemia. The issue of wound toxin has not been finally resolved. However, it is firmly established that toxic substances cannot enter the bloodstream from injured tissues, because reabsorption in them is reduced. The source of toxic substances is a vast area of ​​tissue contusion around the wound channel. It is in this zone that under the influence of potassium, histamine, serotonin, lysosomal enzymes, ATP, AMP, vascular permeability sharply increases. The toxin is formed as early as 15 minutes after ischemia, but has a relative molecular weight of 12,000 and is a product of intense protein breakdown. Administration of this toxin to intact animals results in hemodynamic disturbances typical of shock. The vicious circles that form during traumatic shock can be represented in the form of a diagram shown in Figure 1. Fig. 1. 1. Major vicious circles in shock. Violations of the functions of damaged organs. Most researchers refer to shock as a functional pathology, although an organic component always plays a role in etiology and pathogenesis, which can include a decrease in the volume of circulating blood and, consequently, a decrease in the number of red blood cells.
A significant factor complicating the analysis of the pathogenesis of shock in the clinic is the presence of organic damage that can accelerate the development of shock and modify its course. Yes, damage lower extremities, limiting the mobility of the wounded, forces them to take a horizontal position, often on cold ground, which, causing general cooling, provokes the development of shock. When injured maxillofacial region the victims lose a large amount of saliva, and with it water and protein, which, with difficulty in taking fluids and food, contributes to the development of hypovolemia and blood clots. With craniocerebral injuries, symptoms of brain dysfunctions join, consciousness is lost, excessive vasospasm occurs, which often masks hypovolemia. When the pituitary gland is damaged, neuroendocrine regulation is sharply disrupted, which in itself causes the development of shock and complicates the course of the post-shock period. Fundamentals of pathogenetic therapy of shock The complexity of the pathogenesis of traumatic shock, the variety of disturbances in the activity of many body systems, differences in ideas about the pathogenesis of shock cause a significant difference in the recommendations for the treatment of this process. We will focus on the established things. Experimental studies allow to identify possible directions in the prevention of traumatic shock. For example, the use of some complexes medicines before severe mechanical injury prevents the development of shock. Such complexes include the sharing of drugs (barbiturates), hormones, vitamins. Long-term stimulation of the pituitary-adrenal cortex system by the introduction of ACTH increases the resistance of animals to shock trauma, the introduction of ganglioblockers also has a preventive effect. However, situations where shock prophylaxis seems appropriate may not be very common. Much more often you have to deal with the treatment of developed traumatic shock and, unfortunately, not always in it. early periods and in most cases later. The basic principle of shock treatment is the complexity of therapy. Important in the treatment of shock is taking into account the phase of the development of shock. Treatment should be as quick and energetic as possible. This requirement also determines the methods of administration of certain drugs, most of which are administered directly into the vascular bed. In the treatment of shock in the erectile phase, when circulation disorders have not yet fully developed, deep hypoxia and advanced metabolic disorders have not yet occurred, measures should be reduced to preventing their development. In this phase the means limiting afferent impulsation are widely used; various kinds of novocaine blockades, analgesics, neuroplegic drugs, narcotic substances. Analgesics that inhibit the transmission of impulses, suppress autonomic reactions, limit the feeling of pain, are indicated in the early periods of shock. An important point limiting impulsation from the site of damage is the rest of the damaged area (immobilization, dressings, etc.). In the erectile phase of shock, the use of saline solutions containing neurotropic and energy substances (Popov, Petrov, Filatov, etc.) is recommended. Significant disorders of circulation, tissue respiration and metabolism that occur in the torpid phase of shock require various measures aimed at their correction. In order to correct circulatory disorders, blood transfusion or blood substitutes are used. In severe shock, intra-arterial transfusions are more effective. Their high efficiency is associated with the stimulation of vascular receptors, with an increase in capillary blood flow and the release of part of the deposited blood. Due to the fact that during shock there is predominantly the deposition of formed elements and their aggregation, it seems very promising to use low-molecular colloidal plasma substitutes (dextrans, polyvinol), which have a disaggregating effect and reduce blood viscosity at low shear stresses. Caution should be exercised when using vasopressor substances. Thus, the introduction of one of the most common vasopressor substances - noradrenaline in the initial period of the torpid phase slightly increases the minute volume of blood circulation due to the release of part of the deposited blood and improves the blood supply to the brain and myocardium. The use of norepinephrine in later periods of shock even aggravates the centralization of blood circulation characteristic of it. Under these conditions, the use of noradrenaline is appropriate only as an "emergency" remedy. The use of saline plasma-substituting solutions, although it leads to a temporary revival of blood flow, still does not give a long-term effect. These solutions, with significant disturbances in capillary blood flow and changes in the ratios of colloid osmotic and hydrostatic pressures characteristic of shock, leave the vascular bed relatively quickly. A noticeable effect on blood flow in traumatic shock is exerted by hormones - ACTH and cortisone, administered to normalize metabolic processes. During the development of shock, relative and then absolute adrenal insufficiency is detected first. In light of these data, the use of ACTH appears to be more appropriate in the early stages of shock or in its prevention. Glucocorticoids administered in the torpid phase have a variety of effects. They change the response of blood vessels to vasoactive substances, in particular, potentiate the action of vasopressors. In addition, they reduce vascular permeability. And yet their main action is associated with the influence on metabolic processes and, above all, on the metabolism of carbohydrates. Restoration of oxygen balance in conditions of shock is ensured not only by the restoration of circulation, but also by the use of oxygen therapy. Recently, oxygen therapy has also been recommended. In order to improve metabolic processes, vitamins are used (ascorbic acid, thiamine, riboflavin, pyridoxine, calcium pangamate). In connection with the increase in the resorption of biogenic amines from damaged tissues and, above all, histamine, the use of antihistamines. An important place in the treatment of shock is the correction of acid-base balance. Acidosis is typical of traumatic shock. Its development is determined by both metabolic disorders and the accumulation of carbon dioxide. Violation of excretory processes also contributes to the development of acidosis. The administration of sodium bicarbonate is recommended to reduce acidosis, some consider the use of sodium lactate or Tris buffer to be better.

I did not find a shock prevention :(((

Shock(from the English. shock - shock) - an acutely developing syndrome characterized by a sharp decrease in capillary (metabolic, nutritional) blood flow in various organs, insufficient oxygen supply, inadequate removal of metabolic products from the tissue and manifested by severe impairment of body functions.

Shock must be distinguished from collapse(from lat. collabor - fall, subside), because sometimes the same state is referred to either as a shock or as a collapse, for example, cardiogenic collapse, cardiogenic shock. This is due to the fact that in both cases there is a drop in blood pressure. Collapse is an acute vascular insufficiency, characterized by a sharp decrease in blood pressure, a decrease in the mass of circulating blood. The person then loses consciousness. Shock also lowers blood pressure and darkens consciousness.

