Creation of shock. Shock states of various origins. Vicious circle promoting vasomotor center insufficiency

Story

The state of shock was first described by Hippocrates. The term “shock” was first used in Le Dran. At the end of the 19th century, possible mechanisms for the development of the pathogenesis of shock began to be proposed, among them the following concepts became the most popular:

  • paralysis of the nerves innervating the vessels;
  • depletion of the vasomotor center;
  • neurokinetic disorders;
  • dysfunction of the endocrine glands;
  • decrease in circulating blood volume (CBV);
  • capillary stasis with impaired vascular permeability.

Pathogenesis of shock

From a modern point of view, shock develops in accordance with G. Selye's theory of stress. According to this theory, excessive exposure to the body causes specific and nonspecific reactions in it. The first ones depend on the nature of the effect on the body. The second - only from the force of influence. Nonspecific reactions when exposed to a super-strong stimulus are called general adaptation syndrome. General adaptation syndrome always occurs in the same way, in three stages:

  1. stage compensated (reversible)
  2. decompensated stage (partially reversible, characterized by a general decrease in the body’s resistance and even death of the body)
  3. terminal stage (irreversible, when no therapeutic interventions can prevent death)

Thus, shock, according to Selye, is a manifestation nonspecific reaction body to overexposure.

Hypovolemic shock

This type of shock occurs as a result of a rapid decrease in circulating blood volume, which leads to a drop in the filling pressure of the circulatory system and a decrease in venous return of blood to the heart. As a result, a violation of the blood supply to organs and tissues and their ischemia develops.

Causes

Circulating blood volume can quickly decrease due to the following reasons:

  • blood loss;
  • plasma loss (for example, due to burns, peritonitis);
  • loss of fluid (for example, with diarrhea, vomiting, profuse sweating, diabetes mellitus and diabetes insipidus).

Stages

Depending on the severity of hypovolemic shock, three stages are distinguished in its course, which successively replace each other. This

  • The first stage is non-progressive (compensated). At this stage there are no vicious circles.
  • The second stage is progressive.
  • The third stage is the stage of irreversible changes. At this stage, no modern antishock drugs can bring the patient out of this state. At this stage, medical intervention can return blood pressure and cardiac output to normal for a short period of time, but this does not stop the destructive processes in the body. Among the reasons for the irreversibility of shock at this stage, a violation of homeostasis is noted, which is accompanied by severe damage to all organs, especially damage to the heart.

Vicious circles

With hypovolemic shock, many vicious circles are formed. Among them, the most important is the vicious circle that promotes myocardial damage and the vicious circle that promotes insufficiency of the vasomotor center.

Vicious circle promoting myocardial damage

A decrease in circulating blood volume leads to a decrease in cardiac output and a drop in blood pressure. A drop in blood pressure leads to a decrease in blood circulation in the coronary arteries of the heart, which leads to a decrease in myocardial contractility. A decrease in myocardial contractility leads to an even greater decrease in cardiac output, as well as a further drop in blood pressure. The vicious circle closes.

Vicious circle promoting vasomotor center insufficiency

Hypovolemia is caused by a decrease in cardiac output (that is, a decrease in the volume of blood expelled from the heart in one minute) and a decrease in blood pressure. This leads to a decrease in blood flow in the brain, as well as to disruption of the vasomotor (vasomotor) center. The latter is located in the medulla oblongata. One of the consequences of a disorder in the vasomotor center is considered to be a decrease in the tone of the sympathetic nervous system. As a result, the mechanisms of centralization of blood circulation are disrupted, blood pressure drops, and this, in turn, triggers a violation of cerebral circulation, which is accompanied by even greater depression of the vasomotor center.

Shock organs

Recently, the term “shock organ” (“shock lung” and “shock kidney”) has often been used. This means that exposure to a shock stimulus disrupts the function of these organs, and further disturbances in the condition of the patient’s body are closely related to changes in the “shock organs”.

"Shock Lung"

Story

The term was first coined by Ashbaugh to describe the syndrome of progressive acute respiratory failure. However, back in the year Burford And Burbank described a similar clinical and anatomical syndrome, calling it "wet (moist) lung". After some time, it was discovered that the picture of “shock lung” occurs not only with shock, but also with craniocerebral, thoracic, abdominal injuries, blood loss, prolonged hypotension, aspiration of acidic gastric contents, massive transfusion therapy, increasing cardiac decompensation, pulmonary embolism. Currently, no relationship has been found between the duration of shock and the severity of pulmonary pathology.

Etiology and pathogenesis

The most common cause of the development of “shock lung” is hypovolemic shock. Ischemia of many tissues, as well as a massive release of catecholamines, lead to the entry into the blood of collagen, fat and other substances that cause massive thrombus formation. Because of this, microcirculation is disrupted. A large number of blood clots settle on the surface of the pulmonary vessels, which is due to the structural features of the latter (long convoluted capillaries, double blood supply, shunting). Under the influence of inflammatory mediators (vasoactive peptides, serotonin, histamine, kinins, prostaglandins), vascular permeability in the lungs increases, bronchospasm develops, the release of mediators leads to vasoconstriction and damage.

Clinical picture

Shock lung syndrome develops gradually, usually reaching its apogee after 24-48 hours, often resulting in massive (often bilateral) damage to the lung tissue. The process is clinically divided into three stages.

  1. First stage (initial). Arterial hypoxemia (lack of oxygen in the blood) predominates; the X-ray picture of the lung is usually not changed (with rare exceptions, when X-ray examination shows an increase in the pulmonary pattern). There is no cyanosis (blue discoloration of the skin). The partial pressure of oxygen is sharply reduced. Auscultation reveals scattered dry rales.
  2. Second stage. In the second stage, tachycardia increases, that is, the heart rate increases, tachypnea (respiratory rate) occurs, the partial pressure of oxygen decreases even more, mental disorders intensify, and the partial pressure of carbon dioxide increases slightly. Auscultation reveals dry and sometimes fine rales. Cyanosis is not expressed. X-ray reveals a decrease in the transparency of the lung tissue, bilateral infiltrates and unclear shadows appear.
  3. Third stage. In the third stage, the body is not viable without special support. Cyanosis develops. X-ray reveals an increase in the number and size of focal shadows with their transition to confluent formations and total darkening of the lungs. The partial pressure of oxygen decreases to critical levels.

"Shock Kidney"

Pathological specimen of a kidney from a patient who died of acute renal failure.

The concept of “shock kidney” reflects acute renal dysfunction. In the pathogenesis, the leading role is played by the fact that during shock, a compensatory shunting of arterial blood flow into the direct veins of the pyramids occurs with a sharp decrease in the volume of hemodynamics in the area of ​​the renal cortex. This is confirmed by the results of modern pathophysiological studies.

Pathological anatomy

The kidneys are somewhat enlarged in size, swollen, their cortical layer is anemic, pale gray in color, the peri-cerebral zone and pyramids, on the contrary, are dark red. Microscopically, in the first hours, anemia of the vessels of the cortical layer and a sharp hyperemia of the peri-cerebral zone and direct veins of the pyramids are determined. Microthrombosis of the capillaries of the glomeruli and afferent capillaries is rare.

