Traumatic shock pathogenesis clinic treatment. Scientific electronic library
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 that occurs as a result of damage to organs, irritation of receptors and nerves of injured tissue, blood loss and the entry of biologically active substances into the blood, that is, factors that collectively cause excessive and inadequate reactions of adaptive systems, especially sympathetic-adrenal, persistent violations of neuroendocrine regulation of homeostasis, especially hemodynamics, violations of the 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, environmental conditions are of great importance. 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 of the 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 moments in the origin of traumatic shock, most researchers note the time difference between their inclusion in the general mechanism of the development of the process and far from the same significance in different periods of 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. In recent years, it has been 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 of neurohumoral regulation and circulatory supply. 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 breathing), instability and a sharp decrease in blood pressure, slowing of 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. According to the severity of the clinical course, mild shock, moderate shock and severe shock are distinguished. 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. The type of nervous system, gender, age of the victim, concomitant pathology, infectious diseases, history of trauma accompanied by shock leave a certain imprint on the clinical picture of 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; the entry into the blood of biologically active substances resulting from cell destruction and oxygen starvation of tissues; 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 its most general form, 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, not only receptors, but also other elements - nerve fibers passing through the tissues that make up the nerve trunks. While the receptors have a known specificity with respect 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 the autonomic 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 injury, and then from organs with impaired functions, changes in the lability of nerve elements due to disorders of the blood circulation and oxygen regime determine the subsequent development of the 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 size of which is very variable and depends 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 their effect on the 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 hemodynamic disorders. 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 occurs 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, and the respiratory center of the medulla oblongata is also excited.
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 (respirone 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 in the content of sodium and potassium in mitochondria; - 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 exchange. 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 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. So, damage to the 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 the maxillofacial region is injured, 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 clotting. 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 make it possible to determine possible directions in the prevention of traumatic shock. For example, the use of certain drug complexes 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 administration of ACTH increases the resistance of animals to shockogenic injury, and the administration 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 its early periods, but in most cases in the later ones. 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 impulses 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 - norepinephrine 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 may be important in the treatment of traumatic shock. 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.
Traumatic shock is a severe, polypathogenetic pathological process that develops acutely as a result of an injury, and is characterized by significant dysfunctions of life support systems, primarily blood circulation, against the background of extreme stress on the body's regulatory (adaptive) mechanisms. Traumatic shock is one of the manifestations of the acute period of traumatic disease.
Links in the pathogenesis of shock
The household expression "pain shock", "death from pain shock" is widespread. The true cause of the development of traumatic shock is the rapid loss of a large volume of blood or plasma. Moreover, this loss does not have to be in the form of obvious (external) or latent (internal) bleeding - massive exudation of plasma through the burnt surface of the skin during burns can also cause a shock state.
Important for the development of traumatic shock is not so much the absolute value of blood loss as the rate of blood loss. With rapid blood loss, the body has less time to adjust and adapt, and shock is more likely to develop. Therefore, shock is more likely when large arteries, such as the femoral, are injured.
Severe pain, as well as the neuropsychiatric stress associated with trauma, undoubtedly play a role in the development of shock (although not the main cause) and aggravate the severity of shock.
Factors leading to the development of traumatic shock or aggravating it are also injuries with damage to especially sensitive areas (perineum, neck) and vital organs (for example, a chest wound, rib fractures with impaired respiratory function, traumatic brain injury). In such cases, the severity of shock is determined by the amount of blood loss, the intensity of the pain syndrome, the nature of the injury, and the degree of preservation of the function of vital organs.
Rapid and massive blood or plasma loss leads to a sharp decrease in the volume of circulating blood in the body of the victim. As a result, the victim's blood pressure drops rapidly and strongly, the supply of tissues with oxygen and nutrients worsens, and tissue hypoxia develops. Due to the lack of oxygen in tissues, toxic incompletely oxidized metabolic products accumulate in them, metabolic acidosis develops, and intoxication increases. Lack of glucose and other nutrients by tissues leads to their transition to "self-sufficiency" - lipolysis (fat breakdown) and protein catabolism increase.
The body, trying to cope with blood loss and stabilize blood pressure, reacts with the release of various vasoconstrictor substances into the blood (in particular, adrenaline, norepinephrine, dopamine, cortisol) and spasm of peripheral vessels. This can temporarily stabilize blood pressure at a relatively "acceptable" level, but at the same time worsens the situation with the supply of peripheral tissues with oxygen and nutrients. Accordingly, metabolic acidosis, intoxication with incompletely oxidized metabolic products, and catabolic processes in tissues increase even more. There is a centralization of blood circulation - first of all, the brain, heart, lungs are supplied with blood, while the skin, muscles, abdominal organs receive less blood. Lack of blood by the kidneys leads to a decrease in glomerular filtration of urine and a deterioration in the excretory function of the kidneys, up to complete anuria (lack of urine).
Spasm of peripheral vessels and increased blood clotting as a reaction to bleeding contribute to the blockage of small spasmodic vessels (primarily capillaries) with tiny blood clots - blood clots. The so-called "DIC-syndrome" develops - a syndrome of disseminated intravascular coagulation. Blockage of small vessels further increases the problems with the blood supply to peripheral tissues and, in particular, to the kidneys. This leads to a further increase in metabolic acidosis and intoxication. The so-called "consumption coagulopathy" may develop - a violation of blood clotting due to massive consumption of clotting agents in the process of widespread intravascular coagulation. In this case, pathological bleeding may develop or bleeding from the site of injury may resume, and further aggravation of shock may occur.
A decrease in blood supply to the adrenal glands and their function against the background of an increase in the need for glucocorticoids in “shock” tissues leads to a paradoxical situation. Despite the high level of cortisol in the blood (release!), Relative adrenal insufficiency is observed. This is explained by the fact that less than the tissues need is “thrown out”, and poorly supplied adrenal glands are physically unable to give out more cortisol.
The body's attempts to cope with pain by increasing the secretion of endorphins (endogenous analogues of opiates) lead to a further drop in blood pressure, the development of lethargy, lethargy, and anergy. A reaction to a decrease in blood pressure and a high level of catecholamines in the blood is tachycardia (rapid heartbeat). At the same time, due to the insufficiency of the volume of circulating blood, the cardiac output (stroke volume of the heart) is simultaneously reduced and there is a weak filling of the pulse (up to a thready or undetectable pulse on the peripheral arteries).
