Clear shock. Shock conditions of various origins. Vicious circle that promotes the insufficiency of the Vasomotor Center

History

The state of shock was first described by hippocratic. For the first time, the term "shock" was applied in the city of Le Dran. At the end of the XIX century, possible mechanisms for the development of the pathogenesis of shock were offered, among them the most popular were the following concepts:

  • paralysis of nerves, innervating vessels;
  • exhaustion of the vasomotor center;
  • nervous kinetic disorders;
  • violation of the function of the endocrine glands;
  • reduction of circulating blood volume (BCC);
  • capillary stasis with violation of vessel permeability.

Pathogenesis shock

From a modern point of view, shock develops in accordance with the theory of Stress G. Siele. According to this theory, the excessive effect on the body causes in it specific and non-specific reactions. The first depend on the nature of the impact on the body. The second is only from the force of exposure. Non-specific reactions when influenced by a supercritical stimulus, the name of the general adaptation syndrome was obtained. The total adaptation syndrome always flows the same type, in three stages:

  1. the stage is compensated (reversible)
  2. stage decompensated (partially reversible, is characterized by a general decrease in the body's resistance and even the death of the body)
  3. stage terminal (irreversible, when no therapeutic effects may interfere with death)

Thus, shock, silly, is a manifestation non-specific reaction The body for excessive impact.

Hypovolemic shock

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

The reasons

The amount of circulating blood can quickly decrease due to the following reasons:

  • blood loss;
  • plasmopoter (for example, when burning, peritonitis);
  • loss of fluid (for example, with diarrhea, vomiting, abundant sweating, sugar and nonachon diabetes).

Stages

Depending on the severity of the hypovolemic shock, it is distinguished by three stages, which consistently replace each other. it

  • The first stage is an immanent (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 anti-deposit facilities allow the patient from this state. At this stage, medical intervention can return arterial pressure on a short period of time to normal, but it does not stop the destructive processes in the body. Among the reasons for the irreversibility of the shock at this stage, there is a violation of homeostasis, which is accompanied by severe damage to all organs, the special value has damage to the heart.

Vicious circles

With hypovolemic shock, many vicious circles are formed. Among them, the vicious circle is of the greatest importance, which contributes to damage to the myocardium and the vicious circle, which contributes to the insufficiency of the vasomotor center.

Vicious circle that promotes myocardial damage

Reducing the amount of circulating blood leads to a decrease in the minute volume of the heart and the fall of blood pressure. The 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 reduction. The reduction in myocardial reduction leads to an even greater decrease in the minute volume of the heart, as well as to the further fall of blood pressure. The vicious circle closes.

Vicious circle that promotes the insufficiency of the Vasomotor Center

Hypovolemia is due to a reduction in the minute emission volume (that is, a decrease in the volume of blood exhaled 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 violation of the activity of the vascular (vasomotor) center. The latter is in the oblong brain. One of the consequences of the violation in the Vasomotor Center is the drop in the tone of the sympathetic nervous system. As a result, blood pressure centralization mechanisms are violated, blood pressure drops, and this, in turn, launches a violation of the cerebral circulation, which is accompanied by a large oppression of the vasomotor center.

Shock organs

Recently, the term "shock organ" was often used ("Shock light" and "Shock kidney"). It is understood that the impact of the shock stimulus disrupts the function of these organs, and further disorders of the patient's body are closely related to changes in the "shock organs".

"Shock lung"

History

This term first introduced into the practice ashbaugh (year) in the description of the syndrome of progressive acute respiratory failure. However, another year Burford. and Burbank. described similar clinical and anatomical syndrome by calling it "Wet (wet) light". After some time, it was found that the picture of the "shock light" occurs not only at shocks, but also in the cranial-brain, thoracic, abdominal injuries, with blood loss, long hypotension, aspiration of acidic gastric content, massive transfusion therapy, increasing heart decompensation, Light artery thromboembolism. Currently, no connection was found between the length of the shock and the severity of light pathology.

Etiology and pathogenesis

Most often, the cause of the development of "shock light" is hypovolemic shock. Ischemia of many fabrics, as well as massive emissions of catecholamines lead to the flow of collagen, fat and other substances into the blood, which cause massive thrombosis. Because of this, microcirculation is disturbed. A large number of blood clots are settled on the surface of the vessels of the lungs, which is associated with the characteristics of the latter structure (long convolutions capillaries, double supply with blood, shunting). Under the action of inflammation mediators (vasoactive peptides, serotonin, histamine, kinines, foregnostin) increase the vascular permeability in the lungs, the bronchospasm develops, the release of mediators leads to a narrowing of the vessels and damage.

Clinical picture

Syndrome "Shock Light" develops gradually, reaching its apogee, usually after 24-48 hours, the outcome is often massive (often bilateral) liga-tissue lesion. The process is clinically divided into three stages.

  1. The first stage (initial). The arterial hypoxemia (lack of oxygen in the blood) is dominated, the radiological picture of the lung is usually not changed (with a rare exception, when an increase in the pulmonary pattern is observed during x-ray). Cyanosis (blue skin shade) is absent. The partial oxygen pressure is sharply reduced. Auscultation reveals scattered dry wheels.
  2. Second stage. In the second stage, tachycardia increases, that is, the cardiac abbreviation frequency increases, Tahipne (respiratory frequency) occurs, the partial pressure of oxygen decreases even more, the psyche disorders increase, the partial pressure of carbon dioxide increases somewhat. Auscultation reveals dry, and sometimes fine-pushed wheezes. Cianoz is not expressed. Radiologically determines the decrease in the transparency of the light tissue, bilateral infiltrates appear, obscure shadows.
  3. Third stage. For the third stage, without special support, the body is non-visual. Cyanosis develops. X-ray is revealed to increase the number and sizes of focal shadows with their transition to drain formations and total dim dimum. The partial pressure of oxygen decreases to critical numbers.

"Shock kidney"

Pathoanomatic drug kidney patient who deceased from acute renal failure.

The concept of "shock kidney" reflects the acute violation of the kidney function. In the pathogenesis, the leading role is played by the fact that a compensatory shunting of arterial blood flow occurs in direct veins of pyramids with a sharp decrease in hemodynamic volume in the region of the cortical renal layer. This is confirmed by the results of modern pathophysiological studies.

Pathological anatomy

The kidneys are somewhat increased in size, swollen, the cortical layer of their small-calm, pale gray, the overlooking zone and pyramids, on the contrary, dark red. Microscopically in the first hours is determined by the anemia of the vessels of the cortex layer and the sharp hyperemia of the seaside zone and the pyramids direct veins. Rarely meet microtrombosis of capillaries Glomerul and leading capillaries.

In the future, increasing dystrophic changes in nephrothelia, covering first proximal, and then distal nephrone departments are observed.

Clinical picture

The picture of the "shock" kidney is characterized by a clinic of progressive acute renal failure. In its development, acute renal failure under shock passes four stages:

The first stage flows at that time until the reason caused sharp renal failure. Clinical notes decreased diuresis.