Subsequently, increasing dystrophic changes in the nephrothelium are observed, covering first the proximal and then the distal parts of the nephron.

Clinical picture

The picture of a “shock” kidney is characterized by a clinical picture of progressive acute renal failure. In its development, acute renal failure during shock goes through four stages:

The first stage occurs while the cause that caused acute renal failure is in effect. Clinically, there is a decrease in diuresis.

Second stage (oligoanuric). The most important clinical signs of the oligoanuric stage of acute renal failure include:

  • oligoanuria (with the development of edema);
  • azotemia (smell of ammonia from the mouth, itching);
  • an increase in the size of the kidneys, lower back pain, a positive Pasternatsky sign (the appearance of red blood cells in the urine after tapping in the area of ​​​​the projection of the kidneys);
  • weakness, headache, muscle twitching;
  • tachycardia, expansion of the borders of the heart, pericarditis;
  • dyspnea, congestive wheezing in the lungs up to interstitial pulmonary edema;
  • dry mouth, anorexia, nausea, vomiting, diarrhea, cracks in the mucous membrane of the mouth and tongue, abdominal pain, intestinal paresis;

Third stage (restoration of diuresis). Diuresis can normalize gradually or rapidly. The clinical picture of this stage is associated with the resulting dehydration and diselectrolythemia. The following symptoms develop:

  • weight loss, asthenia, lethargy, lethargy, possible infection;
  • normalization of nitrogen excretory function.

Stage four (recovery). Homeostasis indicators, as well as kidney function, return to normal.

Literature

  • Ado A. D. Pathological physiology. - M., “Triad-X”, 2000. P. 54-60
  • Klimiashvili A.D. Chadayev A.P. Bleeding. Blood transfusion. Blood substitutes. Shock and resuscitation. - M., “Russian State Medical University”, 2006. P. 38-60
  • Meerson F.Z., Pshennikova M.G. Adaptation to stressful situations and physical activity. - M., “Triad-X”, 2000. P. 54-60
  • Poryadin G.V. Stress and pathology. - M., “Miniprint”, 2002. P. 3-22
  • Struchkov V.I. General surgery. - M., “Medicine”, 1978. P. 144-157
  • Sergeev S.T.. Surgery of shock processes. - M., “Triad-X”, 2001. P. 234-338

Notes

Shock(from the French choc - blow, push) is an acute hemodynamic disorder, as a result of which tissue hypoperfusion develops. A more complete definition may be as follows: shock is a severe pathological process, accompanied by the depletion of the vital functions of the body and bringing it to the brink of life and death due to a critical decrease in capillary blood flow in the affected organs. In general, the concept of “shock” until now is not one of the precisely determined ones. Deslauriers famous statement on this matter: “Shock is easier to recognize than to describe, and easier to describe than to define it.”

The initial pathogenetic mechanism of shock, as a rule, is a massive flow of biologically negative afferentation entering the central nervous system from the area of ​​influence of the damaging factor.

Initially, an idea arose about the nature of shock as a result of intolerable painful irritation associated with trauma, causing widespread overexcitation of the central nervous system with subsequent depletion.

Today, the number of conditions that various authors attribute to shock has expanded enormously and currently amounts to dozens in some sources. For example, hemolytic, painful, obstetric, spinal, toxic, hemorrhagic, cardiogenic shock, etc. The inclusion of such a significant number of pathological processes in the concept of shock is often apparently due to the fact that it is not differentiated from collapse and coma. Indeed, shock and collapse have common pathogenetic links: vascular insufficiency, respiratory failure, hypoxia, compensatory reactions.

However, there are also significant differences, for example, with collapse, the process begins precisely with systemic hemodynamic disorders; In case of shock, changes in blood circulation occur secondarily. Other differences are shown in the table (according to A.I. Volozhin, G.V. Poryadin, 1999).

Stages, manifestations and basic mechanisms of shock development. Any shock is characterized by a two-phase change in the activity of the central nervous system: initial widespread excitation of neurons (“erectile stage” or compensation stage); subsequently widespread inhibition of their activity (“torpid stage” or stage of decompensation). Consciousness is usually maintained during both phases of shock. It can be significantly reduced and changed (especially in the torpid phase of shock), but is not completely lost. Reflex reactions to external stimuli of various modalities are also preserved, although significantly weakened.

Sometimes there is a third stage of shock - the so-called terminal stage, in which consciousness is completely absent. This stage is essentially a comatose state with all its characteristic signs.

The erectile stage (compensation) of shock is characterized by increased sympathoadrenal and pituitary-adrenal influences, which increase the activity of most physiological systems. At the beginning of the torpid phase of shock, the level of catecholamines and corticosteroids usually remains elevated, but the effectiveness of their action on various organs is reduced. Subsequently, there is a decrease in the activity of the sympathoadrenal, pituitary-adrenal systems and the content of corresponding hormones in the blood. Therefore, during the first stage of shock, the functions of the circulatory system are activated and, as a result, tachycardia, arterial hypertension, and redistribution of blood flow occur; in addition, there is an increase in breathing rate and an increase in alveolar ventilation; Erythrocytosis may occur due to the release of blood from the depot.

In the second stage of shock, central hemodynamics are weakened: blood pressure decreases, the deposited blood fraction increases, blood volume and pulse pressure decrease, and a “thread-like” pulse is often noted. With mild shock, blood pressure drops to 90–100 mmHg. Art., with moderate severity - up to 70-80, with severe - up to 40-60. Alveolar ventilation decreases, and pathological forms of breathing may appear. In the stage of decompensation, increasing circulatory and respiratory failure leads to the development of severe hypoxia, and it is this that subsequently determines the severity of the shock state.

Characteristics of shock are microcirculation disorders. They can occur already at the first stage due to the redistribution of blood flow and its reduction in a number of organs (kidneys, liver, intestines, etc.). As we move into the torpid phase, microcirculatory disorders become increasingly widespread, manifesting not only as a decrease in microvascular perfusion, but also as a deterioration in the rheological properties of blood, increased permeability of capillary walls, aggregation of formed elements, and perivascular edema.

An obligatory pathogenetic factor in shocks of various etiologies is endotoxemia. Numerous biologically active substances that enter the internal environment of the body in excess (histamine, serotonin, kinins, catecholamines, etc.) have a toxic effect during shock. Denatured proteins and their breakdown products, lysosomal enzymes, toxic intestinal products, microbes and their toxins may appear in the blood. Of significant importance in the development of toxemia are metabolites that are intensively formed in cells due to metabolic disorders: lactic and pyruvic acids, keto acids, potassium, etc. Dysfunctions of the liver and kidneys that arise as a result of hypoxia and microcirculation disorders lead to even greater changes in blood composition: acidosis, ionic and protein imbalance, shifts in osmotic and oncotic pressure in various environments of the body.

The above changes in the body leave an imprint on biochemical processes in the cell (“shock” cell). Cellular disorders are characterized by the well-known triad of hypoxia: ATP deficiency, acidosis, damage to biomembranes.