However, there are fundamental differences between these two states. With collapse, the process develops with a primary insufficiency of the vasoconstrictor reaction. In shock due to activation of the sympathoadrenal system, vasoconstriction is pronounced. It is also the initial link in the development of microcirculation and metabolism disorders in tissues, called shock-specific, which are absent during collapse. For example, with blood loss, hemorrhagic collapse may first develop, and then the process may transform into shock. There are still some differences between collapse and shock. With shocks, especially traumatic ones, one can basically see two stages in their development: excitation and oppression. In the stage of excitation, blood pressure is even elevated. With collapse, there is no stage of excitation and consciousness is turned off completely. With shocks, consciousness is confused and turns off only in the later stages and in severe cases of development.

According to etiology, the following types of shocks are distinguished: 1) hemorrhagic; 2) traumatic; 3) dehydration; 4) burn; 5) cardiogenic; 6) septic; 7) anaphylactic.

Naturally, the pathogenesis of each type of shock has its own developmental features, its leading links. Depending on the nature of the acting cause and the characteristics of the developing damage, the main leading pathogenetic links are: hypovolemia(absolute or relative), pain irritation, infectious process at the stage of sepsis. Their ratio and severity are different for each type of shock. At the same time, a common link can be distinguished in the mechanisms of development of all types of shock. It becomes the sequential inclusion of two types of compensatory-adaptive mechanisms.

The first (vasoconstrictor) type - activation sympathoadrenal and pituitary-adrenal systems. They are included in the leading pathogenetic links. Absolute hypovolemia (loss of blood) or relative (decrease in minute volume of blood and venous return to the heart) leads to a decrease in blood pressure and irritation of baroreceptors, which activates the specified adaptive mechanism through the central nervous system. Pain irritation, like sepsis, stimulates its inclusion. The result of activation of the sympathoadrenal and pituitary-adrenal systems is the release of catecholamines and corticosteroids. Catecholamines cause contraction of blood vessels, which have a pronounced α-adrenoception: mainly skin, kidneys, abdominal organs. Nutritional blood flow in these organs is severely limited. Coronary and cerebral vessels do not have these adrenoreceptors, therefore they do not contract. There is a so-called "centralization of blood circulation", i.e., maintaining blood flow in vital organs - the heart and brain, and maintaining pressure in large arterial vessels. This is precisely the biological significance of the inclusion of the first type of compensatory-adaptive mechanisms.

However, a sharp limitation of perfusion of the skin, kidneys, and abdominal organs causes their ischemia. Hypoxia occurs. This includes second (vasodilatory) type mechanisms aimed at eliminating ischemia. Vasoactive amines, polypeptides and other biologically active substances begin to form, causing vasodilation, an increase in their permeability and a violation of the rheological properties of the blood. A significant contribution to their formation is made by damaged tissues, in which there is a breakdown mast cells, activation of proteolytic systems, release of potassium ions from cells, etc. Inadequacy of the vasodilatory type of compensatory-adaptive mechanisms develops due to excessive formation of vasoactive substances. Taken together, it changes microcirculation in tissues, reducing capillary and increasing shunt blood flow, changing the response of precapillary sphincters to catecholamines, and increasing the permeability of capillary vessels. The rheological properties of the blood change, “vicious circles” turn on. This is the shock-specific changes in microcirculation and metabolism. The result of these disorders is the release of fluid from the vessels into the tissues and a decrease in venous return. A "vicious circle" is activated at the level of the cardiovascular system, leading to a decrease in cardiac output and a decrease in blood pressure. The pain component leads to inhibition of the reflex self-regulation of the cardiovascular system, aggravating the developing disorders. The course of shock passes into the next, more severe stage. There are disorders of lung function ("shock lung"), kidneys, blood coagulation.

With each type of shock, the degree of activation of the sympathoadrenal and pituitary-adrenal systems, as well as the nature, amount and ratio of various types of biologically active substances formed, are different, which affects the speed and degree of development of microcirculatory disorders in various organs. The development of shock also depends on the state of the body. All factors that cause its weakening (the period of convalescence, partial starvation, hypokinesia, etc.) will contribute to the development of shock. And vice versa, favorable working conditions, life, physical activity inhibit its occurrence.

hemorrhagic shock. Occurs with external (knife, bullet wound, arrosive bleeding from the stomach with peptic ulcer, tumors, from the lungs with tuberculosis, etc.) or internal (hemothorax, hemoperitoneum) bleeding under conditions of minimal tissue injury.

Traumatic shock. Occurs with severe injuries of organs, abdominal and chest cavities, musculoskeletal system, accompanied by even minimal blood loss. An increase in blood loss in these cases aggravates the development of shock. In its course, erectile and torpid stages are distinguished. In the erectile stage, speech and motor excitation, pallor are noted. skin, tachycardia, temporary increase blood pressure. These signs are largely associated with the activation of the sympathoadrenal system.

The erectile stage passes into the torpedo stage. The clinical picture of this stage was described in 1864 by the outstanding Russian surgeon N. I. Pirogov: “With a torn off arm or leg, such a stiff one lies motionless at the dressing station .. He does not scream, does not yell, does not complain, does not take part in anything and does not demand anything: the body is cold, the face is pale, like that of a corpse; the gaze is fixed and turned into the distance; pulse, like a thread, barely noticeable under the finger and with frequent alternations. The numb man either does not answer questions at all, or only a barely audible whisper to himself, breathing is also barely noticeable. The wound and skin are almost insensible. The described signs indicate continued activation of the sympathoadrenal system (pale, cold skin, tachycardia) and depression of the function of the central nervous system (consciousness is darkened, although not completely turned off, oppression of pain sensitivity). The leading pathogenetic links are pain irritation and developing hypovolemia.

dehydration shock. It occurs as a result of significant dehydration of the body due to the loss of fluid and electrolytes. With pronounced exudative pleurisy, ileus, peritonitis, fluid from the vascular bed passes into the corresponding cavities. With indomitable vomiting and severe diarrhea liquid is lost to the outside. The consequence is the development of hypovolemia, which plays the role of the leading pathogenetic link. An additional active factor is often an infectious process.

Burn shock. It occurs with extensive and deep burns covering more than 15% of the body surface, and in children and the elderly - even with smaller areas. At the same time, already in the first 12-36 hours, the permeability of capillaries increases sharply, especially in the burn zone, which leads to to a significant release of fluid from the vessels into the tissues. A large amount of edematous fluid, mainly at the site of injury, evaporates. With a burn, 30% of the body surface in an adult patient is lost with evaporation up to 5-6 liters per day, and the volume of circulating blood drops by 20-30%. The leading pathogenetic factors are hypovolemia, pain irritation, a pronounced increase in vascular permeability.