Severe shock without treatment usually results in agony and death. In the case of a relatively mild or moderate shock, in principle, self-healing is possible (at some stage, further promotion of the shock may stop, and later the state stabilizes, the body adapts and recovery begins). But this cannot be relied upon, since the development of a shock state of any degree in itself indicates a breakdown in adaptation, that the severity of the injury has exceeded the compensatory capabilities of this particular organism.
Shock can be primary (early), which occurs immediately after injury and is a direct reaction to injury. Secondary (late) shock occurs 4-24 hours after the injury and even later, often as a result of additional trauma to the victim (during transportation, cooling, renewed bleeding, constriction of the limb with a tourniquet, from gross manipulations in the provision of medical care, etc.). A frequent type of secondary shock is postoperative shock in the wounded. Under the influence of additional trauma, relapses of shock in victims are also possible, usually within 24-36 hours. Often, shock develops after the tourniquet is removed from the limb.
(51) Procedure in case of an accident at the production of AOKhV:
1. Don't panic
2. At the signal "attention everyone!" turn on the TV / radio to get reliable information.
3. Close windows, turn off electrical appliances and gas.
4. Put on rubber boots, raincoat.
5. Take the necessary things with you: documents, necessary warm clothes, a three-day supply of non-perishable food.
6. After notifying the neighbors, quickly (do not panic) leave the zone of possible infection perpendicular to the direction of the wind for a distance of at least 1.5 km.
7. Use PPE (gas mask, cotton-gauze bandage soaked in 2-5% soda/2% citric acid solution (chlorine/ammonia).
8. If it is impossible to leave the infection zone, tightly close and seal/plug all air ducts and cracks. Drink only boiled or bottled water, observe the rules of personal hygiene.
(52) Status epilepticus (a series of epileptic seizures) refers to life-threatening conditions. With it, there are severe violations of breathing, cardiovascular activity, circulation and distribution of blood throughout the organs. The convulsive syndrome is the cornerstone of these changes. As the epileptic status continues, the coma deepens in the patient, muscle hypotension increases (in the period between attacks), reflexes are inhibited. Patients with a series of seizures, and especially those in status epilepticus, require immediate hospitalization and intensive care.
1. Ensure the patency of the upper respiratory tract.
2. Provide peripheral venous access.
3. Then carry out drug treatment aimed at eliminating seizures, normalizing cardiovascular activity and metabolism. Effective measures of anticonvulsant therapy are: intravenous administration of 2 ml of a 0.5% solution of diazepam (seduxen) in 20 ml of a 40% glucose solution. The mixture is injected slowly, over 3-4 minutes. If, after 10-15 minutes after the administration of the indicated solution, convulsions do not stop, the administration should be repeated. If there is no effect, 70-80 ml of a 1% solution of sodium thiopental is administered intravenously. With a drop in blood pressure, cardiac glycosides are indicated.
4. Ensuring adequate oxygenation (either oxygen supply through nasal canulas, or tracheal intubation with low saturation and ineffective administration of anticonvulsants).
5. If there are signs of brain dislocation (anisocoria, decerebral or decortication rigidity, Cushing's syndrome - bradycardia, arterial hypertension, worsening respiratory disorders) - transfer the patient to mechanical ventilation, administer a bolus of mannitol 20% -0.25-0.5 mg / kg in for 15-20 minutes, at the same time 10 mg of a 1% solution of furosemide is injected.
6. Transportation of the patient to the nearest medical institution, which has the possibility of mechanical ventilation.
(53) Burn damage can be of 4 degrees:
1. I degree - redness and swelling of the skin, acute pain.
2. II degree - redness and swelling of the skin with the formation of blisters filled with a yellowish liquid (due to delamination or exfoliation of the epidermis)
3. III degree - the appearance of blisters with jelly-like contents, some of the blisters are destroyed, necrosis of the epidermis and dermis with the formation of a dark red or dark brown scab. There are IIIA and IIIB degrees - with A, the dermal layer of the skin dies partially, with B - completely
4. IV degree - the skin and deeper tissues (fiber, muscles, blood vessels, nerves and bones) are completely affected. There is often charring.
Burns of I, II, IIIA degrees are superficial, IIIB and IV are deep. With superficial burns, the upper layers of the skin are affected, so they heal with conservative treatment (without the use of skin plastics). For deep burns, the death of all layers of the skin and deep tissues is characteristic. In the treatment of these burns, it is necessary to use surgical methods for restoring the skin.
(54) Electrical injury- electric shock, causing deep functional changes in the central nervous system, respiratory and cardiovascular systems, often combined with local tissue damage.
The specific biological effect of the current consists in an exciting effect on the muscles and nerve elements, leading to long-term disturbances in the work of the potassium-sodium pump of cells, and, as a result, to severe neuromuscular disorders (up to ventricular fibrillation and instant death).
Visual signs of electrical injury are "current signs" located at the points of entry and exit of electric charge. At these points, the maximum tissue changes occur under the influence of electric current.
After the termination of the current, symptoms from the central nervous system prevail. General weakness, loss or clouding of consciousness is possible. Signs of electrical injury often resemble the clinical picture of a concussion. There is a headache and dizziness, the patient is lethargic, inhibited, indifferent to the environment. Less commonly, electrical injury is marked by excitation, redness of the skin and restlessness.
On the part of the cardiovascular system, there is first an increase, and then a decrease in blood pressure, increased heart rate and arrhythmia. Quite often expansion of borders of heart comes to light. In severe cases, ventricular fibrillation develops. Moist rales appear in the lungs, and signs of emphysema are found on a chest x-ray. A cough is possible, in some cases (especially with pre-existing pulmonary pathology), signs of acute respiratory failure are noted.
When struck by lightning, in addition to electric shock of very high voltage, it can be accompanied by severe burns up to charring, the victim can also be thrown back by the shock wave and additionally receive traumatic injuries (in particular, the skull)
PP: It begins with the cessation of the effect of current on the victim - disconnection from the current-carrying object. Then it is necessary to assess the condition and, first of all, the preservation of the respiratory function and blood circulation, if necessary, CPR. Regardless of the degree, all victims are subject to hospitalization. Also apply an aseptic bandage to the burn site (if any).
PVP: Victims who are in a state of sharp excitement should be given chloral hydrate in enemas.