It is very important that during the development of shock, so-called “vicious circles” often arise. In this case, the initial disorders of the activity of organs and systems can be potentiated, and the shock tends to “deepen itself.” For example, disorders of the central circulation and microcirculation lead to dysfunction of the liver and kidneys, and the resulting unfavorable changes in the composition of the blood aggravate circulatory disorders. At a certain stage of the torpid stage of shock, hemodynamic disturbances can reach such a degree that secondary collapse develops, which quite often joins shock with its unfavorable development and sharply worsens the patient’s condition.

So, I have outlined, in very general terms, modern ideas about the pathogenesis of shock states. It is clear that the nature, severity and specific significance of each of the pathogenetic factors can vary widely depending on the type of shock, its stage and severity, as well as the reactive properties of the body.

Let me once again emphasize the complexity of the problem of classifying various types of shock states. There is still a lot of discussion around this issue, since there is no single classification. However, most authors, taking into account the main etiological factors and pathogenetic mechanisms, identify the following forms of shock: primary hypovolemic; cardiogenic; vascular-peripheral; traumatic. Examples and brief descriptions of these forms of shock are given in textbooks. It seems to us that shock states are most successfully classified by V.A. Frolov (see diagram).

Previously, we considered the main points of the pathogenesis of anaphylactic and burn shock. Therefore, we will focus only on traumatic, blood transfusion and cardiogenic shock.

Traumatic shock. The cause is usually widespread injuries to bones, muscles, internal organs, accompanied by damage and severe irritation of nerve endings, trunks and plexuses. Traumatic shock is often accompanied or aggravated by blood loss and wound infection.

Here I will dwell on the following point. Views on the mechanism of shock development have undergone significant changes over time. If the neurogenic theory of shock, which was especially popular in the 30-40s. XX century in our country, primarily explained the development of shock as a reflex change in the state of the body in response to pain impulses that arose at the time of injury, then the theory of blood and plasma loss put forward by Blelok (1934) practically did not take into account pain impulses as a significant factor in its development. Currently, most pathophysiologists and clinicians believe that traumatic shock develops as a result of the influence of several pathological factors on the body. First of all, these are pain impulses, blood and plasma loss, and toxemia.

And two more points that you should pay attention to. Firstly, despite the fact that blood loss is one of the significant causes of the development of traumatic shock, it would be wrong to identify changes in blood circulation, including microcirculation, only with a deficiency of bcc. Indeed, in the development of pure blood loss and traumatic shock there are common pathogenetic factors - a state of stress, hypotension accompanied by hypoxia, inadequate afferent impulses from injured tissues during shock or from baro- and chemoreceptors of blood vessels during blood loss. However, disturbances in nervous activity during traumatic shock occur earlier and are more severe than with blood loss. Stimulation of the HPA axis during shock is accompanied by a sharp decrease in the ability of tissues to absorb corticosteroids, which entails the development of extra-adrenal corticosteroid insufficiency. With blood loss, on the contrary, the level of tissue consumption of corticosteroids increases.

Secondly, the activation of defense mechanisms in response to severe injury is accompanied by the activation of antinociceptive defense (see the chapter on the pathophysiology of pain). But here it should be noted that an increase in the content of endogenous opiates, which should have a protective nature in the event of severe trauma, in fact often turns into an irreparable disaster for the body. The fact is that excessive stimulation of all parts of the HPA axis, which always accompanies severe injury, leads to the release of large amounts of enkephalins and endorphins, which, in addition to blocking opiate receptors, perform a number of other functions in the body. First of all, it is involved in the regulation of blood circulation and respiration. It is now known that endorphins can disrupt the regulation of blood circulation and contribute to the development of uncontrollable hypotension.

Thus, efferent manifestations of pain, leading to excessive stimulation of the HPA axis, not only do not protect the body from injury, but, on the contrary, contribute to the development of deep damage to the body’s most important life support systems and the development of traumatic shock.

During the erectile stage, the patient experiences speech and motor agitation: he rushes about, reacts sharply even to ordinary touch; the skin is pale due to spasm of skin microvessels; the pupils are dilated due to activation of the sympathoadrenal system; indicators of central circulation and respiration are increased.

The first stage is replaced by the second - torpid. Its classic clinical picture was described by N.I. Pirogov (1865): “With an arm or leg torn off, such a numb person lies motionless at the dressing station; he does not shout, does not complain, does not take part in anything and does not demand anything; his body is cold, his face is pale; the gaze is motionless and turned into the distance, the pulse is like a thread, barely noticeable under the finger. The numb person either does not answer questions at all, or only to himself, in a barely audible whisper; breathing is also barely noticeable. The wound and skin are almost completely insensitive... The numb man has not completely lost consciousness, not only is he not at all aware of his suffering.”

Typically, patients with severe traumatic shock die from progressive circulatory disorders, respiratory or renal failure. Microperfusion disturbances occur in the lungs, blood shunting increases, and the diffusion properties of alveolar-capillary membranes deteriorate due to their swelling and the development of interstitial edema. Disturbances in the gas exchange function of the lungs during traumatic shock are a very dangerous phenomenon that requires emergency intervention (“shock lung”).

Reduction of blood circulation and microcirculatory disorders in the kidneys lead to kidney failure, manifested by oliguria (or anuria), azotemia and other disorders. In the later stages of shock in the kidneys, along with severe microcirculation disorders, blockage of the tubular apparatus is possible due to the formation of hyaline and myoglobin casts (“shock kidney”). In severe cases of traumatic shock, intestinal autointoxication develops.

Note that the course of shock in childhood has its own characteristics. The most characteristic feature of traumatic shock at an early age is the ability of the child’s body to maintain normal blood pressure levels for a long time even after severe injury. Long-term and persistent centralization of blood circulation in the absence of treatment is suddenly replaced by hemodynamic decompensation. Therefore, the younger the child, the more unfavorable a prognostic sign for shock is arterial hypotension.

Blood transfusion shock. The direct cause of transfusion shock may be incompatibility of the blood of the donor and recipient with respect to group ABO factors, Rh factor or individual antigens. Shock can develop, and its course will worsen significantly in cases where low-quality blood is used (with hemolysis, protein denaturation, bacterial contamination, etc.).

The first signs of shock may appear already during transfusion (in case of group incompatibility) or in the next few hours (in case of Rh incompatibility or incompatibility with individual antigens).

In the occurrence of blood transfusion shock due to group or Rh incompatibility, the main pathogenetic factor is massive agglutination and the formation of erythrocyte conglomerates followed by their hemolysis. As a result, the physicochemical properties of blood change dramatically. It is believed that these changes serve as a trigger for shock as a result of extreme irritation of the wide receptive field of the vascular bed. Significant intravascular hemolysis leads to a sharp deterioration in the oxygen transport functions of the blood and the development of hemic hypoxia, the severity of which subsequently increases as a result of circulatory disorders.

Manifestations. During the erectile stage, motor excitement occurs, rapid breathing with difficulty exhaling, a feeling of heat, and pain in different parts of the body (especially in the kidney area) are noted. Systemic blood pressure may increase and tachycardia may occur.