Cardiogenic shock. Occurs most often as one of the severe complications of acute myocardial infarction. According to B03, it develops in 4-5% of patients under the age of 64 years. The size of the affected part of the myocardium plays an important role in the development of cardiogenic shock. It is believed that it always develops when 40% or more of the mass of the myocardium is damaged. It can also occur with smaller amounts of myocardial damage in cases of additional complications, such as arrhythmias. Perhaps the development of this type of shock and in the absence of a heart attack in cases of mechanical obstacles to filling or emptying the ventricles, with cardiac tamponade, intracardiac tumors. Cardiogenic shock is manifested by pain, up to an anginal state, arterial hypotension, although there are cases of normal blood pressure, activation of the sympathoadrenal system, and peripheral signs of perfusion disorders.

The leading pathogenetic links in the development of cardiogenic shock are: 1) pain irritation; 2) violation of the contractile function of the heart; and 3) cardiac arrhythmias. The severity and combination of these links in each case of cardiogenic shock are different, which gives grounds for isolating different forms this complication. The result of impaired contractile function is a decrease in cardiac output and, as a result, a decrease in the cardiac index. hypovolemia develops. Accession of arrhythmia exacerbates this process.

Septic (synonym: endotoxin) shock. Occurs as a complication of sepsis. Hence the name "septic". Since microbial endotoxins are the main damaging factor, this shock is also called endotoxin. By administering appropriate doses of endotoxins to animals, many of the changes that occur with septic shock in humans can be obtained. The most common cause of septic shock are gram-negative microorganisms - E. coli, Klebsiella, streptococci, pneumococci.

A feature of septic shock is its development against the background of an existing infectious process and a primary septic focus, from which microorganisms and their toxins enter the body (cholangitis or pyelonephritis with obstruction of the excretory tract, peritonitis, etc.). Shock is characterized by fever, chills with profuse sweating, tachycardia, tachypnea, pale skin, rapidly progressive circulatory failure, and impaired lung function.

Leading pathogenetic links of shock: 1) an increase in the body's need for oxygen delivery to tissues. This is caused by fever (increased metabolic processes), increased respiratory function (tachypnea), chills. (increasing the work of skeletal muscles), an increase in the work of the heart - cardiac output increases by 2-3 times. The latter leads to a decrease in the total peripheral vascular resistance; 2) decrease in blood oxygenation in the lungs and insufficient extraction of oxygen from the blood by tissues. Oxygenation is reduced due to circulatory disorders in the small circle caused by microthromboembolism, platelet aggregation on vascular adhesions, as well as impaired ventilation-perfusion relations in the lungs due to the development of atelectasis, pneumonia, and edema. Insufficient extraction of oxygen from the blood is due to several reasons: a) a sharp increase in shunt blood flow in the tissues; b) in the early stages of respiratory alkalosis due to tachypnea and the shift of the oxyhemoglobin dissociation curve to the left caused by this; 3) activation by endotoxins of proteolytic systems in biological fluids (kallikrein-kinin, complement, fibrinolytic) with the formation of products with a pronounced biological effect.

Anaphylactic shock.

Anaphylactic shock proceeds generally standard: a short erectile stage, after a few seconds - torpid. At guinea pig- predominantly bronchospasm (asthmatic type of shock), in dogs - spasm of the sphincters of the hepatic veins, stagnation of blood in the liver and intestines - collapse, in a rabbit - mainly spasm of the pulmonary arteries and blood stagnation in the right half of the heart, in humans - all components: drop in blood pressure due to redistribution of blood and impaired venous return, asthma attack, involuntary urination and defecation, skin manifestations: urticaria (urticaria), edema (oedema), itching (pruritus).

It differs from other types of shock in that the antigen-antibody reaction is the trigger in its pathogenesis, as a result of which blood proteases are activated, histamine, serotonin and other vasoactive substances are released from mast cells, causing primary dilatation of resistive vessels, a decrease in peripheral resistance and arterial hypotension. To anaphylactic hemotransfusion shock is close, where the main mechanism is the interaction of antigens of foreign erythrocytes (incompatible in the AB0 system with blood serum antibodies) - as a result, agglutination of erythrocytes, their hemolysis + release of vasoactive substances → vascular dilatation + blockade microvasculature agglutinated erythrocytes + damage to the epithelium of parenchymal organs by hemolysis products.

Principles of pathogenetic therapy of shock(according to Negovsky). The fight against shock should be complex, simultaneous and aimed at restoring three systems: 1) nervous - relieve pain - blocks, anesthesia, craniocerebral hypothermia, 2) restore blood circulation - infusion of drugs only into the vessels or the heart and no oral administration (inhibition of absorption function and motility of the gastrointestinal tract). Improve nutrition of nerve cells, prevent decortication. 3) Respiration - fight against metabolic acidosis, abundant oxygenation + hyperbaric oxygenation, must take into account the condition of the victim.

Shock - an acutely developing general reflex pathological reaction of the body to the action of extreme stimuli, characterized by a sharp inhibition of all vital functions and based on deep parabiotic disorders in the central nervous system.

Shock is caused by stimuli:

The strength, intensity and duration of the stimulus should be:

unusual

emergency

excessive

Extreme irritants:

Examples of irritants:

Crushing of soft tissues

fractures

damage chest and abdominal cavity

gunshot wounds

extensive burns

incompatibility of blood

The antigenic substances

histamines, peptones

electric shock

ionizing radiation

psychic trauma

Types of shock:

Traumatic

operating (surgical)

· Burn

post-transfusion

· Anaphylactic

Cardiogenic

Electric

Radiation

Mental (psychogenic)

traumatic shock defined as the most common clinical form severe condition of the wounded, which develops as a result of severe mechanical trauma or injury and manifests itself as a syndrome of low minute volume of blood circulation and tissue hypoperfusion.

Clinical and pathogenetic the basis of traumatic shock is the syndrome acute violation blood circulation (hypocirculation), resulting from the combined effect on the body of a wounded person of the life-threatening consequences of an injury, - acute blood loss, damage to vital organs, endotoxicosis, as well as neuro-pain effects. The main link in the pathogenesis of traumatic shock is primary microcirculation disorders. Acute deficiency blood circulation, insufficiency of tissue perfusion with blood leads to a discrepancy between the reduced possibilities of microcirculation and the energy needs of the body. In traumatic shock, unlike other manifestations of the acute period of traumatic disease, hypovolemia due to blood loss is the leading, although not the only, cause of hemodynamic disorders.
An important factor determining the state of blood circulation is the work of the heart. For the majority of victims with severe injuries, the development of a hyperdynamic type of blood circulation is characteristic. With a favorable course, its minute volume after injury can remain elevated throughout the acute period of traumatic disease. This is explained by coronary arteries are not involved in general vascular spasm, venous return remains satisfactory, cardiac activity is stimulated through vascular chemoreceptors by underoxidized metabolic products. However, if hypotension persists, as early as 8 hours after the injury, the one-time and minute performance of the heart in patients with traumatic shock can decrease by about two times compared to the norm. An increase in heart rate and total peripheral vascular resistance is not able to maintain the minute volume of blood circulation at normal values

Insufficient cardiac output in traumatic shock is due to the depletion of the mechanisms of urgent compensation due to myocardial hypoxia, the development of metabolic disorders in it, a decrease in the content of catecholamines in the myocardium, a decrease in its response to sympathetic stimulation and catecholamines circulating in the blood. Thus, a progressive decrease in one-time and minute performance of the heart will be a reflection of developing heart failure even in the absence of direct damage (contusion) of the heart (VV Timofeev, 1983).

