Types of shock Pain, cardiogenic, hypovolemic, infectious toxic shock. General principles of emergency care for shock. SHOCK - Big Medical Encyclopedia

A state of shock is a reaction of the body to traumatic external stimuli, designed, in essence, to support the vital activity of the victim. However, depending on the history of the origin of the shock state, as well as on the individual characteristics of the organism, it can have the opposite, destructive effect.

There are 4 degrees of shock.

1. It is characterized by inhibition of the reaction of the victim and an increase in heart rate up to 100 beats per minute.
2. The pulse rises already to 140 beats per minute, and the systolic pressure drops to 90-80 mm. The reaction is just as inhibited as in the first degree, but in this situation, the implementation of appropriate anti-shock actions is already required.
3. A person does not react to the environment, speaks only in a whisper, and his speech, as a rule, is incoherent. The skin is pale, the pulse is almost not palpable, only on the carotid and femoral arteries. The frequency of beats per minute can reach 180. This condition is characterized by increased sweating and rapid breathing. The pressure drops to 70 mm.
4. This is a terminal state of the body, the negative consequences of which are irreversible. The heartbeat in this case is almost impossible to hear, the state is more unconscious, and breathing is accompanied by convulsive contractions. A person does not respond to external stimuli, and the skin has a cadaverous hue, and the vessels are clearly visible.

Signs of shock

Depending on the degree, the signs of a shock state are different. But it always starts the same way: with a decrease in systolic pressure and an increase in heart rate. Another invariable accompaniment in this case is a slight inhibition of the reaction. That is, a person can answer questions, but at the same time react weakly to what is happening, and sometimes not understand at all where he is and what happened to him.

Causes of shock

Depending on the cause of the shock, there are several types of it.

• hypovolemic shock. Hypovolemic shock is caused, as a rule, by a sudden loss of a large amount of fluid by the body.
• Traumatic. Traumatic is usually a consequence of a recent injury, such as an accident, electric shock, etc.
• Anaphylactic. Anaphylactic is caused by the ingestion of substances that provoke an acute allergic reaction.
• Pain endogenous. Painful endogenous occurs with acute pain associated with diseases of the internal organs.
• Post-transfusion. Post-transfusion may be a reaction to an injection
• Infectious-toxic. Infectious-toxic - shock provoked by severe poisoning of the body.

In any case, this is not an exhaustive list of causes of shock. After all, a lot depends on the person himself and on the circumstances in which he finds himself.

Symptoms

Shock Symptoms

The symptomatology of a shock state depends not only on the degree, but also on its cause. Each variety manifests itself in different ways, with some with less, some with more consequences. But initially, the onset of a state of shock is characterized by an increase in the number of pulse beats per minute, a decrease in systolic pressure, and blanching of the skin.

In cases of anaphylactic shock, bronchospasm may occur, which, if untimely first aid is provided, can lead to death. In hypovolemic shock, a vivid symptom will be constant and intense thirst, because there is a violation of the water-salt balance in the body.

Moreover, we are talking here not only about the loss of blood: the fluid from the body can be actively excreted with vomit and liquid feces. That is, any poisoning with its characteristic features can cause hypovolemic shock. If we are talking about pain endogenous shock, then it all depends on which organ suffers. The primary state of shock may be accompanied by pain in it.

First aid

First aid for shock

First of all, it is necessary to visually inspect the victim and try to determine what caused the state of shock. If necessary, ask him a few clarifying questions. Further, if you did not find any external injuries, carefully give the patient a horizontal position.

If vomiting or bleeding from the mouth is observed, turn his head to the side so that he does not choke. In the event that the victim has a back injury, in no case should he be moved or laid down. You need to leave it in the position in which it is currently located. Provide first aid if open wounds are found: bandage, treat, apply a splint if necessary.

Before the arrival of the ambulance team, monitor the main vital signs, such as pulse, heart rate, breathing.

Features of the treatment of shock conditions

Before prescribing treatment for a shock condition, it is necessary to find out the cause of its origin and. whenever possible. eliminate it. With hypovolemic shock, it is necessary to compensate for the volume of fluid lost with the help of blood transfusions, droppers, etc. This happens, for example, with mountain sickness. To saturate the body with oxygen, oxygen therapy is used in the form of inhalations.

In anaphylactic shock, antihistamines are introduced into the body, and if it comes to bronchospasm, the method of artificial lung ventilation is used. Traumatic shock is eliminated by the introduction of painkillers. Relief may not come immediately. It all depends on the severity of the injury.

The shock caused by poisoning is corrected by removing poisonous toxins from the body. Moreover, in this case, it is necessary to act quickly: if the poisoning is severe, the consequences may be irreversible. With pain endogenous shock, timely assistance will help to get rid of it, and in the future - complex therapy aimed at treating the disease. causing shock.

How long does shock last?

There is no average number of hours that indicate how long a shock can last. A very average indicator suggests that the state of shock can last up to two days. But, as with treatment, it all depends on the type and severity of the injury or other ailment. It also depends on

SHO K I E G O P R O Y A L E N I A

The term "shock" means a blow in translation. .

This is a critical state of the body, between life and death, characterized by deep disorders and depression of all vital functions (respiration, blood circulation, metabolism, liver, kidney functions, etc.). A state of shock can occur with severe injuries, extensive burns and large blood loss. Pain, cooling of the body, hunger, thirst, shaking transportation of the victim contribute to the development and deepening of shock.

Shock is an active defense of the body against environmental aggression..

Depending on the cause that causes the development of a shock state, there are:

1. Shock due to external causes: - traumatic, resulting from mechanical trauma (wounds, bone fractures, tissue compression, etc.);

- burn associated with burn injury (thermal and chemical burns);

- cold , low temperature developing;

- electric resulting from an electrical injury.

2. Shock caused by exposure to internal causes:

- hemorrhagic resulting from acute and massive blood loss;

- To cardiogenic developing with myocardial infarction;

- With optic, which is a consequence of a general purulent infection in the body.

When a person is faced with the threat of death, his body in a state of stress releases a huge amount of adrenaline.

REMEMBER! A colossal release of adrenaline causes a sharp spasm of the precapillaries of the skin, kidneys, liver and intestines.

The vascular network of these and many other organs will be practically excluded from the blood circulation. And such vital centers as the brain, heart, and partly the lungs will receive much more blood than usual. There is a centralization of blood circulation in the hope that after overcoming the extreme situation, they will again be able to start normal life.

REMEMBER! The loss of 1.5 - 2 liters of blood is compensated only due to the spasm of the skin vessels and its exclusion from the blood circulation.

That is why in the first minutes of shock, thanks to the spasm of the precapillaries and a sharp increase peripheral resistance(PS), the body manages not only to maintain the level of blood pressure within normal limits, but also to exceed it even with heavy bleeding.

The first signs of shock development:

Sharp blanching of the skin;

Emotional and motor excitement;

Inadequate assessment of the situation and one's condition;

Absence of complaints of pain even with shockogenic injuries.

The ability to forget about pain at the moment of mortal danger is explained by the fact that a morphine-like substance is produced in the subcortical structures of the brain - endomorphinol( internal, own morphine). Its drug-like action induces a state of mild euphoria and relieves pain even in severe injuries.

On the other hand, pain activates functions endocrine glands and especially the adrenal glands. It is they who secrete the amount of adrenaline, the action of which will cause a spasm of the precapillaries, an increase in blood pressure and an increase in heart rate.

The adrenal cortex secretes and corticosteroids (their analogue is synthetic - prednisolone), which significantly accelerates the metabolism in tissues.

This allows the body to throw out the entire supply of energy in the shortest possible time and concentrate efforts as much as possible in order to get away from danger.

There are two phases of shock:

- short-term erictile(excitation period) phase occurs immediately after the injury and is characterized by motor and speech excitation, as well as complaints of pain. With full preservation of consciousness, the victim underestimates the severity of his condition. Pain sensitivity is increased, the voice is deaf, the words are jerky, the look is restless, the face is pale, the blood pressure is normal or high. An excited state quickly (within a few minutes), less often gradually, turns into an oppressed one, accompanied by a decrease in all vital functions.

- torpid phase (period of oppression: lat. torpidum - inhibition) is characterized by general weakness and a sharp drop in blood pressure. Breathing becomes frequent and superficial. The pulse is frequent, uneven, threadlike (hardly palpable). The face is pale, with an earthy tint, covered with cold clammy sweat. The victim is lethargic, does not answer questions, treats others indifferently, pupils are dilated, consciousness is preserved. In severe cases, vomiting and involuntary urination may occur.

This phase usually ends in death and is considered irreversible..

If within 30-40 minutes the victim does not receive medical care, then prolonged centralization of blood circulation will lead to gross violations of microcirculation in the kidneys, skin, intestines and other organs excluded from blood circulation. Thus, what played a protective role at the initial stage and gave a chance for salvation will become the cause of death in 30-40 minutes.

A sharp decrease in the rate of blood flow in the capillaries, up to a complete stop, will cause a violation of oxygen transport and the accumulation of incompletely oxidized metabolic products in the tissues - acidosis, lack of oxygen - hypoxia and necrosis in a living organism of individual organs and tissues - necrosis.

This stage is very quickly replaced by agony and death. .

A COMPLEX OF ANTI-SHOCK MEASURES.

It is necessary to free the victim from the action of the traumatic factor;

Ensure bleeding stops

To stabilize breathing, provide an influx of fresh air and give a position that ensures breathing;

Give painkillers (analgin, baralgin, pentalgin);

Give funds that tonic the activity of the cardiovascular system (corvalol - 10-15 drops, cordiamine, tincture of lily of the valley);

The victim should be warmed;

Give plenty of warm drink (tea, coffee, water with the addition of salt and baking soda - 1 teaspoon of salt and 0.5 teaspoon of soda per 1 liter of water);

Perform immobilization of injured body parts;

In case of cardiac arrest and breathing, urgent resuscitation measures should be taken (ventilation, external heart massage);

THE INJURED SHOULD NOT BE LEFT ALONE!