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

  • oliganuria (with the development of edema);
  • azotemia (smell ammonia from mouth, itching);
  • an increase in the size of the kidneys, pain in the loins, a positive symptom of Pasternatsky (the appearance of red blood cells in the urine after tapping in the area of \u200b\u200bkidney projection);
  • weakness, headache, muscle sticking;
  • tachycardia, expansion of heart boundaries, pericarditis;
  • the dynake, stagnant wheezing in the lungs up to the interstitial edema of the lungs;
  • dry mouth, anorexia, nausea, vomiting, diarrhea, cracks of the mucous membrane of the mouth and language, abdominal pain, intestinal paresis;

Third stage (recovery of diusca). Diuresis can normalize gradually or rapidly. The clinical picture of this stage is associated with arising dehydration and dielectrictime. The following features are developing:

  • loss of body weight, asthenia, lethargy, inhibition, possibly infection;
  • normalization of nitrogen-excretory function.

Fourth stage (recovery). Gomeostasis indicators, as well as the kidney function comes to normal.

Literature

  • ADO A. D. Pathological physiology. - M., "Triada X", 2000. P. 54-60
  • Klimiashvili A. D. Chadaev A. P. Bleeding. Blood transfusion. Blood substitutes. Shock and resuscitation. - M., "Russian State Medical University", 2006. P. 38-60
  • Meerson F. Z., Prennikova M. G. Adaptation to stressful situations and physical exertion. - M., "Triada X", 2000. P. 54-60
  • Puliardin G. V. Stress and pathology. - M., "Miniprint", 2002. P. 3-22
  • Stolkovkov V. I. General Surgery. - M., "Medicine", 1978. P. 144-157
  • Sergeev S.T. Surgery of shock processes. - M., Triada-X, 2001. P. 234-338

Notes

Shock (from fr. Choc - blow, push) is an acute hemodynamic impairment, as a result of which tissue hypoperfusion develops. A more complete definition may be as follows: shock is a heavy pathological process, accompanied by the exhaustion of vital functions of the body and leading it on a line of life and death due to a critical reduction in capillary blood flow in the affected bodies. In general, the concept of "shock" so far does not apply to the number of precisely deterministic. It is known to say Deloryer on this subject: "Shock is easier to recognize what to describe, and it is easier to describe what to give him a definition."

The initial pathogenetic shock mechanism, as a rule, is a massive stream of biologically negative afforentation entering the CNS from the impact area of \u200b\u200bthe damaging factor.

Initially, an idea of \u200b\u200bthe nature of the shock as a result of an injured injurious pain irritation, which causes the common overexcitation of the CNS, followed by its exhaustion.

Today, the number of states that different authors relate to the shock extremely expanded and currently in some sources is calculated tens. For example, hemolytic, pain, obstetric, spinal, toxic, hemorrhagic, cardiogenic shock, etc. The inclusion of such a significant number of pathological processes in the concept of shock is often due to the fact that it is not differentiated from the collapse and coma. Indeed, shock and collapse have common pathogenetic links: vascular failure, respiratory failure, hypoxia, compensatory reactions.

However, there are significant differences, for example, during the collapse, the process begins precisely with systemic hemodynamic disorders; When shocked, circulatory changes occur again. Other differences are shown in the table (by A.I. Volozhin, G.V. Port, 1999).

Stages, manifestations and main mechanisms for the development of shock.For any shock, a two-phase change in the activities of the central nervous system is characterized: the initial widespread excitation of neurons ("Erectile Stage" or Compensation Stage); In the future, the common oppression of their activity ("Thorpid stage" or the decompensation stage). Usually, consciousness is preserved in both phases of shock. It can be significantly reduced and changed (especially in the flue phase), but does not lose completely. Preserved, although substantially weakened, and reflector reactions to external stimuli of various modalities.

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

For the erectile stage (compensation) of the shock, the strengthening of sympatheadar and pituitary and adrenal influences, which increase the activity of most physiological systems. At the beginning of the turnup phase of the shock, the level of catecholamines and corticosteroids is usually preserved, however, the effectiveness of their action to various organs is reduced. In the future, there is a decrease in the activity of sympathoyadrenal, pituitary and adrenal systems and the content of the corresponding hormones in the blood. Therefore, during the first stage of the shock, the functions of the circulatory system are activated and as a result - tachycardia occurs, arterial hypertension, the redistribution of blood flow; In addition, there is an increase in respiration and an increase in alveolar ventilation; Erythrocytosis may occur due to blood emissions from the depot.

In the second stage of the shock there is a weakening of central hemodynamics: the blood pressure decreases, the deposited fraction of blood increases, ICC and pulse pressure falls, the "thread" pulse is often noted. With a slight shock, hell is reduced to 90-100 mm Hg. Art., with moderate severity - up to 70-80, with severe - up to 40-60. Alveolar ventilation decreases, pathological forms of breathing may appear. In the decompensation stage, the increasing insufficiency of blood circulation and respiration leads to the development of severe hypoxia, and it is it that further determines the severity of the shock state.

Characteristic of shock are microcirculation disorders. They may arise at the first stage due to the redistribution of blood flow and its reduction in a number of organs (kidneys, liver, intestines, etc.). As the microcirculation disorder is transformed into the trapid phase, it is becoming more and more common, manifesting themselves not only by a decrease in the perfusion of microcosuds, but also by the deterioration of the rheological properties of blood, an increase in the permeability of the capillaries walls, aggregation of shaped elements, perivascular edema.

Mandatory pathogenetic factor at seques of different etiology is endotoxmia. The toxic effect with shock is provided by numerous bavos, in the excess of the body (histamine, serotonin, kinines, catecholamines, etc.). Denaterified proteins and their decomposition products, lysosomal enzymes, toxic intestinal products, microbes and their toxins can appear in the blood. Metabolites are essential in the development of toxmia due to metabolism of metabolic disorders: dairy and peeling acids, ketocislotes, potassium, etc. resulting from hypoxia and microcirculation disorders of the violation of the liver and kidney function lead to even greater changes in blood composition: acidosis, Ion and protein imbalance, shifts of osmotic and oncotic pressure in various environments of the body.

The above changes in the body impose an imprint on biochemical processes and in a cell ("shock" cell). For cellular disorders, a known triad of hypoxia is characteristic: ATP deficiency, acidosis, biomembrane damage.

It is very important that the so-called "vicious circles" often occur during the development of shock. At the same time, the initial disorders of the activities of organs and systems can potate, and the shock receives a tendency to "self-smuggling". For example, the disorders of the central blood circulation and microcirculation lead to a violation of the functions of the liver and kidney, and the adverse shifts arising in this regard aggravate blood circulation disorders. At a certain stage of the trapid stage of shock, hemodynamic disorders can achieve an extent that the secondary collapse is developing, it is very often connecting to the shock in its unfavorable development and sharply deteriorating the patient's state.

So, I are set out, in a very general feature, modern ideas about the pathogenesis of shock states. It is clear that the nature, severity and the specific value of each of the pathogenetic factors can fluctuate in wide limits depending on the type of shock, its stage and severity, as well as the reactive properties of the body.