Another main factor that determines the state of blood circulation is vascular tone. A natural response to trauma and blood loss is an increase in the functions of the limbic-reticular complex and the hypothalamic-adrenal system. As a result, in traumatic shock, urgent compensatory mechanisms are activated to maintain blood circulation in vital organs. One of the compensation mechanisms is the development of a widespread vascular spasm (primarily arterioles, metarterioles and precapillary sphincters), aimed at an emergency decrease in the capacity of the vascular bed and bringing it into line with the BCC. The general vascular reaction does not extend only to the arteries of the heart and brain, which are practically devoid of ?-adrenergic receptors that realize the vasoconstrictor effect of adrenaline and norepinephrine.

An urgent compensation mechanism, also aimed at eliminating the discrepancy between the BCC and the capacity of the vascular bed, is autohemodilution. In this case, there is an increased movement of fluid from the interstitial space to the vascular space. The exit of fluid into the interstitium occurs in functioning capillaries, and its entry goes into non-functioning ones. Together with the interstitial fluid, products of anaerobic metabolism penetrate into the capillaries, which reduce the sensitivity of ?-adrenergic receptors to catecholamines. As a result, non-functioning capillaries expand, while functioning ones, on the contrary, narrow. In shock, due to an increase in the concentration of adrenaline and norepinephrine, the ratio between functioning and non-functioning capillaries changes dramatically in favor of the latter.

This creates conditions for increasing the reverse flow of fluid into the vascular bed. Autohemodilution is also enhanced by the dominance of oncotic pressure not only in the venular (as under normal conditions), but also in the arteriolar ends of functioning capillaries due to a sharp decrease in hydrostatic pressure. The mechanism of autohemodilution is rather slow. Even with blood loss exceeding 30-40% of the BCC, the rate of fluid flow from the interstitium into the vascular bed does not exceed 150 ml/h.

In the reaction of urgent compensation for blood loss, the renal mechanism of water and electrolyte retention is of certain importance. It is associated with a decrease in primary urine filtration (a decrease in filtration pressure in combination with spasm of the renal vessels) and an increase in the reabsorption of water and salts in the tubular apparatus of the kidneys under the action of antidiuretic hormone and aldosterone.

With the depletion of the above compensation mechanisms, microcirculation disorders progress. Intensive release by damaged and ischemic tissues of histamine, bradykinin, lactic acid, which have a vasodilating effect; intake of microbial toxins from the intestines; a decrease due to hypoxia and acidosis in the sensitivity of vascular smooth muscle elements to nerve influences and catecholamines leads to the fact that the vasoconstriction phase is replaced by a vasodilation phase. Pathological deposition of blood occurs in metarterioles that have lost their tone and dilated capillaries. The hydrostatic pressure in them increases and becomes greater than the oncotic one. Due to the influence of endotoxins and hypoxia itself vascular wall its permeability increases, the liquid part of the blood goes into the interstitium, the phenomenon of "internal bleeding" occurs. Instability of hemodynamics, impaired vascular tone due to damage to the regulatory function of the brain in such a form of an acute period of traumatic disease as a traumatic coma (severe traumatic brain injury, severe brain contusion) usually develop later - by the end of the first day.

An important link in the pathogenesis of traumatic shock, even with non-thoracic trauma, is acute respiratory failure. By nature, it is usually parenchymal-ventilatory. Its most typical manifestation is progressive arterial hypoxemia. The reasons for the development of the latter are the weakness of the respiratory muscles in conditions of circulatory hypoxia; pain "brake" of breathing; embolization of pulmonary microvessels due to intravascular coagulation, fat globules, iatrogenic transfusions and infusions; interstitial pulmonary edema due to increased permeability of microvascular membranes by endotoxins, hypoxia of the vascular wall, hypoproteinemia; microatelectasis due to reduced formation and increased destruction of surfactant. The predisposition to atelectasis, tracheobronchitis and pneumonia is aggravated by aspiration of blood, gastric contents, increased secretion of mucus by the bronchial glands, difficulty in coughing against the background of insufficient blood supply to the tracheobronchial tree. The combination of pulmonary, hemic (due to anemia) and circulatory hypoxia is a key moment of traumatic shock. It is hypoxia and tissue hypoperfusion that determine metabolic disorders, immune status, hemostasis, and lead to an increase in endotoxicosis.

Traumatic shock occurs in two phases- excitation (erectile) and inhibition (torpid).

erectile phase occurs immediately after the injury and is manifested by motor and speech excitement, anxiety, fear. The consciousness of the victim is preserved, but the spatial and temporal orientations are disturbed, the victim underestimates the severity of his condition. Answers questions correctly, periodically complains of pain. The skin is pale, breathing is rapid, tachycardia is pronounced, the pulse is of sufficient filling and tension, blood pressure is normal or slightly increased.

The erectile phase of shock reflects the body's compensatory response to injury (mobilization stress) and hemodynamically corresponds to the centralization of blood circulation. It can be of different duration - from a few minutes to several hours, and with very severe injuries it may not be detected at all. It has been noted that the shorter the erectile phase, the more severe the subsequent shock.

Torpid phase develops as circulatory insufficiency increases. It is characterized by a violation of consciousness - the victim is inhibited, does not complain of pain, lies motionless, his gaze wanders, is not fixed on anything. He answers questions in a low voice, often requiring repeating the question to get an answer. The skin and visible mucous membranes are pale, with a gray tint. The skin may have a marble pattern (a sign of reduced blood supply and stagnation of blood in small vessels), covered with cold sweat. The extremities are cold, acrocyanosis is noted. Breathing is shallow, rapid. The pulse is frequent, weak filling, thready - a sign of a decrease in the volume of circulating blood. Arterial pressure is reduced.

The severity of the condition in the torpid phase of shock is assessed by pulse rate and blood pressure and is indicated by the degree.

Popkov V. M., Chesnokova N. P., Ledvanov M. Yu.,

2.1. Traumatic shock, etiology, stages of development, pathogenesis

Before defining shock, I would like to recall the well-known Deloyers expression: “shock is easier to recognize than to describe, and easier to describe than to define it.”

Traumatic shock is an acute neurogenic insufficiency of the peripheral circulation that occurs under the influence of an extreme traumatic factor, combined with phase disturbances in the activity of the central nervous system, hormonal balance, and corresponding metabolic and functional disorders of various organs and systems.