The first stage is quickly replaced by the second (torpid). General weakness occurs, redness of the skin gives way to severe pallor, and nausea and vomiting often occur. Against the background of general physical inactivity, convulsions may develop, and blood pressure drops. This type of shock is characterized (to a large extent determine the severity of the condition) by impaired renal function (the so-called blood transfusion nephrosis). The appearance of oliguria or anuria during transfusion shock is always a sign of a dangerous deterioration in the patient's condition.

Cardiogenic shock is a critical condition that develops as a result of acute arterial hypotension caused by a sharp drop in the pumping function of the left ventricle. The primary link in the pathogenesis of cardiogenic shock is a rapid decrease in stroke volume of the left ventricle, which leads to arterial hypotension, despite compensatory spasm of resistive vessels and an increase in total peripheral vascular resistance aimed at restoring blood pressure.

Arterial hypotension and decreased blood flow through the exchange capillaries due to spasm of the smallest arteries, arterioles and precapillary sphincters disrupt blood flow in the organs in the periphery and cause the main symptoms of cardiogenic shock. Namely: disturbances of consciousness; pale skin, cold and damp extremities; oliguria (<20 мл/ч); артериальная гипотензия (систолическое АД < 90 мм рт.ст.).

Cardiogenic shock occurs, according to many authors, in 12–15% of cases of myocardial infarction. The occurrence of cardiogenic shock depends on the size of the zone of myocardial damage, its initial state, central circulation, as well as on the functional characteristics of the nociceptive and antinociceptive system and other factors that determine the reactivity of the body.

When 50–65% of the myocardial mass is affected, either cardiac fibrillation or acute circulatory failure occurs. In this case, shock may not occur. Cardiogenic shock often develops when a smaller mass of the myocardium is affected (up to 50%) against the background of sharp pain, accompanied by chaotic excitation of various autonomic centers and disorders of the neuroendocrine regulation of blood circulation and other physiological systems.

I would like to draw attention to this fundamental distinctive feature of the pathogenesis of this type of shock. Arterial hypotension, which occurs due to traumatic shock, is not the leading link in the pathogenesis of this pathological condition, but a consequence of the failure of compensation for traumatic shock, in which pathological changes in organs and tissues form long before the decrease in blood pressure. In cardiogenic shock, on the contrary, arterial hypotension immediately begins to act as one of the main links in pathogenesis.

Compensatory reactions in response to arterial hypotension and circulatory hypoxia in cardiogenic shock are almost identical to those in patients in a state of traumatic or hypovolemic shock. In particular they include:

Predominantly neurogenic spasm of veins as a result of increased sympathetic vasoconstrictor influences;

Activation of the renin-angiotensin-aldosterone mechanism, including as a result of systemic adrenergic stimulation;

Compensatory autohemodilution, i.e. mobilization of fluid from the interstitial sector to the vascular sector due to changes at the systemic level in the relationship between pre- and postcapillary vascular resistance.

The biological purpose of such compensatory reactions is clear - maintaining IOC and blood pressure through an increase in total venous return, retention of sodium and water in the body, an increase in the intravascular fluid sector and an increase in peripheral vascular resistance. In cardiogenic shock, these protective reactions increase pre- and afterload, and therefore increase the utilization of free energy by cardiomyocytes. The increase in the work of contractile myocardial cells increases the discrepancy between the heart's need for oxygen and the delivery of O 2 to it. As a result, the mass of the hypoxic and hibernating myocardium increases, and its contractility decreases even more.

From the above it follows: the main pathophysiological feature of cardiogenic shock is that compensatory reactions initially have the properties of pathogenesis links, the action of which determines the progression of shock and its acquisition of an irreversible nature. In addition, in cardiogenic shock, the main effector of compensatory reactions aimed at maintaining minute volume of blood circulation, the heart, is affected.

a symptom complex of disorders of the vital functions of the body that arise as a result of a discrepancy between tissue blood flow and the metabolic need of tissues.

During the development of shock, the body's main task is to maintain adequate blood flow to vital organs (heart and brain). Therefore, initially, vasoconstriction occurs in other organs and tissues, thus achieving centralization of blood circulation. Such prolonged narrowing of blood vessels over time leads to the development of ischemia - a decrease in blood supply to an organ or tissue that occurs due to 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 body’s protective adaptive mechanism—centralization of blood circulation—is disrupted, which entails serious consequences.

According to 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 led to the development of this condition. For example, shock can lead to complications such as failure of a number of internal organs, swelling of the lungs and brain. Such dire consequences can lead to death, so shock requires increased attention.

Symptoms


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

With traumatic shock, patients complain of severe pain caused by the injury. 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. In septic shock, elevated body temperature is detected, which is difficult to control by taking antipyretic drugs.

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 the patient has and analyze the situation individually in each case. To diagnose shock, it is necessary to identify signs of insufficient blood circulation to tissues, as well as to detect the inclusion of compensatory mechanisms of the body.

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

It is important to quickly compare all the symptoms, 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 timely medical assistance. Before specialists arrive, people nearby should take first aid measures. First, you need to give the person a horizontal position with the leg end raised. Such actions help to increase venous return to the heart, which leads to an increase in stroke volume of the heart. During shock, the heart can no longer cope with the stroke volume of blood required to deliver the required amount of oxygen to the tissues. A horizontal position with elevated legs, although it does not completely compensate for the insufficiency of the stroke volume of the heart, but helps to improve this condition.

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

The use of medications that constrict blood vessels is necessary to maintain blood pressure.

In case of breathing problems, oxygen therapy or mechanical ventilation is used.

These general measures are aimed at combating the pathogenesis of shock; there is also symptomatic treatment, different for each type of shock. For example, in case of traumatic shock, it is necessary to administer painkillers, immobilize fractures, or apply a sterile dressing to the wound. Cardiogenic shock requires treatment of the cause contributing to the development of 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, squeezing a vessel in the wound, etc.), general measures will not have the desired effect. Septic shock is accompanied by fever, so antipyretics are used as symptomatic treatment, and antibacterial drugs are prescribed to eliminate the cause itself. When treating anaphylactic shock, it is important to prevent delayed systemic manifestations; glucocorticosteroids and antihistamines are used for this purpose. It is also necessary to stop the phenomenon of bronchospasm.

Medicines


When shock develops, it is important to provide access to a vein as quickly as possible, preferably not to one, but to several at once. This is necessary to start infusion therapy, as well as administer drugs directly into the bloodstream. Infusion therapy influences the main links of pathogenesis. It is able to maintain an optimal level of BCC (circulating blood volume), which leads to stabilization of hemodynamics, improves microcirculation, thereby increasing the delivery of oxygen 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, polydesis, polyoxidin, polyglucin, rheopolyglucin).

Usually a combination of crystalloid and colloid 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 promotes 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 effect begins approximately 5 minutes after intravenous administration and lasts about 10 minutes.

Folk remedies


Shock of various etiologies requires exclusively medical care; no recipes of 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 ambulance team to arrive, you should follow the first aid measures that were described earlier (put the person in a horizontal position with the leg end raised, warm the body). Not only the effectiveness of treatment, but also a person’s life depends on correct 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.