Shock (from the English shock - blow, concussion or French choc - push, blow) is an extreme condition resulting from the action of pathogenic factors of extreme force on the body and which is characterized by hemodynamic disturbances with a critical decrease in capillary circulation (tissue perfusion) and progressive violation of all life support systems of the body.

The main manifestations of shock reflect disorders of microcirculation and peripheral circulation (pale or marbled, cold, moist skin), central hemodynamics (decrease in blood pressure), changes in the central nervous system, mental status (lethargy, prostration), dysfunction of other organs (kidneys, liver, lungs, heart, etc.) with the natural development and progression of failure of many organs, if emergency medical care is not provided.

Etiology

Shock can be caused by any pathogenic factors that can disrupt homeostasis. They can be exogenous and endogenous, but they are extremely strong. The action of such factors and the changes that occur as a result of this in the body are potentially fatal. These factors, in strength or duration of action, exceed the limit that can be called the “shock threshold”. So, with bleeding, this is a loss of more than 25% of the BCC, with burns, more than 15% of the body surface is damaged (if more than 20%, shock always develops). Nevertheless, when evaluating the effect of shockogenic factors, it is imperative to take into account the previous state of the body, which can significantly affect these indicators, as well as the presence of influences that can enhance the effect of pathogenic factors.

Depending on the cause of the shock, about 100 different variants of it are described. The most common types of shock are: primary hypovolemic (including hemorrhagic), traumatic, cardiogenic, septic, anaphylactic, burn (combustion; Scheme 23).

Pathogenesis

The shockogenic factor causes changes in the body that go beyond the adaptive and compensatory capabilities of its organs and systems, resulting in a threat to the life of the organism. Shock is a “heroic fight against death”, which is carried out by the maximum tension of all compensatory mechanisms, their sharp systemic activation. At the usual level of pathological influences on the body, compensatory reactions normalize the deviations that have arisen; response systems “calm down”, their activation stops. Under the conditions of the action of factors that cause shock, the deviations are so significant that compensatory reactions are not able to normalize the parameters of homeostasis. The activation of adaptive systems is prolonged and intensified, becoming excessive. The balance of reactions is disturbed, they become out of sync, and at a certain stage they themselves cause damage and worsen the condition of the body. Numerous vicious circles are formed, processes tend to self-sustain and become spontaneously irreversible (Fig. 58). In the future, there is a progressive narrowing of the range of adaptive reactions, simplification and destruction of functional systems that provide compensatory reactions. The result of this is the transition to "extreme regulation" - the gradual disconnection of the CNS from afferent influences, which normally carry out complex regulation. Only the minimum of afferentation necessary to ensure respiration, blood circulation and several other vital functions is preserved. At a certain stage, the regulation of vital activity may pass to an extremely simplified metabolic level.

For the development of most types of shock, a certain period of time is necessary after the action of an aggressive factor, since if the body dies immediately, the state of shock does not have time to develop. For the deployment of compensatory reactions in shock, the initial anatomical and functional integrity of the nervous and endocrine systems is also necessary. In this regard, craniocerebral injuries and primary coma are usually not accompanied by a clinical picture of shock.

At the beginning of the action of the shockogenic factor, the damage is still localized, the specificity of the response to the etiological factor remains. However, with the advent of systemic reactions, this specificity is lost, shock develops along a certain path common to its various types. The features inherent in these individual species are only added to it. Such common links in the pathogenesis of shock are:

1) deficiency of effectively circulating blood volume (ECV), which is combined with a decrease in cardiac output and an increase in total peripheral vascular resistance;

2) excessive release of catecholamines, stimulated by uncorrected hypovolemia, hypotension, hypoxia, acidosis, etc.;

3) generalized release and activation of a large number of biologically active substances;

4) violation of microcirculation - the leading pathogenetic link of the shock state;

5) decrease in blood pressure (however, the severity of the state in shock does not depend on the level of pressure, but mainly on the degree of impaired tissue perfusion);

6) hypoxia, which results in insufficient energy production and
damage to cells under conditions of their increased load;

7) progressive acidosis;

8) development of dysfunction and insufficiency of many organs (multiple organ failure).

In the development of shock, the following main stages can be schematically distinguished:

1) neuroendocrine stage, consisting of:

Perception of information about damage;

Central integration mechanisms;

Neurohormonal efferent influences;

2) hemodynamic stage, which covers:

Changes in systemic hemodynamics;

Violation of microcirculation;

Interstitial lymphatic disorders;

3) cellular stage, which is divided into states:

metabolic stress;

metabolic exhaustion;

Irreversible damage to cellular structures.

These stages condition each other and can occur simultaneously. In the development of each stage, phases are distinguished:

functional changes;

Structural reversible disorders;

irreversible changes.

neuroendocrine responses. In the development of a state of shock, there are always changes in the functions of the nervous system, characterized by a certain sequence and cyclicity. The nervous system receives information about the deviations that have arisen as a result of the action of the shockogenic factor. Reactions are launched aimed at saving the life of the organism, but they are extremely intense, become out of sync, unbalanced. First, excitation of the cerebral cortex develops due to the action of massive afferent impulses entering the central nervous system from the periphery (erectile stage). The cortex causes excitation of subcortical structures, and they, in turn, excite the cortex; positive feedbacks are formed. Excitation is exaggerated. This is also facilitated by the ascending activating influences of the reticular formation. At the same time, the synthesis of GABA is significantly slowed down, the content of opioid peptides (opiates) changes. Excessive long-term excitation can cause CNS depletion and the appearance of irreversible structural damage, which is also enhanced due to humoral effects on the brain. Acetylcholine, adrenaline, vasopressin, corticotropin, histamine, serotonin in high concentrations act in a similar way; a decrease in pH, a decrease in oxygen content similarly affect. If the neurons of the cortex are able to develop active protective inhibition, then the cortex will be protected and, perhaps, its functions will be restored when the body recovers favorably from the state of shock. Against the background of inhibition, the dominant focus remains in the cortex, into which stimuli from the area of ​​shockogenic injury constantly arrive. In this overstressed focus, parabiosis phenomena occur. If the state of the body is not normalized, then the metabolic reserves of the cerebral cortex are depleted, the disturbances progress, and the phase of external passive inhibition develops with further structural damage to neurons and possible death of the brain. The phase of inhibition is called the torpid stage and is manifested by changes in mental status - lethargy, prostration.

The initial excitation also covers the elements of the limbic system, in which the integration of the humoral response to the influence of the shockogenic factor takes place. However, if protective inhibition develops in the cortex, then the subcortical centers remain in an excited state, and the limbic system provides a sharp increase in the tone of the sympathoadrenal system (an increase in the level of catecholamines by 30-300 times is possible), which is transmitted to the hypothalamic-pituitary-adrenal system with the release of the corresponding hormones. . In all types of shock, an increased concentration in the blood of most hormones is determined: corticotropin, glucocorticoids, thyrotropin, thyroid hormones, somatotropin, vasopressin, aldosterone, catecholamines, as well as angiotensin II, endogenous opiates.

Reaction endocrine system in shock, explosive, hormone concentrations increase rapidly and reach extremely high values. The levels of catecholamines, vasopressin, corticotropin and cortisol increase most rapidly. Meanwhile, disturbances in the rhythm of hormone release, fluctuations in the hormonal response, and changes in the concentration of hormones are observed. In general, the reactions of the endocrine system during shock are aimed at preserving the life of the body: ensuring energy genesis, maintaining hemodynamics, BCC, blood pressure, hemostasis, and electrolyte balance. However, the endocrine response is extremely pronounced, so it causes the depletion of effector organs and becomes destructive.

Hemodynamic changes(scheme 24). The leading link in the pathogenesis of shock is hemodynamic disturbances, primarily a decrease in ECTC. This disorder can be caused by:

Loss of body fluid - blood, plasma, water. This is typical for primary hypovolemic, as well as hemorrhagic, traumatic, burn shock;

The movement of fluid from the vessels to other compartments of the body, for example, the accumulation of water in the serous cavities, interstitial space (edema), in the intestine. Such a shock is called redistributive, or distributive (septic, anaphylactic shock);

The development of heart failure, which causes a decrease in cardiac output (cardiogenic shock).

With a decrease in ECOC and a decrease in blood pressure through the impact on baro-, volume-, osmoreceptors, the mechanisms for correcting these parameters are switched on. PAA C, sympathoadrenal and hypothalamic-pituitary-adrenal systems are activated, the release of vasopressin is enhanced. Blood from the depot, interstitial fluid enters the vessels; water is retained by the kidneys. A generalized spasm of peripheral vessels develops. This ensures that the pressure in the central vessels is maintained at a certain level by limiting the flow of blood into the microvasculature of the parenchymal organs, i.e., centralization of blood circulation occurs. That is why the level of blood pressure during shock does not reflect the state of the blood supply to the organs and the severity of the patient's condition. If the pressure is not normalized in the process of further development of the state of shock, then the activation of vasoconstrictor systems not only continues, but also intensifies due to the intense release of catecholamines. Vasoconstriction becomes excessive. It is generalized, but uneven in intensity and duration in different organs. This is due to the peculiarities of the regulation of individual sections of the vascular bed - the presence of a different type and number of adrenoreceptors, different reactivity of the vascular wall, and features of metabolic regulation. Therefore, under conditions of blood supply deficiency, some organs become more vulnerable and are damaged faster, “sacrificed” (organs of the digestive system, kidneys, liver) to maintain cerebral and coronary circulation. The critical pressure of “closing” the movement of blood in the intestines, kidneys is 10.1 kPa (75 mm Hg), in the heart and lungs, blood circulation is disturbed when the pressure drops below 4.7 kPa (35 mm Hg), in the head the brain is below 4 kPa (30 mm Hg), and at a pressure below 2.7 kPa (20 mm Hg), not a single tissue is perfused.