The definition of traumatic shock proposed by us, of course, cannot claim to be an absolute completeness of the characteristics of the entire complex of disorders characteristic of traumatic shock, and can be largely supplemented by the definition of shock, which is offered by G.I. Nazarenko (1994): traumatic shock is a typical evolutionarily formed, phase-developing pathological process of the acute period of traumatic disease.

Peculiarities clinical manifestations traumatic shock, the severity of its course is determined to a large extent by the nature of the injury that induces the development of shock. In this regard, it is necessary to note the variety of classifications of traumatic shock, reflecting mainly the nature of the injury, its severity and localization.

So, in a number of manuals, traumatic shock includes the following types of shock:

1) surgical shock;

2) shock caused by a burn;

3) shock caused by the application of a tourniquet;

4) shock caused by crushing;

5) shock caused by a shock air wave;

6) endotoxin shock.

Proposed by V.K. Kulagin (1978), the classification of traumatic shock is relevant to the present day and includes the following types of traumatic shock:

a) wound, arising from severe mechanical injuries, including components of pain and mental types of shock. Depending on the localization of the injury, it is divided into the following forms: cerebral, pulmonary, visceral, with trauma to the limbs, with prolonged compression of soft tissues, with multiple trauma;

b) hemorrhagic, arising from external and internal bleeding;

c) operational;

d) mixed.

In the dynamics of traumatic shock, most researchers, starting with N.I. Pirogov, there are two stages of development: erectile (excitation) and torpid (inhibition), characterizing, in essence, the functional state of the central nervous system. In the case of an unfavorable course of traumatic shock, a terminal state occurs at the end of the torpid phase. AT terminal state depending on the nature and severity of functional disorders and the nature of clinical manifestations, preagony, agony and clinical death are distinguished.

The erectile stage of shock occurs immediately after exposure to a traumatic factor; its duration is several minutes, in connection with which patients with traumatic shock are delivered to the hospital in the torpid stage of shock. The duration of the torpid stage of shock is usually from several hours to two days.

The leading pathogenetic factors of traumatic shock are: intense pathological afferentation from various receptor zones, in particular, from pain and tactile receptors in the area of ​​injury, psycho-emotional stress, rapidly developing endogenous intoxication, a decrease in the volume of circulating blood and, finally, a violation of the structure and function of various organs and tissues, characteristic of the so-called multiple organ failure in shock.

Regarding the pathogenesis of the erectile stage of shock, it should be noted the general patterns of the formation of stress reactions, which include traumatic shock, discovered by G. Selye and confirmed in numerous studies by domestic and foreign authors.

As is known, the flow of afferent impulses from various inter-, extero- and proprioreceptors, which is formed during the impact of an injury on the body, spreads along the ascending spinocortical pathways not only to the corresponding centers of the cerebral cortex, but primarily to the reticular formation of the brainstem, the limbic system. Activation of the reticular formation of the brain stem is accompanied by an increase in ascending and descending activating influences on the cerebral cortex, centers of the medulla oblongata, hypothalamic structures, and spinal motor centers, which causes the development of the erectile phase of shock. Characteristic signs of the erectile phase, which develops immediately after the action of a traumatic factor, are: general speech and motor excitement, pallor of the skin, sometimes involuntary urination and defecation.

Strengthening the activating influences on the bulbar vasomotor center leads to a short-term increase in neurogenic vascular tone and, accordingly, blood pressure. Nonspecific activation of the bulbar respiratory center in the erectile stage of shock is manifested by the development of tachypnea.

At the same time, activation of the hypothalamus occurs, which is structurally and functionally closely interconnected with the bulbar reticular formation. Activation of the posterior hypothalamic structures, including the higher autonomic centers of the sympathoadrenal system, entails a cascade of reactions characterized by a change in the neurohumoral regulation of the activity of a number of internal organs and systems.

When the sympathoadrenal system is activated in the erectile stage of shock, positive inotropic and chronotropic effects on the heart, tachycardia, hypertension occur. At the same time, a spasm of the afferent vessels of the renal glomeruli develops, which leads to the activation of the renin-angiotensin system, and the production of angiotensin-II, which has a pronounced vasoconstrictor effect, increases.

Activation of the anterior and middle sections of the hypothalamus in the erectile stage of traumatic shock is accompanied by an increase in the production of antidiuretic hormone by the supraoptic nucleus of the anterior hypothalamus and its secretion into the systemic circulation, as well as the formation of the so-called liberins, in particular corticoliberin and thyroliberin. The latter in a humoral way have an activating effect on the adenohypophysis and, accordingly, lead to an increase in the production of adrenocorticotropic and thyroid-stimulating hormones. However, it should be noted that the intensification of thyroid-stimulating hormone production under stressful influences is not an indisputable fact.

One of the important links in the adaptive reactions that are formed already in the erectile stage of shock is the activation of the release of glucocorticoids by the fascicular zone of the adrenal cortex under the influence of adrenocorticotropic hormone. At the same time, the production of mineralocorticoids by the glomerular zone of the adrenal cortex is also stimulated against the background of activation of the renin-angiotensin system.

The endocrine function of the pancreas also undergoes characteristic changes in the erectile and subsequent torpid stages of shock. Against the background of activation of the sympathoadrenal system in the erectile stage of shock, hyperproduction of glucagon occurs, selective inhibition of insulin secretion. However, the hyperglycemia that occurs simultaneously against the background of these hormonal changes is a factor that stimulates the production of insulin.

Instantly developing hormonal imbalance in the erectile stage of shock is accompanied by the occurrence of a complex of metabolic and functional disorders, which are even more intensified in the torpid stage of shock.

Hyperproduction of catecholamines leads to the activation of glycolysis and glycogenolysis enzymes, in particular, liver phosphorylase and glucose-6-phosphatase, which is accompanied by the development of hyperglycemia, and in some cases glucosuria, that is, symptoms of the so-called post-traumatic diabetes mellitus occur.

Excessive production of glucocorticoids leads to the activation of catabolic reactions, the processes of protein breakdown in lymphoid and muscle tissues increase, and a negative nitrogen balance occurs. At the same time, the processes of gluconeogenesis in the liver are stimulated, which provides a sufficiently long hyperglycemic reaction in response to the action of a traumatic agent.

Strengthening adrenergic influences on various organs and tissues in the erectile stage of shock leads to spasm of peripheral vessels, blood flow restriction, the development of ischemia and hypoxia, expressed to a large extent in the skin, skeletal muscles, and abdominal organs. Vasoconstrictor effects of catecholamines are potentiated in the dynamics of shock development due to hyperproduction of vasopressin and angiotensin-II. Oxygen deficiency in tissues also increases due to the activation of the processes of glycolysis, lipolysis, proteolysis under the influence of catecholamines and glucocorticoids, which leads to excessive accumulation of acidic products: lactic, pyruvic, fatty acids, keto acids, amino acids, the further metabolism of which in the tricarboxylic acid cycle is impossible due to with circulatory hypoxia.