Based on the leading trigger factor, the following types of shock can be distinguished:

1. Hypovolemic shock:

  • Hemorrhagic shock (with massive blood loss).
  • Traumatic shock (combination of blood loss with excessive pain impulses).
  • Dehydration shock (excessive loss of water and electrolytes).

2. Cardiogenic shock is caused by a violation of myocardial contractility (acute myocardial infarction, aortic aneurysm, acute myocarditis, rupture of the interventricular septum, cardiomyopathies, severe arrhythmias).

3. Septic shock:

  • Action of exogenous toxic substances (exotoxic shock).
  • The action of bacteria, viruses, endotoxemia due to massive destruction of bacteria (endotoxic, septic, infectious-toxic shock).

4. Anaphylactic shock.

Mechanisms of shock development

Common to shock are hypovolemia, impaired rheological properties of blood, sequestration in the microcirculation system, tissue ischemia and metabolic disorders.

In the pathogenesis of shock, the following are of primary importance:

  1. Hypovolemia. True hypovolemia occurs as a result of bleeding, loss of plasma and various forms of dehydration (primary decrease in blood volume). Relative hypovolemia occurs at a later date during deposition or sequestration of blood (in septic, anaphylactic and other forms of shock).
  2. Cardiovascular failure. This mechanism is primarily characteristic of cardiogenic shock. The main reason is a decrease in cardiac output associated with impaired contractile function of the heart due to acute myocardial infarction, damage to the valvular apparatus, arrhythmias, pulmonary embolism, etc.
  3. Activation of the sympathetic-adrenal system occurs as a result of an increased release of adrenaline and norepinephrine and causes centralization of blood circulation due to spasm of arterioles, pre- and especially post-capillary sphincters, and opening of arteriovenous anastomoses. This leads to impaired organ circulation.
  4. In the zone microcirculation Spasms of pre- and postcapillary sphincters, an increase in arteriovenous anastomoses, and blood shunting, which sharply disrupt tissue gas exchange, continue to increase. There is an accumulation of serotonin, bradykinin and other substances.

Violation of organ circulation causes the development of acute renal and liver failure, shock lung, and dysfunction of the central nervous system.

Clinical manifestations of shock

  1. Decrease in systolic blood pressure.
  2. Decreased pulse pressure.
  3. Tachycardia.
  4. Reduced diuresis to 20 ml per hour or less (oligo- and anuria).
  5. Impaired consciousness (excitement is possible at first, then lethargy and loss of consciousness).
  6. Poor peripheral circulation (pale, cold, clammy skin, acrocyanosis, decreased skin temperature).
  7. Metabolic acidosis.

Stages of diagnostic search

  1. The first stage of diagnosis is to identify signs of shock based on its clinical manifestations.
  2. The second stage is to establish the possible cause of shock based on medical history and objective signs (bleeding, infection, intoxication, anaphylaxis, etc.).
  3. The final stage is to determine the severity of shock, which will allow us to develop patient management tactics and the scope of emergency measures.

When examining a patient at the site of development of a threatening condition (at home, at work, on the street, in a vehicle damaged as a result of an accident), the paramedic can only rely on data from an assessment of the state of the systemic circulation. It is necessary to pay attention to the nature of the pulse (frequency, rhythm, filling and tension), depth and frequency of breathing, and blood pressure level.

The severity of hypovolemic shock in many cases can be determined using the so-called Algover-Burri shock index (AI). By the ratio of pulse rate to systolic blood pressure, the severity of hemodynamic disorders can be assessed and even approximately determined the amount of acute blood loss.

Clinical criteria for the main forms of shock

Hemorrhagic shock as a variant of hypovolemic shock. It can be caused by both external and internal bleeding.
In case of traumatic external bleeding, the location of the wound is important. Profuse bleeding is accompanied by wounds of the face and head, palms, soles (good vascularization and low-fat lobules).

Symptoms. Signs of external or internal bleeding. Dizziness, dry mouth, decreased diuresis. The pulse is frequent and weak. Blood pressure is reduced. Breathing is frequent and shallow. Increase in hematocrit. The rate of blood loss is of decisive importance in the development of hypovolemic hemorrhagic shock. A decrease in blood volume by 30% within 15-20 minutes and a delay in infusion therapy (up to 1 hour) lead to the development of severe decompensated shock, multiple organ failure and high mortality.

Dehydration shock (DS). Dehydration shock is a variant of hypovolemic shock that occurs with profuse diarrhea or repeated uncontrollable vomiting and is accompanied by severe dehydration of the body - exicosis - and severe electrolyte disturbances. Unlike other types of hypovolemic shock (hemorrhagic, burn), direct loss of blood or plasma does not occur during the development of shock. The main pathogenetic cause of DS is the movement of extracellular fluid through the vascular sector into the extracellular space (into the intestinal lumen). With severe diarrhea and repeated profuse vomiting, the loss of body fluid can reach 10-15 liters or more.

DS can occur with cholera, cholera-like variants of enterocolitis and other intestinal infections. A condition characteristic of DS can be detected in cases of high intestinal obstruction and acute pancreatitis.

Symptoms. Signs of intestinal infection, profuse diarrhea and repeated vomiting in the absence of high fever and other manifestations of neurotoxicosis.
Signs of dehydration: thirst, haggard face, sunken eyes, significant decrease in skin turgor. Characterized by a significant drop in skin temperature, frequent shallow breathing, and severe tachycardia.

Traumatic shock. The main factors in this shock are excessive pain impulses, toxemia, blood loss, and subsequent cooling.

  1. The erectile phase is short-lived, characterized by psychomotor agitation and activation of basic functions. Clinically, this is manifested by normo- or hypertension, tachycardia, tachypnea. The patient is conscious, excited, euphoric.
  2. The torpid phase is characterized by psycho-emotional depression: indifference and prostration, a weak reaction to external stimuli. The skin and visible mucous membranes are pale, cold sticky sweat, rapid thready pulse, blood pressure below 100 mm Hg. Art., body temperature is reduced, consciousness is preserved.

However, at present, the division into erectile and torpid phases is losing its meaning.

According to hemodynamic data, there are 4 degrees of shock:

  • I degree - no pronounced hemodynamic disturbances, blood pressure 100-90 mm Hg. Art., pulse up to 100 per minute.
  • II degree - blood pressure 90 mm Hg. Art., pulse up to 100-110 per minute, pale skin, collapsed veins.
  • III degree - blood pressure 80-60 mm Hg. Art., pulse 120 per minute, severe pallor, cold sweat.
  • IV degree - blood pressure less than 60 mm Hg. Art., pulse 140-160 per minute.

Hemolytic shock. Hemolytic shock develops from transfusions of incompatible blood (by group or Rh factors). Shock can also develop when large volumes of blood are transfused.

Symptoms. During a blood transfusion or shortly after it, headache, pain in the lumbar region, nausea, bronchospasm, and fever appear. Blood pressure decreases, the pulse becomes weak and frequent. The skin is pale and moist. There may be convulsions and loss of consciousness. Hemolyzed blood and dark urine are noted. After recovery from shock, jaundice and oliguria (anuria) develop. On the 2-3rd day, shock lung with signs of respiratory failure and hypoxemia may develop.