Simultaneously develop microcirculation disorders(scheme 25). There are also several stages here. First, under the action of vasoconstrictor substances (catecholamines through α-adrenergic receptors, vasopressin, angiotensin II, endothelins, thromboxanes, etc.), a spasm of the vessels of the microvasculature develops - arterioles, metarterioles, precapillary sphincters and venules.

Arteriovenular shunts open (most of all in the lungs and muscles), the blood moves, bypassing the capillaries, thereby, to a certain extent, ensuring the return of blood to the heart. Central venoconstriction is also observed, which causes an increase in central venous pressure and an increase in venous return of blood to the heart, which may have a compensatory value. The rheological properties of blood change, and sludge syndrome develops in the microcirculatory bed. Prolonged vasospasm and impaired perfusion of organs leads to the development of tissue hypoxia, impaired cell metabolism, and acidosis. Acidosis eliminates the spasm of the precapillary sphincters and closes the sphincters of the arteriovenular shunts. A large amount of blood enters the microvasculature, but the postcapillary-venular sphincters are less sensitive to acidosis and remain spasmodic. As a result, a large amount of stagnant acidic blood accumulates in the microcirculation system. Its amount can be 3-4 times the volume of blood contained there under physiological conditions. This phenomenon is called pooling.

At the same time, vascular permeability increases, fluid enters the tissues, which increases the BCC deficiency and aggravates blood clotting. Developing edema, in turn, makes it difficult to supply tissues with oxygen. Thickening of the blood, a violation of its rheological properties and a slowdown in the movement of blood create conditions for the development of DIC. This is facilitated by a decrease in the thromboresistance of the vascular wall, an imbalance in the coagulation and anticoagulation systems of the blood, and activation of platelets. As a result, blood circulation is even more disturbed, the microcirculatory bed is actually clogged, which causes a further increase in hypoxia, damage to organs, and the progression of a state of shock. Arterial vessels lose their ability to maintain their tone, stop responding to vasoconstrictor influences; the postcapillary sections of the vascular bed also expand. Blood stasis mainly occurs in the lungs, intestines, kidneys, liver, skin, which ultimately causes damage to these organs and the development of their insufficiency.

Thus, numerous vicious circles can be traced at the level of the microvasculature, which significantly increase circulatory disorders.

Simultaneously occur changes in lymph circulation. When blockade of the microvasculature develops, the lymphatic system enhances its drainage function by increasing the pores in the lymphocapillaries, venulolymphatic shunting. This significantly enhances lymph drainage from tissues, and thus a significant part of the interstitial fluid accumulated due to microcirculation disorders returns to the systemic circulation. This compensatory mechanism is useful in reducing the venous return of blood to the heart. In the late stages of shock, the lymph flow is weakened, which causes the intensive development of edema, especially in the lungs, liver, and kidneys.

Hemodynamic disorders are largely associated with dysfunction of the heart(scheme 26). Damage to the heart can cause shock (cardiogenic shock) or occurs during its development and aggravates the hemodynamic disorder. Under conditions of shock, damage to the heart is caused by impaired coronary circulation, hypoxia, acidosis, excess free fatty acids, endotoxins of microorganisms, reperfusion, catecholamines, and the action of cytokines. Cardiodepressor factors are also of great importance.

The serum of a patient in a state of shock has a cardiodepressant effect, contains substances that depress the activity of the heart, among which TNF-α plays the greatest role. Its cardiodepressant effect may be due to its ability to trigger cell apoptosis by acting on the corresponding receptors, its influence on the metabolism of sphingolipids, which causes an increase in the production of sphingosine, which can accelerate apoptosis (early effects), as well as the induction of NOS and the formation of a large amount of NO (late effects). NOS is activated by IL-1 and lipopolysaccharides. When NO interacts with AKR, peroxynitrite is formed. In addition to TNF-α, cardiodepressant effects are exerted by FAT, IL-1, IL-6, leukotrienes, peptides formed in the ischemic pancreas. Cardiodepressant factors can disrupt intracellular calcium metabolism, damage mitochondria, affect the conjugation of excitation and contraction; their direct impact on contractile activity is possible. In addition, leukotrienes have a very strong vasoconstrictor effect on the coronary arteries, cause arrhythmias, reduce venous return of blood to the heart, and the C3a complement fragment induces tachycardia, worsens myocardial contractile function and also causes coronary vasoconstriction.

Metabolic disorders and cellular damage. Circulatory disorders in shock necessarily lead to a violation of the metabolism of cells, their structure and function, which are collectively called the “shock cell”. At the first stage, the cell is characterized by a state of hypermetabolism, which develops as a result of nervous and endocrine influences. The exchange rate increases by 2 times or more. Organs and tissues need a much greater supply of substrates and oxygen. Glycogen breaks down and gluconeogenesis increases. Formed insulin resistance. In muscle and other tissues, proteins are broken down using amino acids as substrates for gluconeogenesis. This leads to the development of muscle weakness, including the respiratory muscles. A negative nitrogen balance is created. Ammonium, which is formed during the breakdown of proteins, is not sufficiently neutralized in the liver, which is under shock conditions. In turn, it has a toxic effect on cells, blocking the Krebs cycle. Violations of microcirculation against the background of an increased need for oxygen cause a sharp imbalance between the need and supply of oxygen and nutrients, and the accumulation of metabolic products. In addition, some cytokines, in particular TNF-α, endotoxins of microorganisms (lipopolysaccharides) significantly damage the respiratory chains, disrupting oxidative processes, thereby significantly increasing hypoxic tissue damage.

An integral indicator of the degree of violation of tissue energy metabolism in conditions of limited blood supply and hypoxia can be a gradual increase in the concentration of lactic acid up to 8 mmol/l (normal< 2,2 ммоль/л), что является неблагоприятным прогностическим признаком. Развиваются истощение и нарушение клеточного обмена, которые обусловливают функциональные изменения и структурные повреждения тканей, развитие недостаточности органов (легких, почек, печени, органов пищеварительной системы), что и служит причиной смерти больного. Следует отметить, что причинами гибели клетки являются не только метаболические нарушения вследствие гипоксии, но и повреждения под действием активных кислородных радикалов, протеаз, лизосомальных факторов, цитокинов, токсинов микроорганизмов и др.

The role of cytokines and biologically active substances. Of fundamental importance in the occurrence and progression of pathological changes in shock are the release and activation of a large number of cytokines and other biologically active substances. They interact with each other, forming a cytokine network, and with cells (endotheliocytes, monocytes, macrophages, neutrophilic granulocytes, platelets, etc.). The peculiarity of this interaction is that cytokines stimulate the secretion of each other (TNF-α, FAT, interleukins, etc.) and even their own production. Self-generating, positive feedback loops are formed, which lead to a sharp increase in the level of these substances.

At the same time, there are also inhibitory effects that limit the degree of activation and cytotoxic effect of biologically active substances. When the body responds to pathogenic actions of normal intensity, a balance is maintained between cytotoxic and inhibitory mechanisms, local and general manifestations of the inflammatory process are controlled, which prevents damage to endothelial cells and other cells. With the development of a state of shock, events are forced: excessive production of mediators is observed, which occurs against the background of a critical decrease in the level of inhibitors, positive feedbacks become unregulated, reactions become generalized, systemic. The number of biologically active substances can increase hundreds of times, and then they turn from “defenders” into “aggressors”. With different types of shock, their activation can begin from different stages and at different times, but then, as a rule, systemic activation of biologically active substances occurs, and CCBO develops. In case of further development of shock, hypoxia, accumulation of metabolic products, disorders of the immune system, toxins of microorganisms intensify this “mediator explosion”.

The most important role at the initial stages of the “mediator explosion” is played by TNF-a, PAF, IL-1, then other cytokines and biologically active substances are involved. As a result, TNF-a, FAT, IL-1 are classified as “early” cytokines, IL-6, IL-8, IL-9, IL-11 and other biologically active substances are classified as “late”.

TNF-α is recognized as a central mediator of shock, especially septic shock. It is formed mainly by macrophages after their stimulation (eg, complement fragments C3a, C5a, PAF) during ischemia and reperfusion. Lipopolysaccharides of gram-negative microorganisms are very strong stimulants. TNF-α has a wide range of biological effects:

It is an inducer of apoptosis by binding to specific receptors on cytoplasmic membranes and membranes of the endoplasmic reticulum;

has a depressive effect on the myocardium;

Inhibits intracellular calcium metabolism;

Enhances the formation of active oxygen radicals, stimulating xanthine oxidase;

Directly activates neutrophilic granulocytes, induces the release of proteases by them;

Affects endothelial cells: causes the expression of adhesive molecules, stimulates the synthesis and release of PAF, IL-1, IL-6, IL-8 by endotheliocytes; induces procoagulant functions of the endothelium. May cause damage to the cytoskeleton of endothelial cells and increase vascular permeability;

Activates complement;

Leads to the development of an imbalance of the procoagulant and fibrinolytic systems (weakens the fibrinolytic system and activates the blood coagulation system).

TNF-α can act locally and enter the general circulation. It acts as a synergist with IL-1, FAT. In this case, their influence is sharply enhanced even in microquantities, which do not give independently pronounced effects.