To combat hypoxia, which develops in the first hours after electric shock, oxygen therapy is used.
To reduce headaches, dehydration agents are indicated: 40% glucose solution or 10% sodium chloride solution in an amount of 7-10 ml. With persistent headache associated with increased intracranial pressure, a spinal puncture is performed. The amount of released cerebrospinal fluid during the first puncture should not exceed 5-7 ml, with repeated 10-12 ml.
With functional disorders of the nervous system, sedatives are prescribed.
(55) ixodid ticks
The first signs of a tick bite can appear after two to three hours: weakness, drowsiness, chills, joint pain, photophobia.
Typical symptoms of diseases:
Tick-borne encephalitis: fever, general weakness, headache, dizziness, pain in the eyeballs, pain in the muscles, bones, loss of appetite; in severe forms - impaired consciousness, hemiparesis, bulbar symptoms, movement disorders, paresis of the neck and shoulder muscles and upper limbs; in chronic course - Kozhevnikov's epilepsy.
Borreliosis (Lyme disease): In the acute period- migrating erythema at the site of a tick bite, swollen lymph nodes close to the bite site and conjunctivitis are possible. In a few weeks- neuritis of the cranial nerves, meningitis, radiculoneuritis, multiple erythematous rashes on the skin. When chronized- arthralgia, alternating hr. polyarthritis; polyneuropathy, spastic paraparesis, ataxia, memory disorders and dementia.
PMP: remove the tick, take it to the laboratory for analysis, according to the results - the introduction of human anti-encephalitis immunoglobulin / antibiotic therapy (semi-synthetic penicillins, amoxicillin-clavulanate, sulfonamides - ceftriaxone).
Adrenergic mediator syndrome: list the characteristic symptoms; list drugs (substances) for overdoses and poisonings that are characteristic of the development of this syndrome.
Symptoms: mydriasis, hypertension, tachycardia or heart rate within the upper limit of normal, dry mucous membranes; pale moist skin, intestinal motility is reduced
Typical for the following substances: cold remedies containing adrenomimetics (naphthyzinum); eufillin; cocaine, amitriptyline in the early phase of action; MAO inhibitors (a number of antidepressants and antiparkinsonian drugs - selegiline, tranylcypromine); thyroid hormones; synthetic amphetamines; phencyclidine (general anesthetic, "sernil"); lysergic acid derivatives
Sympatholytic mediator syndrome: list the characteristic symptoms; list drugs (substances) for overdoses and poisonings that are characteristic of the development of this syndrome.
Symptoms: miosis, hypotension, bradycardia, respiratory depression, intestinal motility is reduced, muscle hypotension, skin is pale, wet, cold
drugs (substances): clonidine, b-blockers, Ca-channel blockers, reserpine, opiates
Sting of a bee, bumblebee: list the characteristic symptoms and possible complications; give a detailed description of the full standard for the provision of first and pre-medical, as well as first medical aid.
Symptoms: burning sensation and pain, local tissue swelling, redness and local fever, weakness, dizziness, headache, chills, nausea, vomiting, sometimes urticaria, pain in the lower back and joints, palpitations
Possible complications: upper respiratory tract obstruction, systemic anaphylaxis: generalized urticarial rash, facial edema, skin itching, dry cough, laryngo- and bronchospasm, dyspepsia, shock, pulmonary edema, coma.
First aid:
4) Remove the sting from the wound (preferably with tweezers)
5) Treat the sting site with an antiseptic (treat the wound with ammonia or soap and water). Lay down a person with an elevated position of the limb, immobilization
6) In case of severe pain, give an anesthetic drug
7) Apply cold to the bite
8) Give an antihistamine (suprastin) to drink
9) Plentiful drink
With the phenomena of systemic anaphylaxis a 0.1% solution of adrenaline is injected intravenously - 0.1 ml / year of life (10 mcg / kg), antihistamines (1% diphenhydramine solution, suprastin 2% solution 0.03-0.05 ml / kg or tavegil 0.1 ml/year of life), glucocorticoids (prednisolone 5 mg/kg or dexamethasone 0.5 mg/kg)
With symptoms of bronchospasm- bronchodilators (100-200 mg of salbutamol, 20-80 mcg of ipratropium bromide per inhalation, 10-40 drops of berodual in a nebulizer).
AOXV and suffocating agents: name the substances of this group; pathogenesis of damage by these poisons; list the characteristic syndromes and symptoms when affected by the above substances; give a detailed description of the protective measures and the full standard of first aid.
This group includes agents that, when inhaled, cause damage to the respiratory system and toxic pulmonary edema with the development of acute hypoxia. During World War I, they used chlorine, phosgene, diphosgene. Currently - phosgene, diphosgene, chloropicrin.
Pathogenesis: toxic pulmonary edema develops, which is based on an increase in the permeability of the alveolar and capillary walls as a result of damage to the surfactant system and proteins of the alveolar-capillary membrane, which leads to leakage of the liquid part of the blood and proteins into the alveoli
By severity:
Mild - toxic damage to the mucous membranes of the upper respiratory tract and keratoconjunctivitis (inhalation dose 0.05-0.5 mg x min / l)
Moderate severity - toxic bronchopneumonia (0.5-3 mg x min / l)
Severe - toxic pulmonary edema (3-10 mg x min / l)
Forms of damage:
1) Lightning - a burning sensation in half of the nose, in the nasopharynx and oropharynx. Nausea, severe general weakness, severe dry cough appear, bradypnea increases, cyanosis of the skin and mucous membranes develops. Then the affected person loses consciousness, breathing stops. After cessation of breathing, cardiac activity stops after 3-5 minutes.
2) Delayed form - by periods: increase in pathological manifestations, relative stabilization, recovery. During the period of increasing pathological manifestations, the following phases are distinguished: reflex manifestations, imaginary well-being and clinical manifestations of pulmonary edema
3) The phase of reflex manifestations - smell, unpleasant taste in the mouth, slight irritation of the mucous membranes of the respiratory tract, conjunctiva. Cyanosis appears, breathing slows down. The pulse is quickened, blood pressure rises slightly. Nausea, vomiting, dizziness, general weakness are possible
4) The phase of imaginary well-being (latent) - cyanosis, slight shortness of breath. The affected person is fussy, the movements are discoordinated, there is a percussion box sound above the lungs. Breath sounds are weakened. The duration of the phase is 4-6 hours.