Once again, it emphasizes the complexity of the problem of classification of various types of shock states. There are many discussions around this question to date, since there is no single classification. However, most authors taking into account the main etiological factors and pathogenetic mechanisms allocate the following forms of shock: primary hypovolemic; cardiogenic; vascular peripheral; traumatic. Examples and brief description of these forms of shock are given in textbooks. It seems to us that the most successful shock states are classified by V.A. Frolov (see the scheme).

Earlier, we considered the main points of the pathogenesis of anaphylactic and burn shock. Therefore, we will dwell only on a traumatic, hemotransphusion and cardiogenic shock.

Traumatic shock. The reason is usually common injuries of bones, muscles, internal organs, accompanied by damage and strong irritation of nerve endings, trunks and plexuses. Traumatic shock is often accompanied or its course is aggravated by blood loss and infection of the Russian Academy of Sciences.

Here I will stop at the next moment. Looks at the mechanism of shock development over time undergo significant changes. If the neurogenic shock theory, which was especially popular in the 30-40s. XX century In our country, first of all, explained the development of the shock as a reflex change in the state of the body in response to a painful impulsation, which occurred at the time of injury, the theory of blood and plasmophotheries, put forward by Blek (1934), practically did not take into account the painful impulses as a significant factor in its development. Currently, most pathophysiologists and clinicians believe that traumatic shock develops as a result of the impact on the body of several pathological factors. First of all, it is pain impulse, blood and plasmopoter, toxmia.

And two more points that should be paid attention to. First, despite the fact that blood loss is one of the significant causes of the development of traumatic shock, it would be incorrectly identifying changes in blood circulation, including microcirculation, only with the BCC deficiency. Indeed, in the development of pure bloodstairs and traumatic shock there are common pathogenetic factors - the state of stress, hypotension, accompanied by hypoxia, inadequate afferent impulsation of injured tissues when shocked or from baroque and chemoreceptors of blood vessels during blood loss. However, violations of nervous activity at traumatic shock occur earlier and occur it is heavier than during blood loss. The stimulation of GGAS at shock is accompanied by a sharp decrease in tissue ability to absorb corticosteroids, which entails the development of non-propellate corticosteroidal failure. With blood loss, on the contrary, the level of consumption of corticosteroids with tissues increases.

Secondly, the activation of protective mechanisms in response to severe injury is accompanied by the inclusion of antinocyptive protection (see chapter on pain Pathophysiology). But it should be noted here that the increase in the content of endogenous opiates, which would have to be worn under heavy injury, in fact, often turns around for the body by irreparable catastrophe. The fact is that excessive stimulation of all GGAS links, always accompanying severe injury, leads to the release of a large number of enkephalins and endorphins, which, besides the blockade of opiate receptors, perform a number of functions in the body. First of all, it is part in the regulation of blood circulation and breathing. Currently, it is known that endorphins are able to disturb the regulation of blood circulation and contribute to the development of unmanaged hypotension.

Thus, the efferent manifestations of pain syndrome, leading to excessive stimulation of GGAS, not only do not protect the body from injury, but, on the contrary, contribute to the development of deep damage to the most important livelihood systems and the development of traumatic shock.

During the erectile stage in the patient, speech and motor arousal arises: it is taking place, it also reacts even to the usual touch; Skin covers are pale due to spasmodes of skin microsudes; Pupils are expanded due to the activation of the sympathoadrenal system; Indicators of central blood circulation and respiration are increased.

The second stage comes to replace the second - torpid. The classic clinical picture is described by N.I. Pirogov (1865): "With a torn hand or a nagine lies, such a stubborn on the dressing point is motionless; He does not shout, does not complain, does not accept any participation and does not require anything; his body is cold, face pale; The look is still and addressed in the distance, the pulse is like a thread, barely noticeable under the finger. Okochenaya or not answers questions, or only to yourself, a little heard whisper; Breathing is also barely noten. The wound and the skin are not at all sensitive ... Okocheny did not lose absolutely consciousness, he is not the fact that it is not aware of his suffering. "

Typically, patients with severe traumatic shock are killed from progressive circulatory disorders, respiratory or renal failure. In the lungs there are violations of microperfusion, blood shunting increases, the diffusion properties of alveolar-capillary membranes are worse due to their swelling and the development of interstitial edema. Disorders of the gas exchange function of the lungs at traumatic shock are a very dangerous phenomenon that requires emergency intervention ("shock light").

The reduction of blood circulation and microcirculatory disorders in the kidneys lead to their insufficiency, manifested by Oligira (or Anuria), azotemia and other violations. In the late stages of shock in the kidneys, along with sharp microcirculation disorders, the blockade of the tubular apparatus is possible due to the formation of hyaline and myoglobin cylinders ("shock kidney"). In severe cases, intestinal autointoxication develops at traumatic shock.

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

Hemotransphusion shock. The immediate cause of the hemotransphusion shock may be the incompatibility of blood donor and recipient for group factors AVO, Rh Factor or individual antigens. Shock can develop, and its flow will be significantly aggravated in cases where poor-quality blood is used (with hemolysis, protein denaturation, bacterial contamination, etc.).

The first signs of the shock may appear during transfusion (with group incompatibility) or in the coming hours (with rhesis incompatibility or in individual antigens incompatibility).

In the occurrence of a hemotransfusion shock with a group or rhesiable incompatibility, the main pathogenetic factor is the massive agglutination and formation of erythrocyte conglomerates with their subsequent hemolysis. As a result, the physico-chemical properties of blood change dramatically. These changes believe that these changes serve as a launching mechanism of shock as a result of emergency irritation of a wide recipe field of the vascular bed. Significant intravascular hemolysis leads to a sharp deterioration of oxygen-speaking blood functions and the development of hemic hypoxia, the severity of which increases in the future as a result of circulatory disorders.

Manifestations. In the erectile stage there is a motor excitement, a frequent breathing is noted with a difficult exhalation, a feeling of heat, pain in different parts of the body (especially in the field of kidneys). It may increase systemic blood pressure and tachycardia.

The first stage is quickly replaced by the second (torpid). There is general weakness, redness of the skin is replaced by a sharp pallor, often arise nausea and vomiting. Against the background of general hypodynamies, convulsions may develop, hell drops. For this type of shock, the severity of the state) of the renal function (the so-called hemotransphusion nephrzer) is characteristic of a significant extent. The appearance of Oliguria or Anururia with a hemotransphusion shock always serves as a sign of a dangerous deterioration of the patient's condition.

Cardiogenic shock - This is a critical state that develops due to acute arterial hypotension due to a sharp drop in the pump function of the left ventricle. The primary level of the pathogenesis of the cardiogenic shock is a rapid decrease in the shock volume of the left ventricle, which leads to arterial hypotension, despite the compensatory spasm of resistive vessels and the growth of total peripheral vascular resistance aimed at restoring blood pressure.

Arterial hypotension and reduction of blood flow on the exchange capillaries due to the spasm of the smallest arteries, the arterioles and the prokapillary sphincters violate the bloodstream in organs on the periphery and cause the main symptoms of cardiogenic shock. Namely: disturbances of consciousness; Skin pallor, cold and wet limbs; Oliguria (<20 мл/ч); артериальная гипотензия (систолическое АД < 90 мм рт.ст.).