When TNF-α is administered to animals, generalized effects are observed: systemic arterial hypotension, pulmonary hypertension, metabolic acidosis, hyperglycemia, hyperkalemia, leukopenia, petechial hemorrhages in the lungs and alimentary canal, acute tubular necrosis, diffuse pulmonary infiltration, leukocyte infiltration.

PAF plays an important role in cytokine interactions in shock. It is synthesized and secreted by various cell types (endotheliocytes, macrophages, mast cells, blood cells) in response to the influence of mediators and cytokines, especially TNF-α. FAT causes the following effects:

It is a strong stimulator of adhesion and platelet aggregation, promotes thrombosis;

Increases vascular permeability, since it causes calcium to enter endothelial cells, which leads to their contraction and possible damage;

Probably mediates the action of lipopolysaccharides on the heart; contributes to gastrointestinal damage;

Causes damage to the lungs: increases vascular permeability (which leads to edema) and sensitivity to histamine;

It is a strong chemotactic factor for leukocytes, stimulates the release of proteases, superoxide;

It has a pronounced effect on macrophages: even in small amounts, it triggers or activates the formation of IL-1, TNF-α, eicosanoids.

In an animal experiment, the introduction of FAT recreates a state of shock. In dogs, after this, there is a decrease in blood pressure, a weakening of the coronary blood flow, a decrease in myocardial contractility, changes in the vessels (systemic, pulmonary), hemoconcentration; metabolic acidosis, renal dysfunction, leukopenia, thrombocytopenia develop.

Although TNF-α is considered a central mediator, other cytokines such as IL-1, IL-6, IL-8, arachidonic acid metabolites, plasma proteolytic systems, reactive oxygen radicals, and other factors also play an important role in organ damage in shock. .

The resulting biologically active substances act on various cells: macrophages, endotheliocytes, neutrophilic granulocytes and other blood cells. For the development of shock, the effect of these substances on the vascular endothelium and leukocytes is especially important. In addition to the fact that endothelial cells themselves produce cytokines (IL-1, IL-6, IL-8, PAF), they serve as a target for the action of these same substances. Activation of contractile elements of endothelial cells, disruption of the cytoskeleton, damage to the endothelium occur. This leads to a sharp increase in vascular permeability. At the same time, the expression of adhesion molecules is stimulated, which ensure the fixation of leukocytes on the vascular wall. The accumulation of neutrophilic granulocytes is also facilitated by a large number of substances with a positive chemotactic effect - complement fragments C3a and especially C3a, IL-8, FAT, leukotrienes. Leukocytes play an extremely important role in vascular and tissue damage during shock. Neutrophilic granulocytes activated by cytokines secrete lysosomal enzymes, a large number of proteolytic enzymes, among which elastase is important. At the same time, the activity of leukocytes in relation to the generation and release of active oxygen radicals is enhanced. Massive damage to the endothelium, a sharp increase in vascular permeability are observed, which contributes to the development of the previously described microcirculation disorders. These same substances damage not only blood vessels, but also cells of parenchymal organs, increase the damage caused by hypoxia, contributing to the development of their insufficiency. Complement components, TNF-α, PAF, etc., are also the cause of damage, especially to blood vessels.

Cytokines are also important for the development of DIC in shock. They affect all components of the hemostasis system - blood vessels, platelets and the coagulation hemostasis system. So, under their influence, the thromboresistance of the vascular wall decreases, the procoagulant functions of the endothelium are stimulated, which contributes to thrombosis. FAT, TNF-α activate platelets, cause their adhesion, aggregation. An imbalance develops between the activity of the blood coagulation system, on the one hand, and the activity of the anticoagulant and fibrinolytic systems, on the other.

Insufficiency of organs and systems. The described disorders (hypoxia, acidosis, the influence of active oxygen radicals, proteinases, cytokines, biologically active substances) cause massive cell damage. Dysfunction and insufficiency of one, two or more organs and systems develop. This condition is called multiple organ dysfunction syndrome (MOS) or multiple organ dysfunction syndrome (MODS). The degree of functional organ failure depends on the duration and severity of the shock. When a person is shocked, the lungs are first of all damaged, then encephalopathy, kidney and liver failure, and damage to the digestive canal develop. Perhaps the predominance of insufficiency of one or another organ. Due to dysfunction of the liver, kidneys, intestines, new pathogenic factors arise: infection from the digestive canal, high concentrations of toxic products of normal and pathological metabolism. The mortality rate of such patients is very high: in case of insufficiency in one system - 25-40%, in two - 55-60%, in three - over 80% (75-98%), and if dysfunction of four or more systems develops, mortality approaches to 100%.

One of the organs that are the first to be affected in conditions of shock in humans are the lungs. Injuries can develop hours or days after the onset of shock as acute lung failure, which has been termed acute respiratory distress syndrome in adults (ARDS; acute respiratory distress syndrome, ARDS); the term “shock lungs” is also used. The early stage of ARDS, characterized by a lesser degree of hypoxemia, is called acute pulmonary injury syndrome (ALS). The leading factors in the development of pulmonary insufficiency include a sharp increase in the permeability of the alveolocapillary membrane, damage to the vascular endothelium, lung parenchyma, which causes fluid to escape from the vascular wall and the development of pulmonary edema.

A sharp increase in the permeability of the vascular wall is caused by biologically active substances, which enter the lungs in large quantities from the blood or are formed locally in various cells: pulmonary macrophages, neutrophilic granulocytes, vascular endothelial cells, epithelium of the lower respiratory tract. These substances are not sufficiently inactivated there, since non-respiratory functions of the lungs are disturbed very early in conditions of shock. Of great importance is the activation of complement, the kinin system.

In the lungs, a significant number of leukocytes are sequestered, leukocyte infiltration is observed. The accumulation of leukocytes is facilitated by a high level of chemoattractants in the lungs - complement components, leukotrienes, FAT, IL-8 (excreted from pulmonary macrophages and type II alveolocytes). Leukocytes are additionally activated by TNF-α, FAT, lipopolysaccharides. Proteases, active oxygen radicals, are released from them, which damage the wall of blood vessels. There is also an exit of leukocytes outside the vascular wall and damage to the lung tissue. Collagen, elastin, fibronecgin are destroyed. Exudate rich in proteins and fibrin enters the interstitial space and alveoli, extravascular fibrin deposition occurs, which can later cause the development of fibrosis.

Damage is aggravated due to circulatory disorders, the presence of microthrombi, which are formed as a result of the development of DIC. This leads to a violation of hemostasis in the lungs - an increase in procoagulant and a decrease in fibrinolytic activity of the organ. The production and destruction of endothelin in the lungs increases, which contributes to the development of bronchoconstriction. Decreased lung compliance. A decrease in the production of surfactant causes the collapse of the alveoli and the formation of multiple atelectasis. Shunting occurs - blood is thrown from right to left, which causes a further deterioration in the gas exchange function of the lungs (ventilation-perfusion ratio). Reperfusion that occurs during treatment may also contribute to damage. All this leads to severe progressive hypoxemia, which is difficult to normalize even with the help of hyperoxic gas mixtures. Energy costs for breathing increase. The respiratory muscles begin to consume about 15% of the IOC. The most important indicators indicating the development of pulmonary insufficiency are: pO2 in arterial blood< 71 мм рт. ст., снижение респираторного индекса PaО2/FiО2 < 200 мм рт. ст., при СОЛП - < 300 мм рт. ст. На рентгенограмме определяют двусторонние инфильтраты в легких, давление заклинивания капилляров легочной артерии (ДЗКЛА) - < 18 мм рт. ст.

In the case of the development of ARDSV, the condition of patients worsens significantly. Mortality in an unfavorable course can reach 90%.

Plays a significant role in the development of critical conditions intestinal damage. The intestinal mucosa is constantly updated, has a high metabolic activity, and therefore is very sensitive to hypoxia. Due to a violation of microcirculation and the action of other factors, intestinal cells die, the integrity of the mucous membrane is violated, and erosion is formed. Bleeding is observed, microorganisms and toxins from the intestine enter the mesenteric lymphatic vessels, the pyloric system and the general circulation. Endogenous toxemia occurs, which can cause the development of renal and hepatic failure in the late period of shock. The course of shock is complicated by the development of sepsis.

signs liver damage usually occur a few days after the onset of the underlying disease. These may include encephalopathy, jaundice, coagulopathy, and DIC. In addition, with liver failure, the clearance of circulating cytokines is impaired, which contributes to the long-term maintenance of their high blood levels. Of great importance is the violation of the detoxification function, especially against the background of the receipt of a significant amount of toxic substances and metabolites from the intestine. Shock disrupts protein synthesis in the liver. The deficiency in the synthesis of short-lived proteins, such as blood coagulation factors, is especially pronounced, which leads to the depletion of the coagulation system and the transition of DIC to the stage of hypocoagulation. The metabolism of liver epithelial cells is significantly affected by TNF-α, IL-1, IL-6.

Kidney damage. A decrease in BCC, a decrease in blood pressure, and an extreme degree of spasm of the afferent arterioles cause a decrease in the glomerular filtration rate, a deterioration in the blood supply to the cortical substance of the kidneys, and the development of acute renal failure. In severe shock, renal perfusion slows down and often stops. Oligo- and anuria develop, the concentration of creatinine and urea in the blood increases, azotemia increases. Ischemia that lasts more than 1.5 hours causes damage to the renal tissue; develops glomerular, and then tubular insufficiency associated with necrosis of the epithelium of the renal tubules. In this case, renal failure may persist after the patient is taken out of shock.