5) The phase of clinical manifestations of pulmonary edema is a persistent, debilitating cough, breathing becomes difficult, shortness of breath and cyanosis increase sharply. The affected person is restless, looking for a comfortable position for himself (more often on all fours with his head down). T 38-39. Above the lungs - a boxed sound, there are areas of dullness, usually in the posterior-lower sections, crepitating and moist small bubbling rales are also heard here. Their number is growing. The pulse quickens, heart sounds become muffled, blood pressure decreases. The affected person coughs up an increasing amount of fluid (up to 2.5 liters per day). Breathing becomes noisy, bubbling. The amount of urine is sharply reduced.
In the absence of complications, the recovery period lasts 7-10 days.
Protective measures:
1. Timely use of a filtering gas mask
2. Protective clothing
During the phases of reflex manifestations and imaginary well-being (latent):
1. Inhalation under the mask of a gas mask ficilin (volatile anesthetic) or anti-smoke liquid
2. Shelter from the cold and warm the affected
3. Evacuation on a stretcher with a raised head end or in a sitting position (+ tourniquets on the lower extremities)
4. Abundant washing of eyes with water, nasopharynx and oropharynx
5. Instillation into the conjunctival sac, 2 drops of 0.5% solution of dicaine
6. GCS: beclomethasone dipropionate inhalation to all affected: 1st day - 4 single inhalations of 0.125 mg immediately, and then for 6 hours every 5 minutes 2 inhalations. Then 1-2 inhalations every 10-15 minutes. Until the fifth day, with or without changes in the lungs, 1 inhalation is done hourly; before going to bed - 6 times 4-5 inhalations with 15-minute intervals; after waking up - 5 inhalations. After the 5th day, if there are changes in the lungs, 1 inhalation every hour until complete recovery, in the absence of pathological changes in the lungs - 1 inhalation every 3-4 hours.
The inhalation administration of GCS can be replaced by intravenous metipred: the first day - 1000 mg, the second - the third - 800 mg, the fourth - the fifth - 500-700 mg, from the sixth day the dose is reduced by 100 mg per day - up to 100 mg. Further, it is necessary to reduce the dose by 10 mg per day - up to 50 mg. After that, they switch to taking the drug orally with a dose reduction of 4-6 mg per day. The final dose of 4 mg is taken for a long time.
7. Diprazine (pipolfen) - 2.5% - 2ml
8. Ascorbic acid 5% - up to 50 ml
9. Ca preparations (calcium gluconate 10%-10 ml)
10. Promedol 2%-2 ml IM
With the development of toxic pulmonary edema:
1. Morphine 1%: 1-1.5 ml in 10-15 ml saline
2. GCS locally and systemically
3. Droperidol 0.25% - 2 ml
4. According to indications - diazepam 0.5% - 2 ml
5. 35% or 40% oxygen-air mixture moistened with defoamer vapors
6. Ganglion blockers: pentamine 5% - 1 ml in 9 ml of saline. solution, in / in 3 ml
7. Furosemide 20-40 mg IV
8. According to indications: anticoagulants, vasopressors (dopamine, norepinephrine)
9. Antibiotic therapy
60) AOXV and OV of general toxic (general toxic action): name the substances of this group; pathogenesis of damage by these poisons; list the characteristic syndromes and symptoms when affected by the above substances; give a detailed description of the protective measures and the full standard of first aid ( including antidote therapy).
Substances: hydrocyanic acid and cyanogen chloride
Pathogenesis: these poisons inhibit those enzymes, which include ferric iron, and above all the enzymes of tissue respiration (cytochromes) and the enzyme that catalyzes the breakdown of hydrogen peroxide - catalase. NS NUCL bind cytochrome oxidase and reduce the level of tissue respiration. As a result, the cells do not receive the necessary energy. First of all, the cells of the central nervous system suffer - shortness of breath develops, blood pressure decreases, the pulse changes, convulsions appear.
Oxygen accumulates in the blood, the amount of oxyhemoglobin increases, which gives the blood and tissues a scarlet color.
Characteristic syndromes and symptoms:
Typical initial signs are bitterness and a metallic taste in the mouth, nausea, headache, shortness of breath, convulsions.
Death occurs from the cessation of myocardial activity.
Two clinical forms:
1. Apoplexy: the affected person screams, loses consciousness, falls; after short-term clonic-tonic convulsions, the muscles relax, tendon reflexes disappear; exophthalmos may be noted; pupils dilated, do not react to light. BP drops sharply. Pulse rare, thready. The skin is pale. After a few breaths, breathing stops. Death occurs within 1-3 minutes
2. Lingering shape:
a) Stage of initial manifestations: smell of bitter almonds, slight irritation of the conjunctiva and mucous membranes of the nasopharynx, numbness of the oral mucosa, anxiety, weakness, dizziness, pain in the heart area, a feeling of increased heartbeat, scarlet skin and mucous membranes, breathing deepens and quickens, pulse changes (slows down), blood pressure rises, vomiting, impaired coordination of movements
b) Stage of shortness of breath: symptoms increase, severe general weakness, urge to defecate becomes more frequent, body temperature decreases, breathes with a full mouth, additional respiratory muscles are involved, the pulse is rare, tense, blood pressure is increased, heart sounds are increased, pupils dilated, deep reflexes are increased, shaky gait, depression of consciousness
c) Convulsive stage: depression of consciousness to coma. tonic-clonic convulsions, replaced by relaxation. Convulsive contractions of the masticatory muscles. Breathing fast, deep. Pulse weak voltage, often arrhythmic. During convulsions, the skin and mucous membranes are cyanotic.
d) Coma stage: no consciousness, skin is pale with a cyanotic tint, temperature is lowered, breathing is shallow, arrhythmic, the pulse is weak filling, blood pressure is low, heart sounds are weakened. Death due to respiratory arrest.
A feature of cyanogen chloride poisoning is irritation of the mucous membrane of the upper respiratory tract - sneezing, coughing, dyspnea, lacrimation.