Cardiogenic shock arises, 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 the myocardial damage, its initial state, the central blood circulation, as well as the functional features of the nociceptive and antinocirtable system and other factors that determine the reactivity of the body.

With a defeat of 50-65% of the mass of myocardium, either fibrillation of the heart occurs, or the sharp insufficiency of blood circulation. At the same time, shock may not arise. Cardiogenic shock is more often developing with lesion of the smaller mass of myocardium (up to 50%) against the background of sharp pain, accompanied by chaotic excitation of various vegetative centers and disorders of neuroendocrine regulation of blood circulation and other physiological systems.

I want to pay attention to such a principal distinguishing feature of the pathogenesis of this type of shock. The arterial hypotension arising due to traumatic shock is not the leading link pathogenesis of this pathological state, but a consequence of the insolvency of compensation of traumatic shock, in which pathological shifts in organs and tissues are formed long before decrease in blood pressure. With a cardiogenic shock, on the contrary, the arterial hypotension immediately begins to act as one of the main links of pathogenesis.

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

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

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

Compensatory autogemodilation, i.e. Mobilization of fluid from the interstitial sector into vascular due to the change in the system level of the dining between the pre- and post-patellular vascular resistance.

The biological goal of such compensatory reactions is understandable - maintaining the IOC and blood pressure through the growth of the total venous return, the delay in sodium and water, an increase in the intravascular liquid sector and an increase in the OPS. With a cardiogenic shock, these protective reactions increase the pre- and postload, and therefore increase the utilization of free energy with cardiomyocytes. The growth of the work of crate myocardial cells increases the inconsistency between the need of the heart in oxygen and delivery to it about 2. As a result, the mass of hypoxic and hibernating myocardium is growing, and its reduction is falling.

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

symptom complex of violations of vital functions of the body arising from the inconsistency between the tissue blood flow and the metabolic need of tissues.

During the development of shock, the main task of the body is to preserve adequate blood flow in vital organs (heart and brain). Therefore, initially the narrowing of the vessels in other organs and tissues occurs, thus the centralization of blood circulation is achieved. Such a long narrowing of the vessels with time leads to the development of ischemia - a decrease in the blood supply to the organ or tissue, resulting from the weakening or termination of the inflow of arterial blood. This leads to the formulation of biologically active substances that contribute to an increase in vascular permeability, which ultimately leads to extension of vessels. As a result, the protective adaptive mechanism of the body is disturbed - the centralization of blood circulation, which entails heavy consequences.

By 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 of the development of such a state. For example, shock can lead to such complications as the insufficiency of a number of internal organs, a pulmonary and brain edema. Such formidable consequences are able to lead to death, so shock requires increased attention.

Symptoms


When shock, you can pay attention to the appearance of the patient. Such a person has a pale and cold to touch the skin. The exclusion is septic and anaphylactic shocks, in which the skin is warm at the beginning of development, but then it does not differ from the characteristics at other types of shock. Vividly expressed general weakness, dizziness, nausea. It is possible to develop an excitation that replaces the inhibition or a coma. Blood pressure is significantly reduced, which carries a certain danger. As a result, the shock volume of blood is reduced, necessary to satisfy organs and tissues in oxygen. Therefore, tachycardia occurs - the increase in the number of heartfills. In addition, the appearance of oliganuria is noted, which means a sharp decrease in the amount of urine allocated.

At traumatic shock, patients make complaints against severe pain caused by injury. Anaphylactic shock is accompanied by a shortness of breath, which arises due to bronchospasm. Significant blood loss is also able to lead to the development of shock, in which case attention is drawn to internal or external bleeding. With septic shock, an increased body temperature is revealed, which with difficulty is borne by the reception of antipyretic agents.

Diagnostics


Some time, the state of the shock may be unnoticed, since there is no specific symptom indicating exclusively on the development of shock. Therefore, it is important to assess all the symptoms available in the patient, and an analysis of the situation individually in each case. To make a diagnosis of shock, you need to identify signs of insufficient blood circulation of tissues, as well as detect the inclusion of compensatory mechanisms of the body.

First of all, attention is drawn to the appearance of the patient. Skin is often cold to the touch and has a pale appearance. Cyanosis may be detected (shirt and / or visible mucous membranes). To confirm the hypotension, arterial pressure is measured. Patients make complaints of general weakness, dizziness, nausea, the feeling of heartbeat, sharply decreases the amount of urine allocated.

It is important to most quickly compare all the symptoms, set the correct diagnosis and begin the appropriate treatment.

Treatment


Shock is an urgent state that can lead to irreversible consequences. Therefore, it is extremely important to provide medical care in a timely manner. Before the arrival of specialists nearby people should take first-aid measures. First, you need to give a person a horizontal position with a raised foot end. Such actions contribute to an increase in the venous return to the heart, which leads to an increase in the impact volume of the heart. During the shock, the heart ceases to cope with the impact volume of blood necessary to deliver the desired amount of oxygen to the tissues. Horizontal position with raised legs, though it does not compensate for the fully insufficiency of the impact of the heart, but helps to improve this state.

Medical care is to carry out infusion therapy and the introduction of drugs, the action of which is aimed at narrowing the vessels. Infusion therapy is based on the introduction of various solutions of a certain volume and concentration to fill the vascular bed into the bloodstream.

The use of drugs, narrowing vessels, is necessary to maintain blood pressure.

When impaired breathing uses oxygen therapy or IVL.

These common activities are aimed at combating the pathogenesis of shock, there is also symptomatic treatment, different for each type of shock. For example, at traumatic shock, it is necessary to introduce painkillers, to make immobilization during fractures or impose a sterile bandage on the wound. Cardiogenic shock requires the treatment of the cause that promotes 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, the stopping of bleeding (the imposition of a harness, a gulling bandage, the extension of the vessel in the wound, etc.), the general events will not have a proper effect. Septic shock is accompanied by fever, so antibacterial drugs are administered as symptomatic treatment, and antibacterial drugs are prescribed to eliminate the cause of the cause. 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.

Medicine


When developing shock it is important to ensure the most quickly access to Vienna, it is desirable not to one, but immediately to several. This is necessary for the start of infusion therapy, as well as administration directly into the bloodstream of medicines. Infusion therapy affects the main stars of pathogenesis. It is able to maintain the optimal level of the OCC (the volume of circulating blood), which leads to the stabilization of hemodynamics, improves microcirculation, thereby increases the delivery of oxygen to the tissues, improves metabolism in cells.

The infusion solutions used by shock include:

  • crystaloids (isotonic solution NACI, Ringer's solution, glucose solutions, mannitol, sorbitol);
  • colloids (hemodesis, polydais, polyoxydin, polyglyukin, refooliglukin).

A combination of crystalloid and colloidal solutions is usually used. Such tactics makes it possible to fill the volume of circulating blood, and also regulates the balance of intracellular and interstitial fluids. The choice of volume and the ratio of crystalloid and colloidal solutions depends on each clinical case, which has its own characteristics.