The presence of multiple organ dysfunction and insufficiency is evidenced by certain clinical and laboratory parameters. So, with liver failure, the concentration of bilirubin in the blood exceeds 34 μmol / l, an increase in the level of AcAT, alkaline phosphatase is observed by 2 times or more from the upper limit of the norm; in renal failure, the blood creatinine level exceeds 176 μmol / l, diuresis falls below 30 ml / h; in case of dysfunction in the hemostasis system - an increase in the content of fibrin / fibrinogen degradation products, D-dimer, irothrombin index< 70 %, количество тромбоцитов < 150,0*10в9/л, уровень фибриногена < 2 г/л; при дисфункции ЦНС - менее 15 баллов по шкале Глазго.

Features of the development of various types of shock

hypovolemic shock. Primary hypovolemic shock develops due to fluid loss and a decrease in BCC. This may be the case:

Blood loss during external and internal bleeding (this type of shock is called hemorrhagic);

Loss of plasma during burns, tissue damage, etc.;

Fluid loss with profuse diarrhea, indomitable vomiting, due to polyuria in diabetes or diabetes insipidus.

Hypovolemic shock begins to develop when the volume of intravascular fluid decreases by 15-20% (1 liter per 70 kg of body weight). In young people, the classic manifestations of hypovolemic shock occur with a loss of 30% of BCC. If the loss is 20-40% of BCC (1-2 liters per 70 kg of body weight), moderate shock develops, more than 40% of BCC (more than 2 liters per 70 kg of body weight) - severe shock. The development of shock depends not only on how much the BCC has decreased, but also on the rate of fluid loss. It is the intensity, speed and duration of bleeding that turn it into hemorrhagic shock.

In response to a decrease in BCC, a standard set of compensatory reactions occurs. There is a movement of fluid from the extravascular space to the vessels, so the loss of BCC is accompanied by a deficiency of extracellular fluid, equivalent to a deficiency of plasma. There is water retention by the kidneys, the release of blood from the depot. A spasm of the vessels of the microcirculatory bed, centralization of blood circulation develop. A decrease in venous return of blood to the heart reduces cardiac output, and central hemodynamic insufficiency occurs early. The main hemodynamic parameters characterizing hypovolemic shock include: low PCLA, low cardiac output, high total peripheral vascular resistance. In the future, shock develops according to general patterns. Prolonged centralization of blood circulation causes damage to organs and the development of PON. In the treatment of hypovolemic shock, it is necessary to quickly restore the BCC deficit and eliminate vasoconstriction.

Cardiogenic shock. Cardiogenic shock is called shock, the cause of which is acute heart failure with a sharp decrease in cardiac output. This condition can be caused by:

Decreased contractility of the heart in myocardial infarction, severe myocarditis, cardiomyopathy, complications of thrombolytic therapy with the development of reperfusion syndrome;

Severe heart rhythm disturbances;

Decreased venous return of blood to the heart;

Violations of intracardiac hemodynamics, which are observed with severe defects and ruptures of valves, papillary muscles, interventricular septum, atrial spherical thrombus, heart tumors;

Cardiac tamponade, massive pulmonary embolism, or tension pneumothorax. This type of shock is called obstructive. It develops as a result of a violation of the filling of the heart or the expulsion of blood from it. With cardiac tamponade, a mechanical obstacle to the expansion of its chambers during diastole disrupts their filling, and the venous return of blood to the heart also sharply decreases.

Thromboembolism of the pulmonary arteries causes a restriction of blood flow to the left heart, which is a consequence of a combination of a mechanical factor in case of obstruction by a large thromboembolus and spasm of the pulmonary vessels in the case of embolism by numerous small thromboemboli. In tension pneumothorax, an increase in pressure in the pleural cavity causes a shift in the mediastinum and an inflection of the vena cava at the level of the right atrium, which blocks the venous return of blood to the heart.

The most common cause of cardiogenic shock is myocardial infarction, which in 5-15% of patients is complicated by shock. There are separate clinical variants of cardiogenic shock in heart attacks - reflex, arrhythmic, true cardiogenic. In the development of reflex cardiogenic shock, the leading role is played by the reaction to sharp pain, reflex influences (Bezold-Jarisch reflex) from the focus of necrosis on the work of the heart and vascular tone with blood deposition in the microcirculatory bed. Due to pathological reflex influences, especially with myocardial infarction of the posterior wall, bradycardia may develop, and blood pressure may drop sharply.

Arrhythmic cardiogenic shock is associated with the addition of severe cardiac arrhythmias that significantly reduce cardiac output. Most often, this is paroxysmal ventricular tachycardia with a very high ventricular rate, atrial flutter, or severe bradycardia (for example, with complete atrioventricular block).

True cardiogenic shock is called shock, which develops as a result of a sharp decrease in myocardial contractility. As a rule, it occurs with heart attacks exceeding 40-50% of the mass of the left ventricle, transmural, anterolateral and repeated against the background of a previously reduced myocardial contractility, arterial hypertension, diabetes mellitus, in people over 60 years old.

The initial link in the pathogenesis of cardiogenic shock is a sharp decrease in cardiac output, a decrease in blood pressure (SBP< 90 мм рт. ст., среднее артериальное давление < 60 мм рт. ст. (7,9 кПа) или снижено более чем на 30 мм рт. ст.). При этом повышается давление наполнения желудочков сердца и, соответственно, ДЗКЛА составляет ≥ 20 мм рт. ст., сердечный индекс < 1,8-2 л/(мин*м2). Включаются компенсаторные реакции, направленные на нормализацию артериального давления: активация симпатоадреналовой системы, PAAC и др. Резко повышается периферическое сосудистое сопротивление, что создает дополнительную нагрузку на сердце и ухудшает перфузию тканей. Катехоламины оказывают непосредственное влияние на сердце - проявляется их ино- и хронотропное действие, которое увеличивает потребность сердца в кислороде, а одновременное снижение давления в аорте препятствует поступлению нужного количества крови в венечные сосуды. Это усиливает недостаточность обеспечения миокарда кровью. К ухудшению метаболизма сердца приводит и тахикардия. В ишемизированном миокарде активируется образование метаболитов арахидоновой кислоты, особенно лейкотриенов, продуктов ПОЛ, выделяются лейкоцитарные факторы. Все это дополнительно повреждает сердце. Таким образом, возникает порочный круг. Поражение сердца и тяжесть состояния больного нарастают. Присоединение нарушений легочного кровообращения, развитие отека легких вызывает тяжелую артериальную гипоксемию. В дальнейшем шоковое состояние развивается по общим закономерностям. Смертность при кардиогенном шоке составляет 50-80 %, а при некоторых его видах достигает 100 %.

Septic shock complicates the course of various infectious diseases caused mainly by gram-negative bacteria. Nevertheless, cases of septic conditions with gram-positive and fungal infections have become more frequent.

The development of a state of shock in gram-negative sepsis is mainly associated with the action of endotoxin, which is released during the division or destruction of microorganisms, including against the background of the use of antibiotic therapy. Endotoxin is a lipopolysaccharide capable of binding alone or in combination with blood lipopolysaccharide-binding protein (LBP) to a receptor complex consisting of CD 14, MD2 and TLR-4 receptors (tool-like) on monocytes / macrophages and other cells - endotheliocytes, platelets . In addition, some bacterium molecules are recognized by cytoplasmic receptors NOD-1 and NOD-2. Subsequently, an intracellular cascade is triggered with the activation of the transcription factor NFkB, resulting in the synthesis of TNF-α. The release of other cytokines, pro-inflammatory biologically active substances, is also induced, the formation of adhesion molecules induced by NOS, etc. is stimulated. determined in patients with septic shock. It is released by endotheliocytes and other cells under the action of microorganisms and pro-inflammatory cytokines. Lipopolysaccharide also activates plasma proteolytic systems.

At the beginning of the development of the infectious process, BAS are formed in the focus of infectious inflammation. In case of an excessive response, insufficiency of local protective mechanisms and instability of the barrier, their entry into the blood, uncontrolled distribution of mediators and generalization of the process with the development of SIRS are possible. In this case, bacteremia may be short-term or absent altogether. These substances have a systemic effect primarily on the microvasculature, as well as a powerful direct damaging effect on tissues. Therefore, hemodynamic changes in septic shock begin with microcirculation disorders with further addition of changes in central hemodynamics.

Septic shock is the most "cellular" type of shock, in which tissue damage occurs very early and is much more severe than would be expected from hemodynamic changes alone. Endotoxin (lipopolysaccharide) causes rapid inactivation of cytochrome a, a3 (cytochrome oxidase). TNF-α also damages the respiratory chains, which disrupts mitochondrial oxidative phosphorylation, regardless of the level of oxyhemoglobin or the intensity of blood flow in organs. As a result of dysfunction at the cellular level, the absorption of oxygen from the blood worsens, which is manifested by a decrease in the arteriovenous oxygen difference.

The most important cytokines in septic shock are TNF-α and PAF. It is possible that it is TNF-α that plays a leading role in those cases of shock that end in death, since together with lipopolysaccharide they have a very strong effect, significantly enhance each other's effects, even at low doses. That is why, with the development of septic shock, there is a significant early damage to the vascular endothelium with a sharp increase in permeability, the release of protein and a large amount of fluid into the interstitial space, and a decrease in ECTC. Therefore, such a shock is called distributive, or redistributive. Damage to blood vessels and tissues is also caused by activated leukocytes. Another feature of septic shock is early and persistent vasodilatation of the microcirculatory bed, which, together with sequestration and fluid release into the tissues, causes a significant decrease in blood pressure that cannot be corrected.