Protective measures and first aid:
1. Timely use of a gas mask (brands B, B8, M) and protective clothing
2. Neutralization is not carried out on the ground, but the interior is neutralized with a mixture of steam and formalin
3. Salts of senile acid are degassed with a mixture consisting of 2 parts of 10% solution of vitriol and one part of 10% solution of slaked lime
4. Antidote therapy for cyanide damage
Specific cyanide antidotes - methemoglobin formers (nitrites) - anticyan, amyl nitrite, sodium nitrite; sulfur compounds, carbohydrates, cobalt compounds
A. First aid: amyl nitrite - liquid for inhalation use, 0.5 ml ampoules, under a gas mask
B. First aid (paramedic) assistance: anticyan 20% solution in ampoules of 1 ml, IM 3.5 mg/kg or iv 2.5 mg/kg diluted in 10 ml of 40% glucose; oxygen therapy, according to indications - cordiamine 1 ml / m
C. First aid: re-introduction of anticyan in / in 30 minutes, re-in / m injection after 1 hour. In the absence of anticyan - in / in 10-15 ml of 2% sodium nitrite (2-5 ml / min) under the control of blood pressure. With a weakening of cardiac activity, analeptics are used (1 ml of cordiamine / m); sodium thiosulfate 20-30 ml 30% solution in/in; glucose 40 ml 40% solution IV, oxygen therapy, administration of cytochrome C, vitamins of group B, according to indications - analeptics, pressor amines
Question #61: OV and AOCHV of nerve-paralytic action: name the substances of this group, the pathogenesis of damage by these poisons, list the characteristic syndromes and symptoms in case of damage to the above substances, give a detailed description of protective measures and a full standard of first aid (including antidote therapy).
Substances of this group Key words: tabun, sarin, soman, VX.
Pathogenesis : Organophosphate poisons bind to synapse cholinesterase. The phosphorylated cholinesterase enzyme loses its activity. Inhibition of cholinesterase leads to the accumulation of acetylcholine, disruption of synaptic transmission. There is an excitation of cholinergic receptors, as FOV can have a direct cholinomimetic effect on the postsynaptic membrane, increase the sensitivity of the synapse to acetylcholine.
Clinical picture :
7. central action (anxiety, emotional lability, dizziness, tremor, clonic-tonic convulsions, impaired activity of the respiratory and vasomotor centers, depression of consciousness)
8. muscarine-like action (spasm of smooth muscles, hypersecretion of glands, hypotension, bradycardia)
9. nicotine-like action (muscle weakness, flaccid paresis and paralysis, tachycardia and hypertension)
Protective measures : use of a filtering gas mask, protective clothing, partial sanitization with a liquid from an individual anti-chemical bag, a weak solution of alkali in case of contact with the skin, in case of contact with the eyes, rinse with water, in case of contact with the stomach, induce vomiting, make a gastric tube lavage and give sorbents.
Antidote therapy :
6. Antidote P-10M is used when there is a threat of injury or in the first minutes of intoxication. The drug contains a reversible cholinesterase inhibitor, central anticholinergics and an antioxidant, a tablet of 0.2 grams.
7. Athens in a syringe tube of 1 ml. The drug contains central M-and N-holinolytics, phenamine.
8. Budaxim in a syringe tube of 1 ml. It consists of N- and M-anticholinergic. Entered in \ m.
9. Atropine sulfate 0.1% - M-anticholinergic. In mild forms, IM 1-2 ml, repeated injections of 2 ml IM with an interval of 30 minutes are possible. With a moderate lesion: 2-4 ml intramuscularly, after 10 minutes again 2 ml. In case of severe lesions: 4-6 ml intravenously, again 2-4 ml intramuscularly in 3-8 minutes.
10. Dipiroxime 15% in 1 ml ampoules - cholinesterase reactivator. With a mild degree of damage: 1 ml intramuscularly, after 1-2 hours, again 1 ml. With an average degree: 1-2 ml / m, after 1-2 hours again. For severe lesions: 450-600 mg IV.
11. Equally important is oxygen therapy and all measures to ensure airway patency and respiratory support + anticonvulsant therapy + vasopressors + infusion therapy.
Question #62: Psychomimetic agents (psychomimetics): name the substances of this group, the pathogenesis of damage by these poisons, list the characteristic syndromes and symptoms in case of damage to the above substances, give a detailed description of protective measures and a full standard of first aid (including antidote therapy).
Substances of this group : BZ, lysergic acid diethylamide (DLA), bufotenine, mescaline.
Pathogenesis :
· BZ. The mechanism is due to the blockade of central muscarinic cholinergic receptors and impaired cholinergic transmission in the GM. BZ molecules form a strong complex with M-cholinergic receptors. Due to prolonged blockade of these receptors, the circulation of acetylcholine in synapses is disrupted, morphological damage to the synaptic apparatus develops, which leads to an imbalance in neurotransmitter systems.
· DLK. The ability of this psychotoxicant to cause excitation of the serotonergic, adrenergic and cholinergic systems is noted. There is reason to believe that lysergic psychosis is associated with a violation of the mediator synaptic balance: due to damage to the serotonergic system, the adrenergic and cholinergic systems suffer.
Clinical picture :
7) BZ. Defeats mild severity occur after 1-5 hours: general lethargy, inactivity, low speech activity, drowsiness, mydriasis and accommodation disturbances are possible. Defeats moderate severity occur after 1-2 hours, there is an alternation of delirium syndromes and mild stupor. Periods of clouding of consciousness coincide with manifestations of psychomotor agitation. Illusions and hallucinations are visual, objective. Orientation in space is periodically disturbed. The pulse is speeded up, blood pressure is increased. A severe lesion is formed in 20 minutes - an hour and a half. Prolonged and deep stupefaction of consciousness and sharp psychomotor agitation are characteristic. Disturbed orientation in time and space. Speech contact is not possible, hallucinatory cider is pronounced, various types of hallucinations. Severe mydriasis and disturbances of accommodation. Ataxia is rough, with falls. Dysphonia and dysarthria. The blood pressure is increased, the pulse is quickened. Tachypnea, urinary retention and intestinal atony.
8) DLK. Dizziness, general weakness, nausea, tremor, blurred vision. Distortion in the perception of shapes and colors, difficulty focusing vision on an object. Various mental disorders. Signs of intoxication appear after 20-60 minutes. Reach maximum development in 1-5 hours. Intoxication lasts 8-12 hours.