At present, the fact of centralization of blood circulation, which occurs against the background of severe peripheral vasoconstriction, is generally recognized. The mechanisms of centralization of blood flow are formed in the erectile stage of shock, although they continue to provide it at the initial stages of the torpid stage of shock. The centralization of blood flow is supported by dilatation of the vessels of the heart, brain, adrenal glands and pituitary gland, mainly due to an increase in the activity of the sympathoadrenal system.

Thus, despite the short duration of development, the erectile stage of shock plays an extremely important role in the induction of disadaptation reactions characteristic of the torpid stage of traumatic shock, as well as in providing endogenous mechanisms of anti-stress protection of the body. It is in the erectile stage of shock that the mechanisms that ensure the formation of pathological blood deposition, peripheral circulatory insufficiency, and the transformation of the erectile stage of shock into a torpid stage are deployed.

So, what are the clinical manifestations of the torpid stage of shock and the mechanisms of their development?

The classical description of the torpid stage of traumatic shock was given by N.I. Pirogov in 1865. “With an arm or leg torn off, such a stiff one lies motionless at 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 as pale as that of a corpse, his gaze is motionless and turned into the distance; pulse - like a thread, barely noticeable under the fingers with frequent alternations. The numb man either does not answer questions at all, or only to himself, in a barely audible whisper; breathing is also barely perceptible. The wound and skin are almost not sensitive at all, but if the patient shows signs of feeling with one slight contraction of personal muscles ... "

From a modern point of view, in the development of the torpid stage of traumatic shock, in accordance with the state of hemodynamic parameters, it is customary to distinguish two phases: compensation and decompensation. The compensation phase is characterized by the following manifestations: cold wet skin, progressive tachycardia, pallor of the mucous membranes, relatively high blood pressure, no pronounced hypoxic changes in the myocardium according to ECG, no signs of brain hypoxia. Pupils can be somewhat dilated due to an increase in the tone of the radial muscles due to the activation of the sympathoadrenal system. The duration of filling the capillaries under the nail bed, the so-called spot symptom, is more than 3-5 seconds. To assess the severity of the torpid stage of shock, it is recommended to use a rectal-skin temperature gradient, which is an integrative indicator of the state of microcirculation. This test is easily reproducible in any conditions, it is characterized by the difference between the temperature in the lumen of the rectum at a depth of 8-10 cm and the temperature of the skin on the back of the foot at the base of the 1st toe. Normally, the rectal-skin temperature gradient is 3-5 °C. An increase in this gradient above 6-7 °C indicates the development of shock. G.I. Nazarenko (1994) notes that monitoring the dynamics of this gradient makes it possible to evaluate the effectiveness of antishock therapy. If, despite a set of measures, this gradient continues to increase, the prognosis of a shock state becomes less favorable, an increase in the skin-rectal gradient over 16 ° C indicates the possibility of a fatal outcome in 89% of cases.

In the compensation phase of the torpid shock stage, this gradient increases insignificantly. Central venous pressure in this phase is normal or slightly reduced.

In this way, characteristic features phases of compensation of the torpid stage of shock are: pronounced activation of the sympathoadrenal system with its characteristic functional and metabolic changes, in particular, the development of tachycardia and the hyperdynamic nature of blood circulation. During this period, the centralization of blood flow is still quite pronounced, there are no hypoxic changes in the myocardium and brain structures, the pressor response to intravenous administration norepinephrine, expressed spasm of peripheral vessels of the skin, skeletal muscles, abdominal organs.

However, already in the compensation phase of the torpid stage of traumatic shock, the mechanisms of disadaptation and decompensation are intensively deployed. The compensation phase of the torpid stage of traumatic shock is characterized by the depletion of the body's adaptive capabilities, which is manifested by the hypodynamic nature of blood circulation, there is a progressive decrease in minute blood volume, hypotension, a microcirculation crisis characterized by the development of thrombosis, hemorrhages, and erythrocyte slugging. In this case, the refractoriness of microvessels to nervous and humoral vasoconstrictor effects occurs.

Disorders of microcirculation in the phase of decompensation of traumatic shock are also characterized by progressive pathological deposition of blood.

Concerning the mechanisms of development of pathological deposition of blood, it should be noted that they are formed already in the erectile phase of shock, develop in the compensation phase of the torpid stage of shock, and reach a maximum in the decompensation phase of the torpid stage of shock.

Pathological deposition of blood exacerbates the disproportion between the capacity of the vascular bed and the volume of circulating blood, that is, it is the most important pathogenetic factor in the development of a shock state characterized by insufficiency of regional blood flow and microcirculation.

So, in the erectile stage of shock, due to the activation of the sympathoadrenal system, the renin-angiotensin system, increased release in synaptic structures or into the bloodstream of norepinephrine, adrenaline, angiotensin-II, glucocorticoids, spasm of pre- and postcapillaries of peripheral organs and tissues occurs, a decrease in blood flow velocity through capillaries, aggregation of erythrocytes mainly in venules. In this case, naturally, circulatory hypoxia occurs, accompanied, in turn, by a complex of secondary nonspecific metabolic and functional changes. In particular, in the hypoxia zone, free radical oxidation processes are activated, underoxidized metabolic products begin to accumulate, and initially compensated and then decompensated metabolic acidosis is formed. Under conditions of acidosis, a complex of compensation and damage reactions occurs.

Secondly, the phenomena of degranulation of mast cells are noted, in environment highly active compounds enter in excess, in particular, histamine, serotonin, leukotrienes, heparin, platelet aggregation factor, neutrophil chemotaxis factors, etc., many of which have a vasoactive effect, cause vasodilation of the microvasculature, increase the permeability of the vascular wall, and develop plasma loss and subsequent blood clots.

It should be noted that under the influence of an excess of hydrogen ions in peripheral organs and tissues, destabilization of lysosome membranes occurs, which leads to the release of a large number of lysosomal enzymes into the extracellular environment. The latter cause destruction of the protein, lipid, carbohydrate components of cell membranes and the intercellular substance of the connective tissue. The activation of lysosome phospholipases is accompanied by an increase in the production of polyunsaturated fatty acids, substrate activation of cyclooxygenase and lipoxygenase enzymes, in connection with which an intensive synthesis of prostaglandins and leukotrienes begins, which have a pronounced vasodilatory effect, increase vascular permeability, induce the development of plasma loss, and blood clotting. Damage to the vascular endothelium in the zone of circulatory hypoxia, exposure of vascular wall collagen are accompanied by increased adhesion and platelet aggregation processes, as well as activation of internal and external mechanisms for the formation of prothrombinase activity, that is, prerequisites for the development of thrombohemorrhagic syndrome are created.