There are several mechanisms for acute vasodilation. So, lipopolysaccharides, cytokines (especially TNF-α), endothelium-1 stimulate the formation of iNOS by macrophages, endothelial and smooth muscle cells, which produces a very large amount of NO, as a result of which the tone of both resistive vessels and venules decreases. During the experimental modeling of septic shock, two phases of pressure decrease in response to the action of endotoxin are observed - an immediate phase associated with the activation of constitutive NOS, and a later phase caused by the formation of iNOS. In addition to the vasodilator action, NO, reacting with a large amount of free oxygen radicals, forms highly toxic peroxynitrite (ONOO*), which damages cell membranes, endothelial DNA and cells of nearby tissues. The weakening of vascular tone is also facilitated by the opening of ATP-dependent potassium channels, the release of K + from cells. There is a decrease in the level of vasopressin (depletion of its reserves in the pituitary gland due to previous excessive release). There is an inactivation of catecholamines by superoxide radicals, which are formed in large quantities. Vessels lose sensitivity to the action of vasoconstrictor factors. As a result, the contractility of vascular smooth muscles is weakened, the tone decreases and refractory vasodilation develops. Microcirculation disorders are heterogeneous - there are zones of vasodilation and vasoconstriction. The opening of arterio-lovenular shunts is also characteristic.

Septic shock in Gram-positive infection is due to the direct action of both toxins and biologically active substances. Toxins from gram-positive microorganisms (lipoteichoic acid, peptidoglycans, flagellin, etc.) also bind to the corresponding TLRs (TLR-2, TLR-5, TLR-6, ​​TLR-9), which leads to the release of cytokines. Toxins with the properties of superantigens (toxic shock syndrome toxin, staphylococcal enterotoxin, streptococcal pyrogenic exotoxin) cause nonspecific activation of a large number of lymphocytes, also with the release of biologically active substances.

At the initial stages of the development of septic shock, catecholamines cause an increase in heart rate and UOS. However, in the future, myocardial damage occurs by cardiodepressant factors, the effect of which is significantly enhanced by lipopolysaccharides. Heart failure joins, which significantly aggravates hemodynamic disorders.

Since septic shock causes significant tissue damage, failure of various organs, primarily the lungs and kidneys, develops early. A feature of the development of ARDSV in conditions of septic shock is that the action of lipopolysaccharides, which stimulate the release and enhance the effects of cytokines and leukocytes, is attached to its pathogenesis. This causes rapid and intense damage to the endothelium, pulmonary edema and the development of acute pulmonary insufficiency.

The kidneys respond to vasodilation and a decrease in ECC caused by the action of endotoxin, stimulation of renin release with further formation of angiotensin II and renal vasospasm. There is acute tubular necrosis.

Septic shock is characterized by the early onset of DIC. The central nervous system is also damaged up to the development of a coma.

The main hemodynamic characteristics of septic shock are as follows: low PCLA and total peripheral vascular resistance.

Septic shock is one of the most severe types of shock. Mortality still remains high - 40-60%, and in shock due to abdominal sepsis can reach 100%. Septic shock is the most common cause of death in general intensive care units.

Anaphylactic shock. This type of shock, like septic shock, belongs to the vascular forms of shock. An allergic reaction of the anaphylactic type in case of its generalization can lead to its development. At the same time, mediators secreted from mast cells, as well as other biologically active substances, spread. The vascular tone is significantly reduced, the vessels of the microcirculatory bed expand, and their permeability increases. Blood accumulates in the microvasculature, the fluid goes beyond the vessels, the ECC and the venous return of blood to the heart decrease. The work of the heart also worsens due to impaired coronary circulation, the development of severe arrhythmias. So, leukotrienes (C4, D4) and histamine cause coronary spasm. Histamine (through H1 receptors) inhibits the work of the sinoatrial node, causes (through H2 receptors) other types of arrhythmias up to the development of ventricular fibrillation. Due to a decrease in ECC and a violation of the work of the heart, blood pressure decreases, tissue perfusion is disturbed. The action of histamine, leukotrienes on the smooth muscles of the bronchial tree causes spasm of the bronchioles and the development of obstructive respiratory failure. This greatly enhances hypoxia due to hemodynamic disorders.

In addition to the typical course, other clinical variants of anaphylactic shock are possible. So, a hemodynamic variant can be observed, in which hemodynamic disturbances with heart damage, arrhythmias up to asystole, and the development of acute heart failure come to the fore. The presence of chronic diseases of the respiratory system in a person can contribute to the development of the asphyxial variant of anaphylactic shock, the clinical picture of which is dominated by acute insufficiency of external respiration due to edema of the respiratory tract, bronchospasm, and pulmonary edema.

A feature of anaphylactic shock is the possibility of its rapid, lightning-fast development, when the death of the patient can occur within a few minutes. Therefore, medical care should be provided immediately when the first signs of a shock condition appear. This should be a rapid massive introduction of fluids, catecholamines, glucocorticoids, antihistamines and other anti-shock measures aimed at restoring the functioning of the respiratory and cardiovascular systems.

burn shock develops as a result of extensive thermal lesions of the skin and underlying tissues. The first reactions of the body to a burn are associated with a very strong pain syndrome and psycho-emotional stress, which is a trigger for a sharp activation of the sympathoadrenal system with vasospasm, tachycardia, an increase in UOS and MOS, and a possible increase in blood pressure. In the future, a standard neuroendocrine response develops. At the same time, on a large surface of tissues damaged by a burn, inflammation begins with the release of all its mediators. Vascular permeability increases sharply, protein and liquid parts of the blood exit the vascular bed into the intercellular space (with burns affecting more than 30% of the body surface - 4 ml / (kg * h)); fluid is also lost through the burnt surface to the outside. This causes a significant decrease in BCC, the shock becomes hypovolemic. Hypoproteinemia, resulting from the loss of proteins, enhances the development of edema in unburned tissues (especially in burns with damage to more than 30% of the body surface). This in turn exacerbates hypovolemia. Cardiac output decreases, total peripheral vascular resistance increases significantly, central venous pressure decreases, leading to increased hemodynamic disturbances. Mediators enter the general circulation, generalized activation of biologically active substances and the development of SIRS occur. Due to the destruction of tissues, the breakdown of proteins, a large amount of toxins are formed, which also enter the systemic circulation and cause additional tissue damage. The further course of shock occurs according to general patterns. It is possible to attach an infection with the development of sepsis, which significantly worsens the patient's condition.

traumatic shock occurs as a result of severe mechanical damage - bone fractures, tissue crushing, trauma to internal organs, extensive wounds. Shock may develop immediately after the injury or several hours after it. Its causes, as a rule, are a strong pain reaction, a sharp irritation and even damage to the extero-, intero- and proprioreceptors and a violation of the functions of the central nervous system.

In the development of traumatic shock, the stage of excitation (erectile) and inhibition (torpid) are clearly distinguished. A vivid description of the torpid stage of traumatic shock belongs to N.I. Pirogov. The erectile stage is usually short-lived (5-10 minutes), caused by a sharp excitation of the central nervous system with signs of motor, speech excitation and pain reactions to touch. There is a significant activation of the endocrine system with the release into the blood of a large amount of catecholamines, corticotropin and hormones of the adrenal cortex, vasopressin. The function of the respiratory and cardiovascular systems is enhanced: blood pressure rises, heart rate and respiratory rate increase. Then comes the torpid stage - the stage of CNS inhibition, which extends to the sections of the hypothalamus, brain stem, and spinal cord. It is characterized by adynamia, general lethargy, although the patient is conscious, nevertheless very sluggishly reacts to external stimuli; blood pressure decreases, there are signs of impaired tissue perfusion, diuresis decreases. Due to the bleeding that accompanies the injury, signs of hypovolemic shock are added. In any case, hemodynamic disturbances characteristic of all types of shock develop.

Many inflammatory mediators are released from damaged and nearby tissues, from blood cells, and SIRS develops. In addition, a large amount of toxic substances formed as a result of tissue breakdown, as well as products of impaired metabolism, enter the bloodstream. Significant intoxication enhances damage to organs distant from the site of injury. Traumatic shock is characterized by severe immunosuppression, against which the development of infectious complications with an unfavorable course is possible. All these changes, as in other types of shock, cause the onset of PON.

A variety of traumatic shock is a shock that develops as a result of a compression injury - a syndrome of prolonged squeezing (with a closed injury) or crushing (open injury), a crash syndrome. It occurs after a strong and prolonged (over 2-4 hours or more) compression of soft tissues with clamping of large vessels, when a person falls under rubble in the event of disasters, collapses of buildings, earthquakes, accidents. The limbs are most often subjected to compression. A similar condition occurs after the removal of the tourniquet, imposed for a long time (turnstile shock).

In the pathogenesis of the crash syndrome, the main factors are circulatory disorders with a significant degree of ischemia in compressed tissues, damage to the nerve trunks and the development of a pain reaction, mechanical damage to the muscle tissue array with the release of a large amount of toxic substances. After the tissues are released from compression, after a few hours, edema develops and increases at the site of injury and in the distally located area of ​​the tissues, which leads to a decrease in BCC, a violation of the rheological properties of the blood. From injured tissues, a large amount of toxic substances enter the general bloodstream - decay products of tissues accumulated in damaged areas, creatinine, lactic acid, products of impaired metabolism. Potassium, phosphorus are released, hyperkalemia develops. A feature of the crash syndrome is the entry into the blood of a large amount of myoglobin from destroyed muscle tissue, which serves as an additional factor in kidney damage and causes the development of acute renal failure (myorenal syndrome). Cytokines, biologically active substances are sharply activated. Shock develops according to general patterns.