Protective measures : BZ- gas mask, ChSO, aminostigmine 0.1% 2ml IM, galantamine 0.5% 2ml IM. In the absence of effect, re-introduction. Also, these drugs can be administered intravenously in a 5% glucose solution. With severe psychomotor agitation: triftazin 0.2% 2ML, haloperidol 0.5% 2ml + phenazepam 5 mg per dose. 1% morphine 2ml, anaprilin 0.1% 1ml i/m. Prevention of overheating of the patient. DLK- timely putting on a gas mask, CHSO, antipsychotics, symptomatic therapy.
Question #63: Agents of blistering action: name the substances of this group, the pathogenesis of damage by these poisons, list the characteristic syndromes and symptoms in case of damage to the above substances, give a detailed description of protective measures and a full standard of first aid (including antidote therapy).
Substances of this group : distilled mustard gas, lewisite.
Pathogenesis : mustard gas have both local and resorptive effects on the body. The first is manifested in the development of necrotic inflammation of tissues at the site of entry and penetration into the body. Resorptive action is expressed in a complex symptom complex. There are several leading mechanisms in the pathogenesis of mustard lesions:
4) allergic - a protein + mustard complex is formed, for which antibodies are produced, sensitization and an allergic reaction develop;
5) local action - alkylation of proteins, leading to the destruction of cells;
6) cytostatic effect - as a result of damage to RNA, cell division is disrupted;
7) shock-like effect - develops as a result of blocking a number of body enzymes.
Lewisite binds to enzymes containing sulfur, they are involved in tissue respiration. Foci of necrosis develop in those places where lewisite enters with blood flow. Increases blood clotting, which leads to thrombosis.
Clinical picture :
7. Mustard gas - skin lesions are divided into 3 periods (hidden, erythema stage, vesicular-bullous, ulcerative-necrotic, healing stage); eye damage - catarrhal conjunctivitis, blepharospasm, keratoconjunctivitis; inhalation lesions (mild degree - dryness, runny nose, hoarseness, catarrh of the mucous membranes of the respiratory tract; moderate degree - mustard gas tracheobronchitis, pain behind the sternum, protracted bronchitis: severe degree - mustard pneumonia and necrotic lesions of the mucous membranes); oral lesions - pain in the stomach, salivation, nausea, vomiting, diarrhea; resorptive effect - subfebrile temperature, temperature 38-40 degrees (keeps for 2 weeks, then quickly decreases), shock-like states.
8. Lewisitis - local manifestations (bubbles form that do not tend to merge, tense, surrounded by a bright red corolla of hyperemia, deep tissue necrosis), inhalation lesions (catarrhal rhinopharyngitis, pulmonary edema, chemical burn of the lung, necrotic pneumonia), oral manifestations - education ulcers, lewisite intoxication.
Protective measures : mustard gas- the use of a filtering gas mask, protective clothing, partial sanitization with a liquid from an individual anti-chemical bag, or 10-15% aqueous-alcoholic solution of chloramine, treat the skin with a 2% solution, open the blisters with a sterile needle, treat the surface with a disinfectant solution, inhale in case of inhalation damage ficilin under a gas mask mask, nasopharyngeal and oropharyngeal cavities are washed with a 0.25% solution of chloramine, abundant gastric lavage with a 2-4% aqueous solution of baking soda, activated charcoal. Complex treatment - in / in a 30% solution of sodium thiosulfate 20-30 ml (repeat every 3-4 hours), in order to detoxify 4% sodium bicarbonate. If mustard gas enters the stomach to remove the poison, it is recommended to induce vomiting, wash the stomach with water, or with a 0.02% soda solution, then introduce an adsorbent (25 g of activated carbon in 100 ml of water) and a saline laxative. To combat the phenomena of general poisoning, the following are used: sodium thiosulfate in a 30% solution of 25-50 ml, administered intravenously in order to enhance the processes of neutralization of mustard gas in the body, glucose in a 40% solution of 20-40 ml intravenously, as having a beneficial effect on the heart - vascular disorders, respiratory function of the blood and normalizing impaired metabolism; calcium chloride - 10% intravenous solution of 10 ml, as a means of relieving itching, local inflammatory reactions and reducing the effects of general intoxication; blood substitutes such as polyvinylpyrrolidone (250 ml each), which have a noticeable detoxifying effect; antihistamines, vascular agents (cordiamin, caffeine, ephedrine); if necessary - and heart preparations (strophanthin, corglicon); sodium bicarbonate in a 2% solution of 500 ml intravenously to eliminate the acidotic shift. Lewisite- gas mask, protective clothing, 10-15% aqueous-alcoholic solution of chloramine (neutralization on the skin), 0.25% solution of chloramine for the eyes, if it enters the stomach, wash with 2% solution of baking soda, in case of inhalation damage, anti-smoke mixture. Unithiol - in / m or in / in at the rate of 1 ml per 10 kg, dicaptol 2.5-3 mg / kg / m, berlition - in / in 300 mg in 250 ml of 0.9% NaCl.
Question #64: Irritating agents (lachrymators and sternites): name the substances of this group, the pathogenesis of damage by these poisons, list the characteristic syndromes and symptoms when affected by the above substances, give a detailed description of protective measures and a full standard of first aid (including antidote therapy).
Substances of this group : lachrymator, sternite, CS, CR.
Pathogenesis : these substances affect the sensitive nerve endings of the mucous membranes of the upper respiratory tract and irritate the mucous membranes of the eyes.
Clinical picture : feeling of tickling, soreness, burning in the nose and throat, headache and toothache, in the ears, rhinorrhea, dry painful cough, salivation, nausea, vomiting, mucous membranes are hyperemic, edematous, bradycardia, bradypnea. In severe cases, sensitivity disorder, muscle weakness. Lesions with lachrymators are characterized by a sharp irritation of the conjunctiva and cornea + the above symptoms. When CS is affected, an irritating effect on the skin + the above symptoms still occurs.
Protective measures : filtering gas mask, skin protection, rinsing the mouth and nasopharynx with water or 2% sodium bicarbonate, the affected eyes are washed with water, 2 drops of 0.5% dicaine solution into the conjunctival sac, non-narcotic analgesics, tranquilizers, ficilin inhalations to eliminate reflex disorders.
Question #65: Ammonia: pathogenesis of damage to these AOCs, list the characteristic symptoms and syndromes in case of damage to the above substance, give a detailed description of protective measures and a full standard of first aid.