Under the influence of an excess of hydrogen ions, the opening of arteriovenular shunts and the phenomenon of new formation of capillaries that do not function under normal conditions occur, and the capacity of the vascular bed increases. It should be noted that the discharge of blood through arteriovenous shunts exacerbates the state of hypoxia, since they do not provide transmembrane oxygen exchange with tissues.

Thus, the combined effects of an excess of hydrogen ions, as well as the complex biologically active compounds in the zone of peripheral vasoconstriction induced by the activation of adrenergic influences, they will cause a sharp increase in the capacity of the microcirculatory bed, loss of elasticity of microvessels, and an increase in their permeability, which will ultimately lead to the development of pathological blood deposition and a state of shock. Pathological deposition of blood first develops in the microvessels of the injury zone, skin, subcutaneous tissue, muscle tissue, intestines, and with prolonged hypoxia - and in the liver, kidneys, pancreas.

In connection with the development of pathological deposition of blood, plasma loss, thickening of the blood occurs, the volume of circulating blood decreases sharply, and venous return decreases. A decrease in venous return leads to further stimulation of the sympathoadrenal system, tachycardia is further aggravated. At the same time, the time of diastole and diastolic filling of the cavities of the heart decreases sharply, cardiac output falls, blood pressure falls, and shock syndrome worsens.

Thus, the shock state is based on the disproportion between the volume of circulating blood and the capacity of the vascular bed, when the capacity of the vascular bed tends to progressively increase in the dynamics of shock, and the volume of circulating blood decreases sharply. The decrease in the volume of circulating blood in the dynamics of traumatic shock, as mentioned above, is due to a complex of pathogenetic factors: possible blood loss, obligatory plasma loss due to an increase in the permeability of the vascular wall of the microcirculatory bed of various peripheral organs and tissues, pathological deposition of blood, a decrease in systolic output as a result of a decrease in venous return and activation of the sympathoadrenal system.

One of the key problems in the diagnosis and treatment of shock in severe injuries is the correct assessment of the severity of traumatic shock in the torpid phase.

Currently, there are various criteria for the severity of hemodynamic disorders, including using methods for assessing cardiac output, oxygen flow and the degree of hypoxia, osmolarity and colloid osmotic pressure of plasma, plasma volume, metabolic disorders, coagulation status, water and electrolyte balance and function. kidneys, respiratory function of the lungs, etc.

However, in an emergency clinical practice often use the generally accepted integrative criteria for assessing the severity of hemodynamic disorders in shock - the value of blood pressure and pulse rate.

The most common is the classification of the severity of the shock according to the magnitude of systolic pressure: pressure equal to 90 mm Hg. Art., indicates a shock of the 1st degree, 85-75 mm Hg. Art. - about shock of the 2nd degree, 70 mm Hg. and below - about the shock of the 3rd degree.

To assess the severity of hemodynamic disorders, the Algover index is also used, which is the ratio of the pulse rate to the value of systolic blood pressure. Under normal conditions, this indicator is 0.5-0.6, with shock of the 1st degree - 0.7-0.8, 2nd degree - 0.9-1.2, 3rd degree - 1.3 and higher.

To develop the principles of pathogenetic therapy of shock, it is necessary to clearly understand the mechanisms of development of the torpid stage of traumatic shock, the pathogenetic factors that determine the transformation of the erectile stage of shock into the torpid one.

For a long time, there was a point of view according to which the transformation of the erectile stage of shock into the torpid stage occurs due to progressive hemodynamic disorders, severe circulatory hypoxia, initially in peripheral organs and tissues, and as pathological blood deposition develops and blood pressure drops in the structures of the brain and heart. It should be noted that the fact of progressive circulatory hypoxia in the dynamics of traumatic shock is indisputable, and under conditions of hypoxia, as is known, the formation of free radicals increases, disintegration of biological membranes occurs, macroergic deficiency occurs, all energy-dependent reactions in cells are suppressed, including transmembrane ion transport , phenomena of cell depolarization occur, their excitability and, accordingly, functional activity change.

However, despite the above pattern of metabolic changes and hemodynamic disorders that cause the transformation of the erectile stage of shock into the torpid stage, not all researchers note the instantaneous depletion of energy substrates in the brain tissues in the erectile stage of shock, while the ATP level remains normal even in the torpid stage of shock.

In the mechanisms of transformation of the erectile stage of shock into the torpid stage, an important role should be assigned to pronounced disorders of the neurohormonal and humoral regulation of the function of organs and systems. A sharp activation of the hypothalamic-pituitary-adrenal system in the erectile stage of shock, an increase in the production of ACTH hormones and glucocorticoids are accompanied by an intensification of the metabolism of glucocorticoids in tissues and an equally rapid depletion of the fascicular zone of the adrenal cortex and, accordingly, their production of glucocorticoids. Under conditions of relative deficiency of glucocorticoids, many nonspecific adaptation reactions characteristic of the stress syndrome are suppressed, including a decrease in basal vascular tone, progression of shock, circulatory hypoxia and associated multiple organ failure.

At the same time, excessive activation of the sympathoadrenal system in the erectile stage of shock induces the activation of endogenous anti-stress defense mechanisms - the synthesis of inhibitory mediators in brain structures, in various internal organs and tissues, in particular, gamma-aminobutyric and gamma-hydroxybutyric acids, group E prostaglandins, opioid neuropeptides, which, in turn, limit the stress response; however, being released in inadequate concentrations, they can exacerbate hemodynamic disorders characteristic of shock states, and, accordingly, the severity of the clinical manifestations of shock.

We bring to your attention the journals published by the publishing house "Academy of Natural History"

- This is a pathological condition that occurs due to blood loss and pain in trauma and poses a serious threat to the patient's life. Regardless of the cause of development, it always manifests itself with the same symptoms. Pathology is diagnosed based on clinical signs. An urgent stop of bleeding, anesthesia and immediate delivery of the patient to the hospital is necessary. Treatment of traumatic shock is carried out in the intensive care unit and includes a set of measures to compensate for the violations that have arisen. The prognosis depends on the severity and phase of the shock, as well as the severity of the trauma that caused it.

ICD-10

T79.4

General information

Traumatic shock is a serious condition, which is a reaction of the body to an acute injury, accompanied by severe blood loss and intense pain. It usually develops immediately after an injury and is a direct reaction to injury, but under certain conditions (additional trauma) it may occur after some time (4-36 hours). It is a condition that poses a threat to the life of the patient, and requires urgent treatment in the intensive care unit.

The reasons

Traumatic shock develops in all types of severe injuries, regardless of their cause, location and mechanism of damage. It can be caused by stab and gunshot wounds, falls from a height, car accidents, man-made and natural disasters, industrial accidents, etc. In addition to extensive wounds with damage to soft tissues and blood vessels, as well as open and closed fractures of large bones ( especially multiple and accompanied by damage to the arteries) traumatic shock can cause extensive burns and frostbite, which are accompanied by a significant loss of plasma.