In case of Rh conflict, hemolysis occurs at a later date, and clinical manifestations are less pronounced.

Cardiogenic shock. The most common cause of cardiogenic shock is myocardial infarction.

Symptoms. Pulse is frequent and small. Impaired consciousness. Decrease in diuresis less than 20 ml/hour. Severe metabolic acidosis. Symptoms of peripheral circulatory disorders (skin pale cyanotic, moist, collapsed veins, decreased temperature, etc.).

There are four forms of cardiogenic shock: reflex, “true”, arrhythmogenic, areactive.

The cause of the reflex form of cardiogenic shock is a response to pain mediated through baro- and chemoreceptors. Mortality with erectile shock exceeds 90%. Heart rhythm disturbances (tachy- and bradyarrhythmias) often lead to the development of an arrhythmogenic form of cardiogenic shock. The most dangerous are paroxysmal tachycardia (ventricular and, to a lesser extent, supraventricular), atrial fibrillation, and complete atrioventricular block, often complicated by MES syndrome.

Infectious-toxic shock. Infectious-toxic shock is predominantly a complication of purulent-septic diseases, in approximately 10-38% of cases. It is caused by the penetration into the bloodstream of a large number of toxins of gram-negative and gram-positive flora, affecting the microcirculation and hemostasis systems.
There is a hyperdynamic phase of ITS: an initial (short-term) “hot” period (hyperthermia, activation of the systemic circulation with an increase in cardiac output with a good response to infusion therapy) and a hypodynamic phase: a subsequent, longer “cold” period (progressive hypotension, tachycardia, significant resistance to intensive therapy. Exo- and endotoxins, proteolysis products have a toxic effect on the myocardium, lungs, kidneys, liver, endocrine glands, reticuloendothelial system. Severe disturbance of hemostasis is manifested by the development of acute and subacute DIC syndrome and determines the most severe clinical manifestations of toxic-infectious shock.

Symptoms. The clinical picture consists of the symptoms of the underlying disease (acute infectious process) and symptoms of shock (drop in blood pressure, tachycardia, shortness of breath, cyanosis, oliguria or anuria, hemorrhages, hemorrhages, signs of disseminated intravascular coagulation).

Diagnosis of shock

  • Clinical assessment
  • Sometimes lactate is detected in the blood, a deficiency of bases.

Diagnosis is primarily clinical, based on evidence of inadequate tissue perfusion (stunning, oliguria, peripheral cyanosis) and evidence of compensatory mechanisms. Specific criteria include stupor, heart rate >100/min, respiratory rate >22, hypotension, or 30 mmHg. drop in baseline blood pressure and diuresis<0,5 мл/кг/ч. Лабораторные исследования в пользу диагноза включают лактат >3 mmol/l, base deficiency, and PaCO 2<32 мм рт. Однако ни один из этих результатов не является диагностическим и каждый оценивается в общем клиническом контексте, в т.ч. физические признаки. В последнее время, измерение сублингвального давления РСO 2 и ближней инфракрасной спектроскопии были введены в качестве неинвазивных и быстрых методов, которые могут измерять степень шока, однако эти методы до сих пор не подтверждены в более крупном масштабе.

Diagnosis of the cause. Knowing the cause of shock is more important than classifying the type. Often the cause is obvious or can be discovered quickly based on the history and physical examination, using simple testing techniques.

Chest pain (with or without shortness of breath) suggests MI, aortic dissection, or pulmonary embolism. A systolic murmur may indicate ventricular rupture, atrial septal rupture, or mitral valve regurgitation due to acute MI. A diastolic murmur may indicate aortic regurgitation due to aortic dissection involving the aortic root. Cardiac tamponade can be judged by the jugular vein, muffled heart sounds and paradoxical pulsation. Pulmonary embolism is severe enough to cause shock, usually causes a decrease in O2 saturation, and is more common in characteristic situations, including. with prolonged bed rest and after surgery. Tests include ECG, troponin I, chest x-ray, blood gases, lung scan, spiral CT, and echocardiography.

Abdominal or back pain suggests pancreatitis, rupture of an abdominal aortic aneurysm, peritonitis, and in women of childbearing age, rupture of an ectopic pregnancy. A pulsatile mass in the midline of the abdomen suggests an abdominal aortic aneurysm. A tender adnexal mass on palpation suggests an ectopic pregnancy. Testing usually includes a CT scan of the abdomen (if the patient is unstable, bedside ultrasound may be used), a complete blood count, amylase, lipase and, for women of childbearing age, a urine pregnancy test.

Fever, chills, and focal signs of infection suggest septic shock, especially in immunocompromised patients. Isolated fever depends on medical history and clinical conditions and may indicate heatstroke.

In several patients the cause is unknown. Patients who do not have focal symptoms or signs suggestive of a cause should have an ECG, cardiac enzymes, chest x-ray, and blood gas studies. If the results of these tests are normal, the most likely causes are drug overdose, obscure infections (including toxic shock), anaphylaxis, and obstructive shock.

Prognosis and treatment of shock

If left untreated, shock is fatal. Even with treatment, mortality from cardiogenic shock after MI (60% to 65%) and septic shock (30% to 40%) is high. The prognosis depends on the cause, pre-existing or complication of the disease, the time between onset and diagnosis, as well as the timeliness and adequacy of therapy.

General leadership. First aid is to keep the patient warm. Monitor external hemorrhages, check the airway and ventilation, and provide respiratory assistance if necessary. Nothing is given by mouth, and the patient's head is turned to one side to avoid aspiration if vomiting occurs.

Treatment begins at the same time as the assessment. Additional O 2 is delivered through the mask. If shock is severe or ventilation is inadequate, intubation of the airway with mechanical ventilation is necessary. Two large (16- to 18-gauge) catheters are inserted into separate peripheral veins. A central venous line or intraosseous needle, especially in children, provides an alternative when peripheral venous access is not available.

Typically, 1 L (or 20 ml/kg in children) of 0.9% saline is infused over 15 minutes. For bleeding, Ringer's solution is usually used. If clinical parameters do not return to normal levels, the infusion is repeated. Smaller volumes are used for patients with signs of high right-sided pressure (eg, distension of the jugular veins) or acute myocardial infarction. This strategy and volume of fluid administration should probably not be used in patients with signs of pulmonary edema. In addition, infusion therapy against the background of the underlying disease may require monitoring of central venous pressure or blood pressure. Bedside ultrasound of the heart to evaluate the contractility of the vena cava.

Critical illness monitoring includes ECG; systolic, diastolic and mean blood pressure, intra-arterial catheter is preferred; control of breathing rate and depth; pulse oximetry; installation of a permanent renal catheter; monitoring body temperature, and assessing clinical condition, pulse volume, skin temperature and color. Measurement of central venous pressure, pulmonary arterial pressure, and thermodilution of cardiac output using the balloon tip of a pulmonary artery catheter may be useful in the diagnosis and initial treatment of patients with shock of undetermined or mixed etiology or with severe shock, especially with oliguria or pulmonary edema. Echocardiography (bedside or transesophageal) is a less invasive alternative. Serial measurements of arterial blood gases, hematocrit, electrolytes, serum creatinine, and blood lactate. Sublingual CO 2 measurement, when available, is a non-invasive monitoring of visceral perfusion.