Clinical picture : under the influence of small concentrations of ammonia, mild phenomena of rhinitis, pharyngitis, tracheitis, bronchitis are observed. The duration of poisoning is 3-5 days. When exposed to high concentrations, there is a strong cough, pain and tightness in the chest, diffuse mucopurulent bronchitis. In some cases, at very high concentrations of ammonia, pulmonary edema, spasm of the glottis, and pneumonia occur. With eye damage, lacrimation, photophobia, eyelid spasm, conjunctivitis are observed; if liquid ammonia gets on the skin, a burn with erythema and blisters is observed. Ammonia vapors cause more erythema.
Protective measures :
9. the victim should immediately be taken out of the affected area;
10. if it is impossible to leave the affected area, it is important to provide oxygen access;
11. the mouth, throat and nose are washed with water for about 15 minutes (additional rinsing is provided by adding citric or glutamic acid to the water);
12. during the next day after the defeat, absolute rest is provided, which is important even with a slight degree of poisoning;
13. 0.5% solution of dicaine should be used for the eyes, additionally they can be closed with a bandage;
14. if poison gets on the skin area, rinse it with water as soon as possible, then apply a bandage;
15. Getting poison into the stomach requires washing it.
Acute poisoning with a drug from the group of benzodiazepines: pathogenesis of the lesion; description of the clinical picture (characteristic symptoms); a detailed description of the provision of assistance - first and pre-medical; first medical (including measures to remove unabsorbed poison and antidote therapy).
Pathogenesis
Inhibition in the CNS is achieved by stimulation of GABA A receptors with an increase in the flux of chloride ions. In addition, the inactivation and reuptake of adenosine is suppressed, which leads to stimulation of adenosine receptors.
Clinic
The state of intoxication with hypnotics generally resembles alcohol intoxication. Characteristic features are increasing lethargy, drowsiness, and discoordination of movements. The affective sphere is characterized by emotional lability. A mild degree of habitual intoxication may initially be accompanied by an increase in mood. But at the same time, fun, a feeling of sympathy for the interlocutor can easily turn into anger, aggression towards others. Motor activity increases, but the movements are erratic, not coordinated. Sexual desire may increase, appetite may increase.
For intoxication with hypnotics and sedatives of moderate and severe severity, severe somatic and neurological disorders are characteristic. Often there is hypersalivation, hyperemia of the sclera. The skin becomes sebaceous.
With an increase in the degree of intoxication, a person falls asleep, a deep sleep. Bradycardia and hypotension are noted. The pupils are dilated, their reaction to light is sluggish, nystagmus, diplopia, dysarthria, decreased superficial reflexes and muscle tone, and ataxia are noted. There may be involuntary defecation, urination. With severe intoxication, oppression of consciousness increases, deep sleep turns into a coma. Arterial pressure falls sharply, the pulse is frequent, superficial. Breathing is shallow, frequent, with the deepening of the coma becomes rare, even more superficial, acquires periodicity (Cheyne-Stokes breathing). The patient turns pale sharply, body temperature drops, deep reflexes disappear.
characteristic feature traumatic shock is the development of pathological deposition of blood. Concerning the mechanisms of pathological deposition of blood, it should be noted that they are formed already in the erectile phase of shock, reaching a maximum in the torpid and terminal stages of shock. The leading factors of pathological blood deposition are vasospasm, circulatory hypoxia, the formation of metabolic acidosis, subsequent degranulation of mast cells, activation of the kallikrein-kinin system, the formation of vasodilatory biologically active compounds, microcirculation disorders in organs and tissues, characterized initially by prolonged vasospasm. Pathological deposition of blood leads to the exclusion of a significant part of the blood from the active circulation, exacerbates the discrepancy between the volume of circulating blood and the capacity of the vascular bed, becoming the most important pathogenetic link in circulatory disorders in shock.
An important role in the pathogenesis of traumatic shock is played by plasma loss, which is caused by an increase in vascular permeability due to the action of acid metabolites and vasoactive peptides, as well as an increase in intracapillary pressure due to blood stasis. Plasma loss leads not only to a further deficit in the volume of circulating blood, but also causes changes in the rheological properties of the blood. At the same time, the phenomena of aggregation of blood cells, hypercoagulation with the subsequent formation of DIC syndrome develop, capillary microthrombi are formed, completely interrupting the blood flow.
Under conditions of progressive circulatory hypoxia, there is a deficiency in the energy supply of cells, suppression of all energy-dependent processes, pronounced metabolic acidosis, and an increase in the permeability of biological membranes. There is not enough energy to ensure the functions of cells and, above all, such energy-intensive processes as the operation of membrane pumps. Sodium and water rush into the cell, and potassium is released from it. The development of cell edema and intracellular acidosis leads to damage to lysosomal membranes, the release of lysosomal enzymes with their lytic effect on various intracellular structures.
In addition, during shock, numerous biologically active substances, which enter the internal environment of the body in excess, exhibit a toxic effect. Thus, as shock progresses, another leading pathogenetic factor, endotoxemia, comes into play. The latter is also enhanced by the intake of toxic products from the intestine, since hypoxia reduces the barrier function of the intestinal wall. Of particular importance in the development of endotoxemia is a violation of the antitoxic function of the liver.
Endotoxemia, along with severe cellular hypoxia caused by a crisis of microcirculation, restructuring of tissue metabolism to the anaerobic pathway, and impaired ATP resynthesis, plays an important role in the development of irreversible shock phenomena.
trauma shock clinic pathogenesis
Of the numerous theories of the pathogenesis of traumatic shock, neurogenic, plasma and blood loss, as well as toxemic, deserve attention. However, each of the listed theories in the form in which it was proposed by the authors with a claim to universality does not stand up to serious criticism.
neurogenic theory- proposed by Krail in the First World War as a theory of exhaustion, supported by scientists of our country (N.N. Burdenko, I.R. Petrov). As a result of excessive irritation, exhaustion occurs in the cells of the cerebral cortex, and to prevent them from dying, diffuse inhibition develops, which then spreads to subcortical formations, resulting in depression of the centers of respiration and blood circulation, a decrease in temperature, etc. However, numerous clinical observations and experimental data do not fit into this theory. Firstly, diffuse inhibition is observed during sleep and anesthesia, and during shock, the wounded person is conscious. Secondly, if inhibition begins in the cortex to protect it from exhaustion and death, then this contradicts evolution and the emergence of man: inhibition must arise in older structures to protect younger ones from death. Thirdly, neurophysiologists have proven that inhibition is not a passive process, but an active one, and it occurs in the thalamic region, so the excess flow of impulses does not enter the reticular formation, which is responsible for the emotional coloring of human behavior, and the cerebral cortex. Therefore, indifference, indifference to the environment, adynamia and others are striking. symptoms of torpidity, but these are not symptoms of diffuse inhibition! An attempt to use stimulants in the treatment of severe shock has not paid off. However, this theory should not be simply discarded. From the standpoint of neurogenic theory, the trigger mechanism of shock can be explained.