General principles of antishock therapy. The prognosis is largely determined by the timely resuscitation. The main goal of treatment is to stabilize hemodynamics and restore organ perfusion to maintain adequate systemic and regional oxygen transport. With the development of shock, the following general measures are appropriate:

Termination or weakening of the action of the shock factor (for example, stopping bleeding);

Anesthesia in the presence of severe pain - with injuries, burns;

Ensuring the patency of the respiratory tract and the functioning of the external respiration system - artificial ventilation of the lungs, the use of appropriate gas mixtures;

Restoration of perfusion of organs and tissues, which requires normalization of the BCC (infusion therapy - the introduction of fluids), restoration and maintenance of hemodynamics, normalization of vascular tone;

Normalization of the hemostasis system (due to the development or threat of DIC);

Correction of acidosis, hypoxia, electrolyte balance, hypothermia;

Detoxification measures, possibly using extracorporeal detoxification (plasmapheresis, hemosorption, lymphosorption, hemodialysis, ultrahemofiltration), the introduction of antidote agents;

Infection control (septic shock, burn lesions, open injuries, as well as in case of sepsis with other types of shock).

Methods are being developed to eliminate excess amounts of cytokines and other biologically active substances - the use of protease inhibitors, monoclonal antibodies (for example, to TNF-α), blockers of some receptors (including TLR) in septic shock, endothelin receptors; the introduction of soluble receptors, such as CD-14, antibodies to adhesion molecules, etc. Some of the effects of TNF-α are blocked by cyclooxygenase inhibitors, glucocorticoids.

a symptom complex of violations of the vital functions of the body, arising as a result of a discrepancy between tissue blood flow and the metabolic need of tissues.

During the development of shock, the main task of the body is to maintain adequate blood flow in the vital organs (heart and brain). Therefore, initially there is a narrowing of blood vessels in other organs and tissues, thus achieving centralization of blood circulation. Such prolonged vasoconstriction over time leads to the development of ischemia - a decrease in the blood supply to an organ or tissue resulting from a weakening or cessation of arterial blood flow. This leads to the production of biologically active substances that increase vascular permeability, which ultimately leads to vasodilation. As a result, the protective adaptive mechanism of the body is disrupted - the centralization of blood circulation, which entails serious consequences.

According to the pathogenesis, the following types of shock are distinguished:

• hypovolemic;
• traumatic;
• cardiogenic;
• infectious-toxic;
• anaphylactic;
• septic;
• neurogenic;
• combined (contains all pathogenetic elements of various shocks).

The consequences of shock depend on the cause that served to develop such a condition. For example, shock can lead to complications such as failure of a number of internal organs, pulmonary and cerebral edema. Such formidable consequences can lead to death, so the shock requires increased attention.

Symptoms

In shock, you can pay attention to the appearance of the patient. Such a person has pale and cold skin to the touch. The exceptions are septic and anaphylactic shocks, in which the skin is warm at the beginning of development, but then it does not differ in any way from the characteristics in other types of shock. General weakness, dizziness, nausea are pronounced. Perhaps the development of excitation, followed by lethargy or coma. Blood pressure is significantly reduced, which carries a certain danger. As a result, the stroke volume of blood is reduced, which is necessary to satisfy organs and tissues in oxygen. Therefore, tachycardia occurs - an increase in the number of heart contractions. In addition, there is the appearance of oligoanuria, which means a sharp decrease in the amount of urine excreted.

In traumatic shock, patients complain of severe pain caused by trauma. Anaphylactic shock is accompanied by shortness of breath, which occurs due to bronchospasm. Significant blood loss can also lead to the development of shock, in which case attention is drawn to internal or external bleeding. With septic shock, an elevated body temperature is detected, which is difficult to stop by taking antipyretics.

Diagnostics

For some time, the state of shock may go unnoticed, since there is no specific symptom indicating exclusively the development of shock. Therefore, it is important to evaluate all the symptoms that the patient has and to analyze the situation individually in each case. To make a diagnosis of shock, it is necessary to identify signs of insufficient blood circulation in tissues, as well as to detect the inclusion of compensatory mechanisms of the body.

First of all, attention is paid to the appearance of the patient. The skin is often cold to the touch and looks pale. Cyanosis (bluish discoloration of the skin and/or visible mucous membranes) may be detected. Blood pressure is measured to confirm hypotension. Patients complain of general weakness, dizziness, nausea, palpitations, and the amount of urine excreted sharply decreases.

It is important to compare all the symptoms as quickly as possible, make the correct diagnosis and begin appropriate treatment.

Treatment

Shock is an emergency condition that can lead to irreversible consequences. Therefore, it is extremely important to provide medical assistance in a timely manner. Prior to the arrival of specialists, nearby people should take first aid measures. First, you need to give the person a horizontal position with a raised foot end. Such actions contribute to an increase in venous return to the heart, which leads to an increase in the stroke volume of the heart. During shock, the heart can no longer cope with the stroke volume necessary to deliver the right amount of oxygen to the tissues. Although the horizontal position with raised legs does not fully compensate for the insufficiency of the stroke volume of the heart, it helps to improve this condition.

Medical care consists of infusion therapy and the introduction of drugs whose action is aimed at vasoconstriction. Infusion therapy is based on the introduction into the bloodstream of various solutions of a certain volume and concentration to fill the vascular bed.

The use of drugs that narrow blood vessels is necessary to maintain blood pressure.

If breathing is disturbed, oxygen therapy or mechanical ventilation is used.

These general measures are aimed at combating the pathogenesis of shock, and there is also a symptomatic treatment that is different for each type of shock. So, for example, in case of traumatic shock, it is necessary to administer painkillers, immobilize fractures, or apply a sterile bandage to the wound. Cardiogenic shock requires treatment of the underlying cause of the shock. Hypovolemic shock is often associated with blood loss, so it is important to understand that without eliminating the cause, that is, stopping the bleeding (application of a tourniquet, pressure bandage, clamping the vessel in the wound, etc.), general measures will not have the desired effect. Septic shock is accompanied by fever, so antipyretics are used as a symptomatic treatment, and antibacterial drugs are prescribed to eliminate the cause itself. In the treatment of anaphylactic shock, it is important to prevent delayed systemic manifestations; for this purpose, glucocorticosteroids and antihistamines are used. It is also necessary to stop the phenomenon of bronchospasm.

Medications

With the development of shock, it is important to provide access to the vein as quickly as possible, preferably not to one, but to several at once. This is necessary to start infusion therapy, as well as the introduction of drugs directly into the bloodstream. Infusion therapy has an impact on the main links of pathogenesis. It is able to maintain an optimal level of BCC (volume of circulating blood), which leads to stabilization of hemodynamics, improves microcirculation, thereby increasing oxygen delivery to tissues, and improves metabolism in cells.

Infusion solutions used for shock include:

• crystalloids (isotonic NaCl solution, Ringer's solution, glucose solutions, mannitol, sorbitol);
• colloids (hemodez, polydez, polyoxidin, polyglucin, reopoliglyukin).

Usually a combination of crystalloid and colloidal solutions is used. This tactic allows you to replenish the volume of circulating blood, and also regulates the balance of intracellular and interstitial fluids. The choice of volume and ratio of crystalloid and colloid solutions depends on each clinical case, which has its own characteristics.

Of the drugs that cause narrowing of the lumen of blood vessels, the main one is adrenaline. Intravenous administration contributes to the accumulation of the required concentration of the drug directly in the blood, which leads to the most rapid manifestation of the effect than with other methods of administration. Dobutamine and dopamine also have this effect. Their action occurs approximately 5 minutes after intravenous administration and lasts about 10 minutes.

Folk remedies

Shock of various etiologies requires exclusively medical care, no recipes for folk remedies can improve the patient's condition. Therefore, it is important not to waste precious time, but to immediately call specialists who will provide the necessary assistance and save you from possible irreversible consequences. While waiting for the arrival of the ambulance, the first aid measures that were described earlier should be performed (put the person in a horizontal position with the foot end raised, warm the body). Not only the effectiveness of treatment, but also the life of a person depends on the right actions!

The information is for reference only and is not a guide to action. Do not self-medicate. At the first symptoms of the disease, consult a doctor.

The term "shock" was first used in his writings by the French physician Henri Le Dran in the 18th century, but this designation of the pathological condition has been familiar since the time of Hippocrates, who described various shock reactions in his writings. If we classify the types of shock in accordance with the main mechanisms of pathological genesis, then we can distinguish traumatic, anaphylactic, dehydration (or infectious-toxic), cardiogenic, septic and other types. Some of them are detailed below.

Traumatic type of shock: symptoms of the condition and emergency care

traumatic shock- this is an acutely developing and life-threatening condition that occurs as a result of a severe injury and is characterized by a progressive disruption of the activity of all body systems. The main pathogenesis factors in traumatic shock are: pain, toxemia, bleeding, BCC and plasma deficiency and subsequent cooling.

With prolonged compression syndrome and extensive soft tissue damage, one of the causes of this type of shock is early toxicosis. Insufficiency of kidney function occurs as a result of toxic damage to the renal epithelium and blockage of convoluted tubules by hyaline and pigment cylinders containing myoglobin. In some cases, oliguria and anuria, even with a satisfactory level of blood pressure, make it possible to judge the severity of shock.

In burn shock, in addition to pain and toxemia, an important pathogenetic factor is plasma loss from the burn surface, which determines protein and potassium deficiencies.

There are three stages of this type of shock.

The main symptoms of traumatic shock of the 1st degree (mild shock) in humans:

• lethargy;
• skin pale and cold;
• the symptom of the "white spot" is sharply positive;
• tachypnea;
• tachycardia up to 100 beats / min;
• SBP 90-100 mmHg Art.;
• timely initiation of treatment stabilizes the condition at the prehospital stage.

Signs of the development of traumatic shock of the 2nd degree (moderate shock):

• lethargy and adynamia;
• skin pale and cold, marbled;
• tachycardia up to 110-120 beats / min;
• SBP 80-75 mmHg Art.;
• diuresis is reduced;
• significant efforts and resuscitation are required to stabilize the condition at the prehospital stage.