Of the drugs causing the narrowing of the lumen of the vessels, the main is adrenaline. Intravenous administration contributes to the accumulation of the necessary concentration of the drug directly in the blood, which leads to the most rapid manifestation of the effect than with other methods of administration. Also, dobutamine and dopamine have such an effect. Their action occurs approximately 5 minutes after intravenous administration and lasts about 10 minutes.

Folk remedies


The shock of various etiologies requires exclusively medical care, no folk recipes are capable of improving the patient's condition. Therefore, it is important not to lose precious time, and immediately call specialists who will provide the necessary assistance and save on possible irreversible consequences. During the emergence of the arrival of the ambulance brigade, you should perform the first aid measures that were described early (give a person a horizontal position with an elevated foot end, warm the body). Not only the effectiveness of the treatment, but also the life of a person depends on the right action!

Information is referenced and is not a guide to action. Do not self-medicate. At the first symptoms of the disease, consult a doctor.

On the leading starting 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 impulsation).
  • Dehydration shock (abundant loss of water and electrolytes).

2. Cardiogenic shock is due to a violation of the contractile ability of myocardium (acute myocardial infarction, aortic aneurysm, acute myocarditis, gap of the interventricular partition, cardiomyopathy, heavy arrhythmias).

3. Septic shock:

  • The effect of exogenous toxic substances (exotoxic shock).
  • The effect of bacteria, viruses, endotoxmia due to the massive destruction of bacteria (endotoxic, septic, infectious-toxic shock).

4. Anaphylactic shock.

Shock development mechanisms

The total for shock is hypovolemia, violation of the rheological properties of blood, sequestration in the microcirculation system, tissue ischemia and metabolic disorders.

In the pathogenesis of the shock, the main meaning is:

  1. Hypovolemia. True hypovolemia occurs as a result of bleeding, plasma loss and various forms of dehydration (primary decrease in the BCC). Relative hypovolemia occurs in a later date when depositing or sequestration of blood (with septic, anaphylactic and other forms of shock).
  2. Cardiovascular failure. This mechanism is characteristic primarily for cardiogenic shock. The main reason is a reduction in heart rate associated with a violation of the contractile function of the heart due to the acute myocardial infarction, damage to the valve apparatus, during arrhythmias, TEL, etc.
  3. Activation of the sympathetic adrenal system It occurs as a result of increased emissions of adrenaline and norepinephrine and causes the centralization of blood circulation due to spasm arterioles, and especially postpillar sphincters, the disclosure of arteriovenous anastamans. This leads to a violation of organ blood circulation.
  4. In zone microcirculationthe spasmodation of pre- and post-tillar sphincters continue to grow, an increase in arteriovenous anastasics, blood shunting, sharply disturbing tissue gas exchange. Serotonin, bradyikinin and other substances are accumulated.

Violation of organ blood circulation causes the development of acute renal and liver failure, shock light, violation of the functions of the CNS.

Clinical manifestations of shock

  1. Reduced systolic blood pressure.
  2. Reduced pulse pressure.
  3. Tachycardia.
  4. Reduced diurea to 20 ml per hour and less (oligo and anory).
  5. Violation of consciousness (initially an excitement is possible, then the injection and loss of consciousness).
  6. Violation of peripheral blood circulation (pale, cold, sticky leather, acrocyanosis, ledging of the skin temperature).
  7. Metabolic acidosis.

Stages of diagnostic search

  1. The first stage of diagnosis is to establish signs of shock on its clinical manifestations.
  2. The second stage is to establish a possible cause of shock on the basis of anamnesis and objective signs (bleeding, infection, intoxication, anaphylaxis, etc.).
  3. The final stage is to determine the severity of the shock, which will allow you to develop the tactics of the patient and the amount of urgent events.

When examining the patient at the site of the development of the threatening state (at home, at work, on the street, in the vehicle damaged as a result of the accident), the paramedher can rely only on these estimates of the state of systemic blood circulation. It is necessary to pay attention to the character of the pulse (frequency, rhythm, filling and voltage), depth and frequency of respiration, blood pressure.

The severity of the hypovolemic shock in many cases can be determined by the so-called shock index of Alghera - Bururi (Shi). With respect to the pulse rate to systolic blood pressure, you can estimate the severity of hemodynamic disorders and even approximately determine the magnitude of acute blood loss.

Clinical criteria for the main forms of shock

Hemorrhagic shock as an option is hypovolemic. It can be caused by both outer and internal bleeding.
With traumatic outer bleeding, the localization of the injury is important. Heated bleeding is accompanied by injuries of the face and head, palms, soles (good vascularization and innovative lobes).

Symptoms. Signs of outdoor or internal bleeding. Dizziness, dry mouth, reduced diurea. Pulse frequent, weak. Hell is reduced. Breathing is frequent, superficial. Increase hematocrit. The rate of blood loss is crucial in the development of the hypovolemic hemorrhagic shock. The decrease in the BCC is 30% for 15-20 minutes and delay with infusion therapy (up to 1 hour) lead to the development of severe decompensated shock, polyorgan deficiency and high mortality.

Dehydration shock (DH). Dehydration shock - an option of the hypovolemic shock, which occurs during a profuse diarrhea or by re-indomitable vomiting and accompanied by a pronounced dehydration of the body - an excaciousness - and severe electrolyte violations. Unlike other types of hypovolemic shock (hemorrhagic, burn), direct loss of blood or plasma when developing shock does not occur. The main pathogenetic cause of DSh is the movement of extracellular fluid through the vascular sector into the extracellular space (in the intestinal lumen). With a pronounced diarrhea and repeated abundant vomiting the loss of the liquid component of the body can reach 10-15 liters and more.

DH can occur during cholera, cholera-like embodiments of enterocolitis and other intestinal infections. The condition characteristic of DSh can be detected at high intestinal obstruction, acute pancreatitis.

Symptoms. Signs of intestinal infection, abundant diarrhea and multiple vomiting in the absence of high fever and other manifestations of neurotoxicosis.
Symptoms of dehydration: thirst, loose face, spawned eyes, a significant decrease in the leather turgora. A significant drop in skin temperature is characterized, frequent surface breathing, pronounced tachycardia.

Traumatic shock. The main factors at the same shock are excessive pain impulse, toxemia, blood loss, subsequent cooling.

  1. The erectile phase is short-lived, characterized by psychomotor excitation and activation of basic functions. Clinically, this is manifested by standard or hypertension, tachycardia, Tahipne. The patient in consciousness is excited, euphoric.
  2. The trapid phase is characterized by psycho-emotional oppression: indifference and prostration, weak reaction to external irritation. Skin and visible mucous pale, cold sticky sweat, frequent threaded pulse, blood pressure below 100 mm RT. Art., The body temperature is reduced, consciousness is saved.

However, at present, dividing on the erectile and trapid phase is losing its meaning.