The development of traumatic shock is based on massive blood loss, severe pain syndrome, dysfunction of vital organs and mental stress caused by acute trauma. In this case, blood loss plays a leading role, and the influence of other factors can vary significantly. So, if sensitive areas (perineum and neck) are damaged, the influence of the pain factor increases, and if the chest is injured, the patient's condition is aggravated by impaired respiratory function and oxygen supply to the body.

Pathogenesis

The trigger mechanism of traumatic shock is largely associated with the centralization of blood circulation - a state when the body directs blood to vital organs (lungs, heart, liver, brain, etc.), removing it from less important organs and tissues (muscles, skin, adipose tissue). The brain receives signals about the lack of blood and responds to them by stimulating the adrenal glands to release adrenaline and norepinephrine. These hormones act on peripheral vessels, causing them to constrict. As a result, the blood flows from the limbs and it becomes enough for the functioning of the vital organs.

After a while, the mechanism starts to fail. Due to the lack of oxygen, peripheral vessels dilate, so blood flows away from vital organs. At the same time, due to violations of tissue metabolism, the walls of peripheral vessels stop responding to signals from the nervous system and the action of hormones, so there is no re-constriction of the vessels, and the “periphery” turns into a blood depot. Due to insufficient blood volume, the work of the heart is disrupted, which further exacerbates circulatory disorders. The blood pressure drops. With a significant decrease in blood pressure, the normal functioning of the kidneys is disturbed, and a little later - the liver and intestinal wall. Toxins are released from the intestinal wall into the blood. The situation is aggravated due to the occurrence of numerous foci of tissues that have become dead without oxygen and a gross metabolic disorder.

Due to spasm and increased blood clotting, some of the small vessels are clogged with blood clots. This causes the development of DIC (disseminated intravascular coagulation syndrome), in which blood clotting first slows down and then practically disappears. With DIC, bleeding may resume at the site of injury, pathological bleeding occurs, and multiple small hemorrhages appear in the skin and internal organs. All of the above leads to a progressive deterioration of the patient's condition and becomes the cause of death.

Classification

There are several classifications of traumatic shock, depending on the causes of its development. So, in many Russian guidelines on traumatology and orthopedics, surgical shock, endotoxin shock, shock due to crushing, burns, air shock and tourniquet are distinguished. The classification of V.K. is widely used. Kulagina, according to which there are the following types of traumatic shock:

• Wound traumatic shock (resulting from mechanical trauma). Depending on the location of the damage, it is divided into visceral, pulmonary, cerebral, with an injury to the limbs, with multiple trauma, with compression of soft tissues.
• Operational traumatic shock.
• Hemorrhagic traumatic shock (developing with internal and external bleeding).
• Mixed traumatic shock.

Regardless of the causes of occurrence, traumatic shock occurs in two phases: erectile (the body tries to compensate for the disorders that have arisen) and torpid (compensatory capabilities are depleted). Taking into account the severity of the patient's condition in the torpid phase, 4 degrees of shock are distinguished:

• I (easy). The patient is pale, sometimes a little lethargic. Consciousness is clear. Reflexes are reduced. Shortness of breath, pulse up to 100 beats / min.
• II (moderate). The patient is lethargic and lethargic. Pulse about 140 beats / min.
• III (severe). Consciousness is preserved, the possibility of perception of the surrounding world is lost. The skin is earthy gray, the lips, nose and fingertips are cyanotic. Sticky sweat. The pulse is about 160 beats / min.
• IV (pre-agony and agony). Consciousness is absent, the pulse is not determined.

Symptoms of traumatic shock

In the erectile phase, the patient is agitated, complains of pain, and may scream or moan. He is anxious and scared. Often there is aggression, resistance to examination and treatment. The skin is pale, blood pressure is slightly elevated. There is tachycardia, tachypnea (increased breathing), trembling of the limbs or small twitching of individual muscles. The eyes are shining, the pupils are dilated, the look is restless. The skin is covered with cold clammy sweat. The pulse is rhythmic, body temperature is normal or slightly elevated. At this stage, the body still compensates for the violations that have arisen. There are no gross violations of the activity of internal organs, there is no DIC.

With the onset of the torpid phase of traumatic shock, the patient becomes apathetic, lethargic, drowsy and depressed. Despite the fact that the pain does not decrease during this period, the patient ceases or almost ceases to signal it. He no longer screams or complains, he can lie silently, moaning quietly, or even lose consciousness. There is no reaction even with manipulations in the area of ​​damage. Blood pressure gradually decreases and heart rate increases. Pulse on peripheral arteries weakens, becomes filiform, and then ceases to be determined.

The patient's eyes are dim, sunken, the pupils are dilated, the gaze is motionless, shadows under the eyes. There is a pronounced pallor of the skin, cyanosis of the mucous membranes, lips, nose and fingertips. The skin is dry and cold, tissue elasticity is reduced. Facial features are sharpened, nasolabial folds are smoothed out. The body temperature is normal or low (it is also possible to increase the temperature due to a wound infection). The patient is chilled even in a warm room. Often there are convulsions, involuntary excretion of feces and urine.

Symptoms of intoxication are revealed. The patient suffers from thirst, the tongue is lined, the lips are parched and dry. Nausea and, in severe cases, even vomiting may occur. Due to progressive impairment of kidney function, the amount of urine decreases even with heavy drinking. Urine is dark, concentrated, with severe shock, anuria (complete absence of urine) is possible.

Diagnostics

Traumatic shock is diagnosed when the corresponding symptoms are identified, the presence of a fresh injury or other possible cause occurrence of this pathology. To assess the condition of the victim, periodic measurements of the pulse and blood pressure are performed, and laboratory tests are prescribed. Scroll diagnostic procedures determined pathological condition that caused the development of traumatic shock.

Treatment of traumatic shock

At the stage of first aid, it is necessary to temporarily stop bleeding (tourniquet, tight bandage), restore patency respiratory tract, perform anesthesia and immobilization, as well as prevent hypothermia. Move the patient should be very careful to prevent re-traumatization.

In the hospital, at the initial stage, resuscitators-anesthesiologists transfuse saline (lactasol, Ringer's solution) and colloidal (rheopolyglucin, polyglucin, gelatinol, etc.) solutions. After determining the Rh and blood group, the transfusion of these solutions is continued in combination with blood and plasma. Ensure adequate breathing using airways, oxygen therapy, tracheal intubation, or mechanical ventilation. Continue anesthesia. Perform bladder catheterization exact definition amount of urine.

Surgical interventions are carried out according to vital indications in the amount necessary to save life and prevent further aggravation of shock. They stop bleeding and treat wounds, blockade and immobilization of fractures, eliminate pneumothorax, etc. Hormone therapy and dehydration are prescribed, drugs are used to combat cerebral hypoxia, and metabolic disorders are corrected.