Clinical symptoms of traumatic shock of the 3rd degree (severe shock):

• lethargy and adynamia, indifference to the environment;
• earthy skin, cold;
• tachycardia up to 130-140 beats / min;
• SBP 60 mmHg Art. and below, diastolic blood pressure is often not determined;
• anuria;
• resuscitation measures are required in the conditions of the intensive care unit (trauma center). The prognosis is extremely doubtful.

For successful assistance with this type of shock, the following are important:

• early diagnosis;
• therapy ahead of the development of shock;
• compliance with the rule of the "golden hour": the chances of the victim to survive are higher if he is provided with specialized resuscitation and surgical care within an hour;
• "golden hour" is counted from the moment of injury, and not the start of assistance;
• any action at the scene should be only life-saving in nature.

In children, the symptoms of traumatic shock are more pronounced, the condition is characterized by a long phase of centralization of blood circulation, often even with severe trauma, and then the transition to decentralization.

Diagnosis of external bleeding is not difficult, it is more difficult to diagnose internal bleeding. In simple cases, it is enough to determine the pulse rate and the value of systolic blood pressure. Having these indicators, it is possible to approximately determine the volume of blood loss according to the Algover index.

The determination of the volume of blood loss is based on the ratio of pulse rate to the level of systolic blood pressure. The normal ratio (Algover index) is about 0.5 (P8/BP=60/120).

With an index equal to 1 (PS / BP = 100/100), the volume of blood loss is 20% of the BCC, which corresponds to 1-1.2 liters in an adult.

With an index equal to 1.5 (PS / BP = 120/80), the volume of blood loss is 30-40% of the BCC, which corresponds to 1.5-2 liters in an adult.

With an index equal to 2 (PS / BP = 120/60), the volume of blood loss is 50% of the BCC, i.e. more than 2.5 liters of blood.

There is data on the dependence of blood loss on the nature of the injury (in a middle-aged person):

• with an ankle fracture, blood loss is 250 ml;
• with a fracture of the shoulder, blood loss is 300-500 ml;
• with a fracture of the lower leg, blood loss is 300-350 ml;
• with a hip fracture, blood loss is 500-1000 ml;
• with a pelvic fracture, blood loss is 2500-3000 ml;
• with multiple fractures or combined trauma - 3000-4000 ml.

When providing first aid for this type of shock, you must:

1. Conduct a survey.
2. Calling the resuscitation team.
3. Temporary stop of external bleeding.
4. Providing intravenous access through a needle/cannula of the largest diameter.
5. Elimination of the deficit of the BCC.
6. Correction of violations of gas exchange.
7. Interruption of shockogenic impulses from the site of injury.
8. transport immobilization.
9. Medical therapy.

Secondary examination (takes no more than 10 minutes, in case of a diagnosis of "traumatic shock" is performed during transportation). The purpose of the secondary examination is to clarify the diagnosis (clarification of the nature of traumatic injuries, assessment of the reaction).

Inspection is carried out in the following order:

• head - signs of bleeding, injury;
• neck - signs of tension pneumothorax, trauma;
• chest - signs of tension pneumothorax, trauma, rib fractures;
• stomach - tension, soreness;
• pelvis - signs of injury, fractures;
• limbs - signs of injury, fractures;
• soft tissues - signs of injury;
• CNS - assessment of the activity of consciousness according to the Glasgow Coma Scale.

Emergency care for this type of shock after a secondary examination includes:

• Immobilization for fractures - only after anesthesia.
• Infusion therapy - continuation of previously prescribed infusion therapy, correction depending on the state of hemodynamics.
• Hormone therapy - methylprednisolone for adults 90-150 mg, children - 5 mg / kg intravenously or hydrocortisone - 15-25 mg / kg intravenously;
• 20-40% glucose solution - 10-20 ml intravenously.

Attention!

• When providing first aid for symptoms of traumatic shock, one should not seek to increase blood pressure (systolic) above 90-100 mm Hg. Art.
• The introduction of pressor amines (mezaton, norepinephrine, etc.) is contraindicated.
• Narcotic analgesics should not be administered if internal organ damage or internal bleeding is suspected and if systolic blood pressure is less than 60 mm Hg. Art.
• Droperidol, which has vasodilating properties, should not be used!

Anaphylactic type of shock: the first clinical signs and medical care

Anaphylactic shock- this is an allergic reaction of an immediate type, in which reagin antibodies (immunoglobulin E) are fixed on the surface of mast cells (labrocytes). More often it develops in response to parenteral administration of drugs (penicillin, sulfonamides, serums, vaccines, protein preparations, etc.). Anaphylactic shock may occur when biting insects, eating food and inhaling air with allergens, contact with household allergens.

As a result of the antigen-antibody reaction, the mediators of the allergic reaction are released (early phase). These are physiologically active substances that act on smooth muscles and vascular endothelium. At the same time, collapse develops, pronounced hemodynamic disturbances. However, the development of a late phase is also possible, due to the repeated release of biologically active substances from other cells attracted to the site of action of the allergen.

Anaphylactic shock is the most severe form of an immediate allergic reaction.

All the main symptoms of this type of shock occur within a few seconds or minutes after contact with the allergen (after injection of the drug) or within 2 hours after eating. The more severe the reaction, the faster the symptoms develop.

Clinical signs in anaphylactic shock depend on the severity of the condition.

For mild flow:

• rash and erythema, itching and tingling appear in the area of ​​the skin of the face, hands, head, tongue;
• burning sensation and heat in the body;
• sudden headache;
• severe numbness of the limbs;
• rapidly growing weakness;
• dyspnea, bronchospasm;
• chest pain;
• dizziness;
• hyperhidrosis;
• severe dry mouth;
• pronounced injection of the sclera;
• hyperemia of the face is replaced by pallor;
• tachypnea, stridor, wheezing, shortness of breath or apnea;
• hypotension, thready pulse;
• angioedema of the eyelids, face, larynx and other parts of the body.

In severe cases, symptoms of shock are manifested, such as:

• sudden loss of consciousness;
• a sharp decrease in blood pressure (not determined!).

All symptoms of shock with a delayed reaction (late phase) to an allergen may increase again after 2-24 hours, which is observed in 30% of all patients.

Attention!

• During the provision of first aid for this type of shock, epinephrine (adrenaline) must be prescribed with a decrease in blood pressure against the background of preserved consciousness! Do not use unreasonably low doses of glucocorticoids!
• It is unacceptable to / in the introduction of epinephrine (adrenaline)!
• The appointment of antihistamines (promethazine (pipolfen) with reduced blood pressure is contraindicated!
• The use of calcium gluconate and calcium chloride is contraindicated (they are ineffective, their effect gives an unpredictable result in the further course of the disease)!
• The appointment of diuretics is contraindicated (in shock, they increase the deficiency of BCC, hypovolemia and arterial hypotension)!
• Be sure to hospitalize the patient after the relief of symptoms due to the delayed phase of the allergic reaction of anaphylactic shock!

Infectious-toxic shock: clinical symptoms and first aid for shock

Infectious-toxic or dehydration shock (ITS) is one of the most severe emergency conditions, an extreme manifestation of the syndrome of intoxication and dehydration that develops in various infectious diseases. Each disease has its own clinical and pathogenetic features. The leading mechanism of infectious-toxic shock is acute toxic vascular insufficiency with a progressive decrease in venous blood return, disorganization of microcirculation, accompanied by the development of metabolic acidosis, DIC syndrome, and multiple organ lesions.

Clinically, the following main stages of this type of shock conditions are distinguished:

The first signs of infectious-toxic shock I degree:

• body temperature 38.5-40.5 ° C;
• moderate tachycardia;
• BP is normal or elevated;
• tachypnea, hyperpnea;
• diuresis is satisfactory or somewhat reduced (25 ml/h);
• general hyperreflexia;
• consciousness is preserved, excitement, anxiety are possible;
• in infants - often convulsive readiness.

The main symptoms of infectious-toxic shock II degree:

• body temperature is normal or subnormal;
• severe tachycardia, weak pulse;
• BP is reduced (60-90 mm Hg);
• pronounced tachypnea;
• diuresis is reduced (25-10 ml/h);
• lethargy, lethargy.

The main signs of infectious-toxic shock III degree:

• sharp tachycardia;
• pulse is thready or not defined;
• BP is very low or zero;
• diuresis is reduced (less than 10 ml / h) or anuria;
• severe tachypnea;
• consciousness is clouded;
• muscle hypertension (mask face);
• hyperreflexia;
• foot pathological reflexes;
• the pupils are narrowed, the reaction to light is weakened;
• possible strabismus, meningeal symptoms;
• convulsions.

Symptoms of infectious-toxic shock IV degree (agonal state):

• consciousness is absent (coma);
• pronounced respiratory disorders;
• pupils are dilated, without reaction to light;
• tonic convulsions.

When providing first aid for this type of shock, children are administered:

• prednisone 5-10 mg/kg intravenously (if impossible - intramuscularly), with positive dynamics - re-introduction after 6 hours, with insufficient effectiveness - re-introduction in full or half dose with an interval of 30-40 minutes;
• intravenous infusion therapy to restore BCC - colloidal solutions (rheopolyglucin, albumin) at a dose of 15-20 ml / kg, crystalloid solutions at a dose of 130-140 ml / kg per day;
• oxygen therapy;
• hospitalization in the infectious diseases department.

First aid for signs of infectious-toxic shock for adults:

• puncture of two peripheral veins and infusion of crystalloid solutions in / in at a rate of 80-100 ml / min in a volume of 10% of the initial body weight;
• call for the resuscitation team.