According to hemodynamics, 4 degrees of shock are distinguished:

  • I degree - no severe hemodynamic disorders, ad00-90 mm Hg. Art., pulse up to 100 per minute.
  • II degree - hell of 90 mm RT. Art., pulse up to 100-110 per minute, the skin is pale, the veins are sleeping.
  • III degree - hell 80-60 mm RT. Art., pulse 120 per minute, sharp pallor, cold sweat.
  • IV degree - hell less than 60 mm Hg. Art., Pulse 140-160 per minute.

Hemolytic shock. Hemolytic shock develops when incompatible blood overflows (by group or rhesus factors). Shock can also develop during transfusion of large volumes of blood.

Symptoms. During blood transfusion or shortly after it, headache appears, pain in the lumbar region, nausea, bronchospasm, the temperature rises. Reduced blood pressure, the pulse becomes weak, frequent. Pale skin, wet. There may be cramps, loss of consciousness. It has hemolyzed blood, dark urine. After removal from shock, jaundice develops, Oliguria (Anuria). On the 2-3rd day, shock lights can develop with signs of respiratory failure and hypoxemia.

With a rhesus conflict, hemolysis occurs in a later date, clinical manifestations are expressed to a lesser extent.

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

Symptoms. Pulse frequent, small. Violation of consciousness. Reduced diurea less than 20 ml / hour. Pronounced metabolic acidosis. Symptoms of impaired peripheral blood circulation (pale cyanotic leather, wet, sleeping veins, decrease in temperature, etc.).

There are four forms of cardiogenic shock: reflex, "true", arrhythmogenic, and isactive.

The cause of the reflex form of cardiogenic shock is the reaction to pain indired through baro- and chemoreceptors. Mortality with arotic shock exceeds 90%. Disturbances of the heart rhythm (tachy and bradyarithmia) often lead to the development of the arrhythmogenic form of cardiogenic shock. Paroxysmal tachycardia (ventricular and to a lesser degree is sufficiently sufficient), flickering arrhythmia, complete atrioventricular blockade, often complicated by MES syndrome.

Infectious toxic shock.Infectious-toxic shock is predominantly a complication of purulent-septic diseases, approximately 10-38% of cases. It is due to the penetration into the bloodstream of a large amount of toxins of gram-negative and gram-positive flora, affecting microcirculation systems and hemostasis.
The Hypendynamic phase is distinguished by the Hypendynamic phase: the initial (short) "hot" period (hyperthermia, activation of systemic blood circulation with an increase in cardiac output with a good reaction to infusion therapy) and the hypodynamic phase: a subsequent, longer "cold" period (progressive hypotension, tachycardia, significant resistance To intensive therapy. Ex-and endotoxins, proteolysis products have a toxic effect on myocardium, light, kidneys, liver, endocrine glands, reticulosendothelial system. The pronounced hemostasis disorder is manifested by the development of acute and subacuteistics of the syndrome and determines the most severe clinical manifestations of toxic-infectious shock.

Symptoms. The clinical picture consists of symptoms of the underlying disease (acute infectious process) and shock symptoms (drop of blood pressure, tachycardia, shortness of breath, cyanosis, oliguria, or anouria, hemorrhage, hemorrhage, signs of KHS syndrome).

Diagnosis of Shock

  • Clinical Evaluation
  • Sometimes lactate in the blood is found, the basis deficit.

The diagnosis is mainly clinical, based on evidence of insufficient tissue perfusion (stunning, oliguria, peripheral cyanosis) and signs of compensatory mechanisms. Specific criteria include stunning, heart rate\u003e 100 per minute, respiratory frequency\u003e 22, hypotension or 30 mm Hg. Falling Basic Hell and Diuresis<0,5 мл/кг/ч. Лабораторные исследования в пользу диагноза включают лактат >3 mmol / l, deficiency of foundations, and raso 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 cause. Know the reason for shock is more important than classifying type. Often, the reason is obvious or it can be learned quickly on the basis of the history of the disease and physical examination, based on simple research methods.

Pain in the chest (with or without shortness of breath) assumes them, the bundle of aorta or a pulmonary embolism. Systolic noise may indicate the gastroincing gap, the interpresent partition or the insufficiency of the mitral valve as a result of the acute it. The diastolic noise may indicate the aortic regurgitation, due to the latalization of the aorta with the participation of the root of the aorta. About Tamponade Hearts can be judged by the jugular vein, the mutedness of the heart tones and paradoxical pulsation. The pulmonary embolism is quite serious to cause shock, it usually causes a decrease in saturation O 2 and is more common in characteristic situations, incl. With long bed mode and after surgical intervention. Research methods include ECG, determining troponin I, chest radiography, determination of blood gases, lung scans, spiral CT, and echocardiography.

Pains in the abdomen or in the back suggest pancreatitis, the gap of the abdominal aorta aneurysm, peritonitis, and in women of childbearing age, the gap during ectopic pregnancy. The pulsating mass of the middle line of the abdomen implies the aneurysm of the abdominal aorta. Gently with palpation The formation of appendages implies an ectopic pregnancy. The study usually includes CT abdominal cavity (if the patient is unstable, a bedside ultrasound can be used), a clinical analysis of blood, the definition of amylase, lipase and for women of childbearing age, a pregnancy urine test.

Fever, chills and coordination features of infection involve septic shock, especially in patients with immunodeficiency. Isolated fever depends on the history of the disease and clinical conditions, it may indicate a thermal blow.

In several patients, the reason is unknown. Patients who do not have focal symptoms or signs indicating the reasons should be made ECG, heart enzymes, chest x-rays and blood gas research. If the results of these studies are normal, the most likely reasons may be an overdose of drugs, little-known infections (including toxic shock), anaphylaxis and obstructive shock.

Forecast and Treatment of Shock

In the absence of treatment, the shock ends with a fatal. Even in the treatment of mortality from cardiogenic shock after it (from 60% to 65%) and septic shock (from 30% to 40%) is high. The forecast depends on the cause that existed earlier or complications of the disease, the time between the beginning and the formulation of the diagnosis, as well as the timeliness and adequacy of therapy.

General leadership. First aid - detention in the patient of heat. Control of external hemorrhages, checking the respiratory tract and ventilation, respiratory assistance is provided if necessary. Nothing is given through the mouth, and the patient's head is turned on one side to avoid aspiration if vomiting occurs.

Treatment begins simultaneously with the assessment. Additional O 2 is delivered through the mask. If a shock is severe or insufficient ventilation, the intubation of the respiratory tract with mechanical ventilation is necessary. Two large (from 16 to 18 - sensor) catheter are embedded in separate peripheral veins. The central venous line or intraskoy needle, especially in children, provides an alternative when there is no access to peripheral veins.

As a rule, 1 l (or 20 ml / kg in children) 0.9% of the physiological solution is poured within 15 minutes. When bleeding, Ringer's solution is usually used. If clinical parameters have not returned to a normal level, infusion is repeated. Smaller volumes are used for patients with high right-hand pressure signs (for example, a stretching of the cervical veins) or acute myocardial infarction. Such tactics and the volume of injection of the liquid probably should not be carried out with patients with signs of pulmonary edema. In addition, infusion therapy against the background of the main disease may require monitoring of FLOLD or DED. Bedside ultrasound of the heart, in order to assess the reduction of the vein hollow.