All parenteral drugs are given intravenously. Opioids are generally avoided because they can cause blood vessels to dilate. However, severe pain can be treated with morphine 1 to 4 mg intravenously over 2 minutes and repeated over 10 to 15 minutes if necessary. Although cerebral hypoperfusion may be concerning, sedatives or tranquilizers are not prescribed.

After initial resuscitation, specific treatment is aimed at the underlying disease. Additional supportive care depends on the type of shock.

Hemorrhagic shock. In hemorrhagic shock, surgical control of bleeding is the first priority. Intravenous resuscitation accompanies, rather than precedes, surgical control. Blood products and crystalloid solutions are used for resuscitation, however, packed red blood cells and plasma are considered first in patients who will require a 1:1 mass transfusion. Lack of response usually indicates insufficient volume or an unrecognized source of bleeding. Vasopressor agents are not indicated for the treatment of hemorrhagic shock if cardiogenic, obstructive, or distributive causes are also present.

Distribution shock. Distributive shock with profound hypotension after initial fluid resuscitation with 0.9% saline can be treated with inotropes or vasopressors (eg, dopamine, norepinephrine). Parenteral antibiotics should be used after blood samples are collected for culture. Patients with anaphylactic shock do not respond to fluid infusion (especially if accompanied by bronchospasm), they are shown epinephrine, and then epinephrine infusion.

Cardiogenic shock. Cardiogenic shock caused by structural abnormalities is treated surgically. Coronary thrombosis is treated either by percutaneous intervention (angioplasty, stenting), if a multi-vessel lesion of the coronary arteries is detected (coronary artery bypass grafting) or thrombolysis. For example, tachyform of atrial fibrillation, ventricular tachycardia are restored by cardioversion or medications. Bradycardia is treated by implantation of a percutaneous or transvenous pacemaker; atropine can be given intravenously in up to 4 doses over 5 minutes while awaiting pacemaker implantation. Isoproterenol may sometimes be prescribed if atropine is ineffective, but is contraindicated in patients with myocardial ischemia due to coronary artery disease.

If pulmonary artery occlusion pressure is low or normal, shock after acute MI is treated with volume expansion. If the pulmonary artery catheter is not in place, infusions are carried out with caution, while auscultation of the chest is performed (often accompanied by signs of overload). Shock after right ventricular infarction is usually accompanied by partial volume expansion. However, vasopressor agents may be necessary. Inotropic support is most preferred in patients with normal or above-normal filling. Tachycardia and arrhythmia sometimes occur during dobutamine administration, especially at higher doses, which requires a dose reduction of the drug. Vasodilators (eg, nitroprusside, nitroglycerin), which increase venous capacity or low systemic vascular resistance, reduce stress on the damaged myocardium. Combination therapy (eg, dopamine or dobutamine with nitroprusside or nitroglycerin) may be more beneficial but requires frequent ECG and pulmonary and systemic hemodynamic monitoring. For more severe hypotension, norepinephrine or dopamine may be given. Intraballoon counterpulsation is a valuable method for temporarily relieving shock in patients with acute myocardial infarction.

In obstructive shock, cardiac tamponade requires immediate pericardiocentesis, which can be done in bed.

Shock (English - blow, push)- an acute, life-threatening pathological process that occurs under the influence of a very strong irritant for the body and is characterized by disorders of the central and peripheral circulation with a sharp decrease in blood supply to vital organs. This leads to severe disturbances in cellular metabolism, resulting in changes or loss of normal cell function, and in extreme cases, cell death.

ETIOLOGY AND PATHOGENESIS

Many diseases potentially contribute to the development of shock and the following main groups of causes of its occurrence can be distinguished:

1. Primary decrease in circulating blood volume (hypovolemic shock) - with bleeding, dehydration, loss of plasma due to burns.
2. Impaired peripheral hemodynamics (redistribution or vasogenic shock) - sepsis, anaphylaxis, intoxication, acute adrenal insufficiency, neurogenic shock, traumatic shock.
3. Primary heart failure (cardiogenic shock) - with arrhythmias, myocarditis, acute left ventricular failure, myocardial infarction.
4. Obstruction of venous blood flow or cardiac output (obstructive shock) - in diseases of the pericardium, tension pneumothorax, pulmonary embolism, fat and air embolism, etc.

The essence of shock is a disruption of gas exchange between blood and tissues, followed by hypoxia and microcirculation disorders. The main pathogenetic links of shock are caused by hypovolemia, cardiovascular failure, impaired tissue circulation as a result of changes in capillary and post-capillary resistance, blood shunting, capillary stasis with aggregation of cellular elements of the blood (sludge syndrome), increased permeability of the vascular wall and blood rejection. Impaired tissue perfusion negatively affects all organs and systems, but the central nervous system is especially sensitive to hypoxia.

DIAGNOSTICS

There is no single generally accepted classification of shock in pediatrics. More often, the origin, phase of development, clinical picture and severity of shock are taken into account.

By origin they distinguish hemorrhagic, dehydration (anhydremic), burn, septic, toxic, anaphylactic, traumatic, endogenous pain, neurogenic, endocrine in acute adrenal insufficiency, cardiogenic, pleuropulmonary, post-transfusion shocks, etc.

According to the phases of development of peripheral circulatory disorders, the following are indicated:

  • early (compensated) phase
  • phase of pronounced shock c) late (decompensated) phase of shock.

According to the severity, shock can be classified as mild, moderate, or severe. Techniques that allow one to assess, first of all, the state of the cardiovascular system and the type of hemodynamics come to the fore in diagnosing shock of any etiology. As the degree of shock increases, heart rate progressively increases (1st degree - by 20-40%, 2nd degree - by 40-60%, 3rd degree - by 60-100% or more compared to the norm) and decreases blood pressure (1st degree - decreases pulse pressure, 2nd degree - the value of systolic blood pressure drops to 60-80 mmHg, the phenomenon of “continuous tone” is characteristic, 3rd degree - systolic blood pressure is less than 60 mmHg or not determined).

Shock of any etiology has a phased development of peripheral circulatory disorders, at the same time, their severity and duration can be very diverse.

The early (compensated) phase of shock is clinically manifested in a child by tachycardia with normal or slightly elevated blood pressure, pale skin, cold extremities, acrocyanosis, slight tachypnea, and normal diuresis. The child is conscious, states of anxiety and psychomotor excitability are possible, reflexes are strengthened.

The phase of pronounced (subcompensated) shock is characterized by a violation of the child’s consciousness in the form of lethargy, muffledness, weakened reflexes, a significant decrease in blood pressure (60-80 mm Hg), severe tachycardia up to 150% of the age norm, severe pallor and acrocyanosis of the skin, thread-like pulse , more pronounced superficial tachypnea, hypothermia, oliguria.