Theory of plasma and blood loss most common among American scientists, but has a significant number of supporters in our country (A.N. Berkutov, N.I. Egurnov). Indeed, with any mechanical injury, blood loss is observed. So, with a closed fracture of the femur, even without damage to the main vessels, it can be up to 1.5 liters, but not all at once, but during the day, and thus, from the standpoint of this theory, it is impossible to explain the triggering mechanism of shock. In the future, circulatory disorders in both traumatic shock and hemorrhagic shock are of the same type. Microcirculation disorders have been especially well studied.
Theory of toxemia proposed in 1918 by the American pathophysiologist W. Kennon. Of course, toxemia occurs, especially in the late period, as toxins accumulate due to impaired peripheral circulation. Therefore, in the treatment it is necessary to include drugs for detoxifying the body, but not to start with them! From the standpoint of this theory, it is also impossible to explain the triggering mechanism of shock. It is suitable for explaining the pathogenesis of tourniquet shock and traumatic toxicosis.
An attempt to combine these three theories into one has not yet found wide support, although many scientists, including extreme supporters of the theory of blood loss (G.N. Tsybulyak, 1994), recognize the presence of all three mechanisms in the pathogenesis of shock. The essence of the idea is that at each separate stage of the post-traumatic reaction, one of the factors is the leading cause of shock, and at the next stage, another.
So, the trigger is a neurogenic factor: a powerful stream of specific pain and nonspecific afferent impulses enters the central nervous system (thalamus as the main collector of all types of sensitivity). Under these conditions, in order to survive at this moment from imminent death, a new emergency functional system (EFS) is formed in order to adapt the functions of the body to the suddenly changed conditions of existence. Thus, the main meaning of the inclusion of new regulatory mechanisms is to transfer from a high level of vital activity to a more ancient, primitive level that ensures the activity of the heart and central nervous system by turning off all other organs and systems. Hypobiosis develops (according to D.M. Sherman), which is clinically manifested by a drop in blood pressure, the onset of adynamia, a decrease in muscle and skin temperature, and as a result of all this (which is extremely important!) - a decrease in oxygen consumption by tissues! If the CFS does not have time to form, then in case of severe trauma, primary collapse and death occur. Thus, from a general biological point of view, shock is a protective reaction of the body.
At the second stage of the post-traumatic reaction, circulatory disorders are the leading link in the pathogenesis of shock.(according to the theory of blood loss), the essence of which can be reduced to the following:
- 1. “Centralization of blood circulation” - after a drop in blood pressure, under the influence of adrenaline and norepinephrine released into the blood at the time of injury, a spasm of arterioles and precapillaries occurs, due to this, the total peripheral resistance of the arteries increases, blood pressure rises and venous return of blood to the heart is ensured, but the tissues are cut off from the "blood supply".
- 2. The second adaptive reaction is the opening of arterio-venous shunts, through which blood bypassing the capillaries immediately enters the veins.
- 3. Disturbances of microcirculation - in disconnected tissues, a large amount of under-oxidized products accumulate, including histamine-like ones, under the influence of which capillary sphincters open, and blood rushes into dilated capillaries. There is a discrepancy between the BCC and the increased capacity of functioning capillaries (“bleeding into own capillaries”). In dilated capillaries, blood flow is slowed down. At the same time, under conditions of hypoxia, the porosity of the capillary wall increases, and the liquid part of the blood begins to go into the interstitial space, the electrostatic charge of the erythrocyte membrane decreases, their mutual repulsion decreases, and so-called. "slugs" of erythrocytes. Develops DIC (disseminated intravascular coagulation). Violations of microcirculation become universal. As a result, generalized hypoxia develops, i.e. all tissues and organs are affected
Signals are sent to the CNS about a continuing deterioration in the nutrition of organs, and, according to the feedback law, a new NFS is formed upon recovery from shock. However, if it fails, the process progresses.
At the third stage of the post-traumatic reaction, the leading factor in the development of shock is toxemia.. All toxins can be divided into 3 groups. The first is the decay products of tissues damaged at the time of injury. The second is under-oxidized metabolic products. Under conditions of hypoxia, all types of metabolism suffer, primarily carbohydrate metabolism. Under normal conditions, during the aerobic oxidation pathway, 38 ATP molecules are formed from one glucose molecule, which are used to replenish energy costs that ensure the vital activity of the cell. During hypoxia, the anaerobic oxidation pathway predominates, in which one glucose molecule gives only two ATP molecules with the formation of a huge amount of underoxidized products. Glucose consumption is clearly uneconomical - “this is a high road to death” (V.B. Lemus). Glucose reserves are quickly depleted, which leads to neoglycolysis: fats and proteins become energy sources, and again with the formation of underoxidized products. In addition, due to hypoxia, individual cells die with the release of cellular (lysosomal) enzymes into the blood, which leads to self-poisoning of the body. The third group of toxins are toxins of the intestinal flora that enter the bloodstream from the intestinal lumen, since the porosity of the intestinal wall increases during hypoxia. Due to hypoxia, the barrier and detoxification functions of the liver are sharply impaired. With low blood pressure, the kidneys do not work. Therefore, toxins are not excreted from the body. The irreversibility of shock is formed.
Thus, the trigger mechanism of shock is a neurogenic factor, then circulatory disorders become dominant, and at the third stage - toxemia. Such an understanding of the pathogenesis of shock provides a rational construction of a shock treatment program.
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 to the chest and abdomen
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 is defined as the most common clinical form of a serious 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 of acute circulatory disorders (hypocirculation), which occurs as a result of the combined effect on the body of the wounded person of the life-threatening consequences of trauma - 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 circulatory failure, 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 the fact that 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 a 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 of the vascular wall itself, its permeability increases, the liquid part of the blood goes into the interstitium, and 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 elevated.
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 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.