Monitoring critical states includes ECG; systolic, diastolic and average blood pressure, preferred intraarterial catheter; control of the frequency of respiration and depth; Pulse oximetry; Installation of a permanent accounting catheter; Control of body temperature, and an assessment of the clinical condition, the volume of the pulse, the temperature of the skin and the color. Measuring FED, dreet and thermodyailing of cardiac emission using a pulmonary artery catheter tip can be useful for diagnosing and initial treatment of patients with a shock of uncertain or mixed etiology or with heavy shock, especially accompanied by oliginia or pulmonary edema. Echocardiography (bedside or perchive) is a less invasive alternative. Sequential measurements of blood blood gases, hematocrit, electrolytes, serum creatinine, and lactate in the blood. Sublingual measurement of CO 2, if this is possible, is non-invasive monitoring of visceral perfusion.

All parenteral preparations are given intravenously. Opioids are usually avoiding because they can cause the expansion of blood vessels. However, expressed pain syndrome, can be treated with morphine 1 to 4 mg intravenously for 2 minutes and repeated from 10 to 15 minutes if necessary. Although brain hypoperfusion can cause concern, sedative or tranquilizers are prescribed.

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

Hemorrhagic shock. When hemorrhagic shock, surgical bleeding control is the first priority. Intravenous resuscitation accompanies, and not precedes surgical control. Blood products and crystalloid solutions are used for resuscitation, however, the erythrocyte mass and plasma are considered primarily in patients who need mass transfusion in a 1: 1 ratio. The absence of an answer usually indicates an insufficient volume or unrecognized source of bleeding. Vasopressor agents are not shown for the treatment of hemorrhagic shock, if cardiogenic, obstructive or distribution causes are also present.

Distribution shock. Distribution shock with deep hypotension after the initial replenishment of the liquid with 0.9% physiological solution can be treated with inotropic or vasopressor preparations (for example, dopamine, norepinephrine). Paranteral antibiotics should be used after the samples of blood samples. Patients with anaphylactic shock are not responding to fluid infusion (especially if accompanied by bronchospasm), adrenaline is shown, and then adrenaline infusion.

Cardiogenic shock. Cardiogenic shock caused by structural disorders is treated surgically. Coronary thrombosis is treated either with percutaneous intervention (angioplasty, stenting), when identifying a multi-propelled lesion, the coronary arteries (coronary shunting) or thrombolesis, for example, atrial flicker tachy formation, ventricular tachycardia are restored by cardioversion or drugs. Bradycardia is treated with an implantation of a percutaneous or transgeneous pacemaker; Atropine can be given intravenously to 4 doses for 5 minutes, waiting for the implantation of the pacemaker. Isoproterenol can sometimes be prescribed if atropine is ineffective, but contraindicated in patients with myocardial ischemia due to the disease of the coronary arteries.

If the occlusal pressure of the pulmonary artery is low or normal, the treatment of shock after acute it is carried out by an increase in volume. If the catheter in the pulmonary artery is not in place, with caution carried out infusions, simultaneously conduct an auscultation of the chest (often accompanied by signs of overload). Shock after the infarction of the right ventricle is usually accompanied by partial volume extension. However, vasopressor agents may be needed. Inotropic support is most preferable in patients with normal or above normal filling. Sometimes during the introduction of dobutamine, tachycardia and arrhythmia occur, especially at higher doses, which requires a reduction in the dose of the drug. Vasodilators (for example, nitroprusside, nitroglycerin), which increase the venous capacity or low systemic vascular resistance, reduce the load on damaged myocardium. Combined therapy (for example, dopamine or dobutamine with nitroprusside or nitroglycerin) can be more useful, but requires frequent ECG, pulmonary and systemic hemodynamic monitoring. With more severe hypotension, norepinephrine or dopamine can be given. Intrabalon counterpulcation is a valuable method for temporary shock removal in patients with acute myocardial infarction.

With obstructive shock, the head of the heart requires immediate pericardiocente, which can be done in bed.

Shock (eng. - blow, push)- acute, threatening life pathological process arising under the action of a very strong irritant for the body and is characterized by the disorders of the central and peripheral blood circulation with a sharp decrease in the blood supply to vital organs. This leads to severe violations of cellular metabolism, as a result of which the normal function of cells changes or is lost, and in extreme cases - their death.

Etiology and pathogenesis

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

1. Primary decrease in the volume of circulating blood (hypovolemic shock) - when bleeding, dehydration, loss of plasma for burns.
2. Violation of peripheral hemodynamics (redicient or vasogenic shock) - sepsis, anaphylaxis, intoxication, acute adrenal insufficiency, neurogenic shock, traumatic shock.
3. Primary heart failure (cardiogenic shock) - with arrhythmias, myocardits, acute left venture defartments, myocardial infarction.
4. Obstruction of the venous inflow of blood or cardiac output (obstructive shock) - with pericardial diseases, intense pneumothorax, thromboembolism of pulmonary artery, fatty and air embolism, etc.

The essence of shock is a violation of gas exchange between blood and tissues with subsequent hypoxia, microcirculation disorders. The main pathogenetic shock links are due to hypovolemia, cardiovascular insufficiency, disruption of tissue circulation as a result of changes in capillary and post-cellular resistances, blood shunt, capillary state with aggregation of cellular elements of blood (sweet-syndrome), an increase in the permeability of the vascular wall and transshipment of blood. The violation of the 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 taken into account, phase of development, clinic and severity of shock.

By the origin, hemorrhagic, dehydration (anhydrous), burn, septic, toxic, anaphylactic, traumatic, endogenous pain, neurogenic, endocrine, with acute adrenal insufficiency, cardiogenic, pleurpulmonal, post-transfusion shocks, etc.

According to the phases of the development of peripheral circulation disorders indicate:

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

By severity, it is possible to release shock as light, moderate, heavy. The first plan in the diagnosis of shock of any etiology is the techniques that allow us to estimate first of all the state of the cardiovascular system, the type of hemodynamics. At increasing the degree of shock, heart rate increases progressively (1 degree - by 20-40%, 2 degree - by 40-60%, 3 degree - by 60-100% and more compared to regulatory) and blood pressure decreases (1 degree - decreases The pulse pressure, 2 degree - the magnitude of the systolic blood pressure is falling to 60-80 mm Hg. Art., It is characterized by the phenomenon of "continuous tone", 3 degree - systolic blood pressure less than 60 mm Hg. Art. or not determined).

The shock of any etiology has the phase of the development of peripheral circulation disorders, at the same time, the severity and duration of them can be very diverse.

An early (compensated) shock phase is clinically manifested by tachycardia with normal or somewhat elevated arterial pressure, skin pallor, cold limbs, acricyanosis, minor tachipne, normal diuresis. The child is conscious, the states of anxiety, psychomotor excitability, reflexes are reinforced.

The phase of the pronounced (subcomensive) shock is characterized by a violation of the child's consciousness in the form of inhibition, mutedness, weakening of reflexes, a significant decrease in blood pressure (60-80 mm Hg. Art.), Pronounced tachycardia to 150% of the age norm, a sharp pallness and acricyanosis of the skin, threaded pulse , more pronounced superficial tachipne, hypothermia, oliginia.