The late (decompensated) phase of shock is characterized by an extremely severe condition, impaired consciousness up to the development of coma, pallor of the skin with an earthy tint or widespread cyanosis of the skin and mucous membranes, hypostasis, a critical decrease in blood pressure or its uncertainty (less than 60 mm Hg), thread-like pulse or its absence on peripheral vessels, arrhythmic breathing, anuria. With further progression of the process, the clinical picture of an atonal state (terminal stage) develops.

Sometimes the early phase of shock is very short-lived (severe forms of anaphylactic shock, fulminant form of infectious-toxic shock with meningococcal infection, etc.). And therefore the condition is diagnosed in the phase of severe or decompensated shock. The early phase can manifest itself quite fully and for a long time with the vascular origin of shock, less so in the presence of primary hypovolemia.

It is always necessary to pay attention to the possibility of circulatory decompensation: progressive pallor of the skin and mucous membranes, cold sticky sweat, cold extremities, a positive capillary refill test (after pressing on the fingernail, the color is normally restored after 2 s, and with a positive test - more than 3 s, indicates about impaired peripheral circulation) or a positive symptom of a “pale spot” (more than 2 s), progressive arterial hypotension, an increase in the Algover shock index (the ratio of pulse rate to systolic pressure, which normally does not exceed 1 in children over 5 years of age and 1.5 in children under 5 years of age), a progressive decrease in diuresis.

With severe insufficiency of perfusion, multiple organ failure can form - simultaneous or sequential damage to the vital systems of the body (“shock organs” - the central nervous system, lungs, kidneys, adrenal glands, heart, intestines, etc.).

FIRST AID FOR SHOCK

1. Place the patient in a horizontal position with the lower limbs raised.
2. Ensure patency of the upper respiratory tract - remove foreign bodies from the oropharynx, throw back the head, remove the lower jaw, open the mouth, establish a supply of humidified, heated 100% oxygen through a breathing mask or nasal catheter.
3. If possible, reduce or eliminate the effect of a developmentally significant shock factor:

  • for anaphylaxis: stop administering medications; remove the insect sting; above the injection or bite site, apply a tourniquet for up to 25 minutes, inject the injection site or lesion with 0.3-0.5 ml of a 0.1% solution of adrenaline in 3-5 ml of saline, cover the injection site with ice for 10-15 minutes, when if the allergen enters through the mouth, if the patient’s condition allows, rinse the stomach, give a laxative, do a cleansing enema, if allergens get into the nose or eyes, rinse with running water;
  • in case of bleeding, stop external bleeding using tamponade, bandages, hemostatic clamps, clamping of large arteries, a tourniquet with recording the time of its application;
  • for traumatic pain syndrome: immobilization; analgesia intravenously, intramuscularly with a 50% solution of analgin at a dose of 0.1 ml/year of life or even, if necessary, with a 1% solution of promedol at a dose of 0.1 ml/year of life, inhalation anesthesia - with nitric oxide mixed with oxygen (2 :1 or 1:1), or intramuscularly or intravenously by administration of 2-4 mg/kg Kalip-Sol;
  • for tension pneumothorax - pleural puncture.

4. Catheterization of central or peripheral veins for intensive infusion therapy, starting with the introduction of crystalloids in a volume of 10-20 ml / kg (Ringer's solutions, 0.9% sodium chloride) and colloids (reopolyglucin, polyglucin, 5% albumin, Gecodez, gelatinol , Gelofusin). The choice of drugs, their ratio, volume of infusion and rate of administration of solutions is determined by the pathogenetic variant of shock and the nature of the underlying disease. For shock, IV infusions are carried out until the patient comes out of this state, or until minimal signs of congestion appear in the pulmonary or systemic circulation. To prevent excessive administration of solutions, central venous pressure is constantly monitored (normally its value in mm H2O is equal to 30/35 + 5 x number of years of life). If it is low, the infusion continues, if it is high, it stops. Monitoring blood pressure and diuresis is also mandatory.

5. In the presence of acute adrenal insufficiency, hormones are prescribed:

Hydrocortisone 10-40 mg/kg/day;
or prednisolone 2-10 mg/kg/day, with half the daily dose in the first administration, and the other half evenly throughout the day.

6. In case of hypoglycemia, administer a 20-40% glucose solution at a dose of 2 ml/kg intravenously.
7. In case of refractory arterial hypotension and in the presence of metabolic acidosis, its correction is with a 4% solution of sodium bicarbonate at a dose of 2 ml/kg under the control of the acid-base state.
8. Symptomatic therapy (sedatives, anticonvulsants, antipyretics, antihistamines, hemostatics, antiplatelet agents, etc.).
9. If necessary, comprehensive resuscitation support.

Patients with manifestations of shock should be hospitalized in the intensive care unit, where, taking into account the etiopathogenesis, the clinic will carry out further conservative or surgical treatment.

Anaphylactic shock

Anaphylactic shock- the most severe manifestation of an immediate allergic reaction that occurs to the introduction of an allergen against the background of sensitization of the body and is characterized by severe disturbances of blood circulation, breathing, and central nervous system activity and is truly life-threatening.

Causally significant allergens for the development of arterial shock in children may be:

  • medications (antibiotics, sulfonamides, local anesthetics, radiopaque contrast agents, antipyretics, heparin, streptokinase, Asparaginase, plasma expanders - dextran, gelatin)
  • foreign proteins (vaccines, serums, donor blood, plasma)
  • allergen extracts for diagnosis and treatment;
  • poison of insects, snakes;
  • some food products (citrus fruits, nuts, etc.);
  • chemical compounds;
  • plant pollen;
  • cooling the body.

On the frequency and time of development arterial shock influences the route of introduction of the allergen into the body. In the case of parenteral administration of the allergen, AS is observed more often. The intravenous route of administration of the drug is especially dangerous, although the development of AS is quite possible with any option for the drug to enter the child’s body.

DIAGNOSTICS

Arterial shock develops quickly, within the first 30 minutes (maximum up to 4 hours) from the moment of contact with the allergen, and the severity of the shock does not depend on the dose of the allergen. In severe cases, collapse develops at the moment of contact with the allergen.

There are five clinical forms of arterial shock:

1. Asphyxial (asthmatoid) variant- weakness, a feeling of constriction in the chest, lack of air, persistent cough, throbbing headache, pain in the heart, fear appear and increase. The skin is sharply pale, then cyanotic. Foaming at the mouth, suffocation, expiratory shortness of breath with wheezing on exhalation. Angioedema of the face and other parts of the body may develop. In the future, with the progression of respiratory failure and the addition of symptoms of acute adrenal insufficiency, death may occur.

2. Hemodynamic (cardiac-vascular) variant- weakness, tinnitus, heavy sweating, anginal pain in the heart area appear and increase. Pallor of the skin and acrocyanosis increase. Blood pressure drops progressively, the pulse is threadlike, heart sounds are sharply weakened, cardiac arrhythmias, loss of consciousness and convulsions are possible within a few minutes. A lethal outcome can occur with an increase in cardiovascular insufficiency.

3. Cerebral variant- focal neurological and cerebral symptoms rapidly increase.

4. Abdominal option- spastic diffuse abdominal pain, nausea, vomiting, diarrhea, gastrointestinal bleeding.

5. Mixed option.

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