Late (decompensated) shock phase is characterized by an extremely difficult state, violation of consciousness up to the development of coma, skin pallion with an earthly tint or common cyanosis of the skin and mucous membranes, hypostasis, critical decrease in blood pressure or the uncertainty of it (less than 60 mm Hg), a filamental pulse or its absence on peripheral vessels, arrhythmical breathing, Anuria. With the further progression of the process, the atonal state clinic is developing (terminal stage).

Sometimes the early phase of shock is very short-lived (severe forms of anaphylactic shock, the lightning form of infectious-toxic shock during meningococcal infection, etc.). And therefore, the state is diagnosed in the phase of pronounced or decompensated shock. A long enough and a long early phase can manifest themselves with the vascular genesis of shock, less - in the presence of primary hypovolemia.

It is always necessary to pay attention to the possibility of decompensation of blood circulation: the progressive paleness of the skin and mucous membranes, cold sticky sweat, cold limbs, a positive test of capillary filling (after pressing the finger, the color is restored after 2 s, and with a positive sample - more than 3 s, testifies On the impaired peripheral blood circulation) or a positive symptom of the "pale spot" (more than 2 C), progressive arterial hypotension, the growth of the alfreker's shock index (the ratio of the pulse rate to the size of the systolic pressure, which is normal in the normal one in children over 5 years and 1, 5 In children up to 5 years), progressive reduction in Diurea.

In pronounced deficiency of perfusion, polyorgan deficiency can be formed - simultaneous or consistent damage to vital systems of the organism ("shock authorities" - CNS, lungs, kidneys, adrenal glands, heart, intestines, etc.) ..

First aid for shock

1. Put the patient in a horizontal position with raised lower limbs.
2. To ensure the passability of the upper respiratory tract - to remove foreign bodies from the oornych, to throw off the head, remove the lower jaw, open the mouth, set the supply of moisture, heated 100% oxygen through the breathing mask or the nasal catheter.
3. If possible, reduce or eliminate the action of a meaningful for the development of a shock factor:

  • by anaphylaxis: stop the introduction of drugs; Remove the sting of the insect; Above the place of injection or bite to impose harness up to 25 minutes, the place of injection or damage to the knotting of 0.3-0.5 ml of 0.1% of the adrenaline solution in 3-5 ml of physiological solution, the place of administration to put ice for 10-15 minutes, admission of allergen through the mouth, if the patient's condition is allowed to rinse the stomach, give a laxative, make a cleansing enema, when you get allergens into the nose or eyes, rinse with running water;
  • when bleeding, stop the outer bleeding by means of tamponades, dressings, hemostatic clamps, grinding large arteries, harness with the fixation of its overlay time;
  • with traumatic, pain syndrome: immobilization; Anesthesias in / in, a 50% analgin solution at a dose of 0.1 ml / year of life or even if necessary, 1% priedol solution at a dose of 0.1 ml / year of life, annesthetic inhalation - nitrogen oxide in a mixture with oxygen (2 : 1 or 1: 1), or in / m or in / in the introduction of 2-4 mg / kg calip-salt;
  • with a strained pneumothorax - pleural puncture.

4. Catheterization of central or peripheral veins for conducting 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 (REOPOLIGLUKIN, Polyglucina, 5% albumin, hectober, gelatinoly , Gelofusin). The choice of drugs, their ratio, the volume of infusion and the rate of administration of solutions is determined by the pathogenetic variant of the shock and the nature of the underlying disease. By shock in / in infusion, they are carried out until the patient leaves this state, or until the minimum signs of stagnation in a small or large circulation circle will appear. To prevent excessive injection of solutions, the central venous pressure is constantly monitored (its value in mm water. Art. Equal to 30/35 + 5 x the number of years of life). If it is low - infusion continues, high - stops. Mandatory is also control of blood pressure, diuresis.

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

Hydrocortisone 10-40 mg / kg / day;
Or prednisone 2-10 mg / kg / day, while in the first introduction half of the daily dose, and the other half is evenly within the day.

6. In hypoglycemia, in / in introducing a 20-40% glucose solution at a dose of 2 ml / kg.
7. With refractory arterial hypotension and in the presence of metabolic acidosis, its correction is a 4% sodium bicarbonate solution at a dose of 2 ml / kg under the control of acid-alkaline state.
8. Symptomatic therapy (sedative, anticonvulsant, antipyretic, antihistamines, hemostatic, disagrement, etc.) ..
9. If necessary, a comprehensive resuscitation provision.

Patients with shock manifestations should be hospitalized into the resuscitation department, where, taking into account etiopathogenesis, clinics will be further conservative or operational treatment.

Anaphylactic shock

Anaphylactic shock - The most severe manifestation of an allergic reaction of an immediate type that occurs to the administration of allergen against the background of the body sensitization and is characterized by severe circulatory disorders, respiration, and the activities of the central nervous system and is really threatened with life.

Causal significant allergens of the development of arterial shock in children can be:

  • medicines (antibiotics, sulfonamides, local anesthetics, x-ray protection, antipyrtic, heparin, streptocinase, aspara-hynoses, plasma substitutes - dextran, gelatin)
  • alien proteins (vaccines, serums, donor blood, plasma)
  • extracts of allergens for diagnosis and treatment;
  • poison insects, snakes;
  • some foods (citrus, nuts, etc.);
  • chemical compounds;
  • pollen plants;
  • cooling body.

On frequency and development time arterial shock The path of administration of allergen in the body is affected. In the case of parenteral administration, Allergen AS is observed more often. Especially dangerous to / in the path of administration of a drug drug, although the development of AS is quite possible with any embodiment of drugs in the child's body.

DIAGNOSTICS

Arterial shock Developing quickly, during the first variation (as much as possible to 4 hours) from the moment of contact with the allergen, and the severity of the shock does not depend on the dose of allergen. In severe cases, the collapse develops at the time of contact with the allergen.

Severe five clinical form of arterial shock:

1. Asfactic (asthmatoid) option - weakness appear and grow up, feeling in breast, lack of air, adsatory cough, pulsating headache, pain in the heart area, fear. Skin covers are sharply pale, then cyanotic. Foam at the mouth, suffocity, expiratory shortness of breath with wheezing in exhale. It is possible to develop angioedema swelling of the face and other parts of the body. In the future, with the progression of respiratory failure and accession of symptoms of acute adrenal insufficiency, lethal output may occur.

2. Hemodynamic (cardiac-vascular) option - Weakness appear and grow, noise in the ears, pouring sweat, anginal pain in the heart. The skin pallor, acricyanosis increases. It is progressively falling blood pressure, the threaded pulse, the tones of the heart are sharply weakened, arrhythmia of cardiac activity, in a few minutes there are loss of consciousness, convulsions. Female outcome may occur with the growth of cardiovascular failure.

3. Cerebral version - quickly increasing focal neurological and international symptoms.

4. Abdominal option - Spastic spilled pain in the abdomen, nausea, vomiting, diarrhea, gastrointestinal bleeding.

5. Mixed version.

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