What is a state of shock. SHOCK - Big Medical Encyclopedia

V.K. Kulagin distinguishes the following stages:

1. Nervous stage - the name emphasizes the leading role of the nervous factor in the initial stage of shock.

2. Vascular (the leading pathogenetic factors are a decrease in the volume of circulating blood, centralization of blood circulation, microcirculation disorders, followed by the development of hypoxia in many tissues).

3. Metabolic (hemodynamic disorders are accompanied by metabolic disorders that aggravate the course of the process - metabolic acidosis, the release of various cells, including lysosomal enzymes, into tissues and blood).

The following stages of shock are more common:

1) The stage of compensated shock, arousal - erectile.

2) The stage of decompensated shock, inhibition - torpid.

3) Stage of thermal shock, preagonal.

In the erectile stage, there is an increase in blood pressure, an increase in heart rate, and an acceleration of blood flow. A spasm of the vessels of many peripheral organs is also detected against the background of activation of blood flow in vital organs - centralization of blood circulation. The stage is most pronounced in traumatic and burn shock, with anaphylactic and blood transfusion it is short-lived.

In the torpid stage, blood pressure decreases and the degree of this decrease determines, along with other indicators, the severity of shock. A decrease in hourly urine output of less than 40 ml subsequently leads to the development of metabolic, and then, during the transition to the next, the thermal stage and irreversible morphological disorders. They are based on congestive hypoxia - anoxia, often taking on an irreversible character.

2.1.1. Etiology and pathogenesis of hypovolemic shock (HSH)

This shock develops with extensive loss of fluids. The most common cause of HSH is acute blood loss as a result of trauma or internal bleeding (from peptic ulcer, esophageal varices, aortic aneurysm). Blood loss may be obvious (eg, bloody stools) or latent (eg, ectopic pregnancy).

At the same time, HSH can develop with large losses not only of blood, but also of other fluids. In these cases, its symptoms do not appear immediately, but after a few hours and are accompanied by thickening of the blood. Fluid may be lost:

with massive thermal and chemical burns;

with its accumulation in the abdominal cavity (peritonitis).

with profuse diarrhea and indomitable vomiting.

with urine in diabetes and diabetes insipidus, adrenal insufficiency, with an overdose of strong diuretics.

In addition to absolute hypovolemia, there is a relative one, in which there can be enough and even a lot of blood in the vessels, but a smaller part of it takes part in the circulation, and a large part is deposited (sequestered) in the capillary and venous bed. This situation is typical for septic, anaphylactic and, to some extent, cardiogenic shock, giving all these variants of shock a certain similarity with hypovolemic, including hemorrhagic shock.

An adult easily copes with the loss of 10% of the total circulating blood volume (CBV) using the mechanisms of maintaining blood pressure, which, first of all, include vasoconstriction under the influence of catecholamines. If, however, a person rapidly loses 20 to 25% of the circulating blood, compensatory mechanisms usually no longer work fully and symptoms of shock develop.

In hemorrhagic shock, the most striking changes in hemodynamics are observed.

Immediately after blood loss, compensatory mechanisms are activated to maintain blood pressure:

1) a decrease in cardiac output (CO) is accompanied by an increase in the tone of arterioles due to an increase in the sensitivity of peripheral vessels to catecholamines and other vasoconstrictors;

2) capillaries overlap and blood begins to flow through arteriolovenous shunts;

3) renal ischemia triggers renin secretion, and through it, the renin-angiotensin-aldosterone system with sodium and water retention and an increase in BCC.

Peripheral vasoconstriction (or spasm of arterioles) on the one hand maintains blood pressure, and on the other hand, impedes tissue perfusion. In this regard, hypoxia develops in tissues, substances that reduce vascular tone accumulate. These are lactate, adenosine and many other intermediate products. Microvessels, especially exchange ones, overflow with blood. This can be regarded as a compensatory reaction of the body in response to hypoxia (to solve oxygen starvation) in an extreme situation. As a result, venous stasis develops and a lot of fluid leaves the active circulation, blood flow weakens. In this phase, all muscle microvessels lose their sensitivity to vasoconstrictors.

The perfusion of the heart and brain is maintained for the longest time, but then it also fails. Vasoconstriction. compensatory in fact, can cause ischemic necrosis of the intestine or fingers of the extremities. A myocardial depression factor appears in the blood, weakening heart contractions.

In addition to hypoxia, endotoxin of gram-negative intestinal bacteria plays an important role in the decrease in peripheral vascular tone in any form of shock. If microcirculation disorders were associated only with metabolic acidosis, they would be relatively easily eliminated after the body was removed from hypoxia. However, this does not happen, because in addition to hypoxia, a series of highly active "shockogenic" mediators of leukocytes and microvascular endothelium, formed under the influence of endotoxin, participate in the paralytic expansion of microvessels (see septic shock).

The fact is that any shock is accompanied by ischemia of the large intestine. In turn, ischemia makes the intestinal wall permeable to endotoxin, which enters the liver through the portal vein system. Under normal conditions, almost all endotoxin settles and is neutralized in the hepatic RES. At the same time, during shock, the liver loses its ability to capture and neutralize endotoxin. The latter, bypassing the liver, seeps into the systemic circulation, connecting to the pathogenesis of shock.

Shock is a pathological change in the functions of the vital systems of the body, in which there is a violation of breathing and blood circulation. This condition was first described by Hippocrates, but the medical term appeared only in the middle of the 18th century. Since various diseases can lead to the development of shock, for a long time scientists have proposed a large number of theories of its occurrence. However, none of them explained all the mechanisms. It has now been established that shock is based on arterial hypotension, which occurs with a decrease in circulating blood volume, a decrease in cardiac output and total peripheral vascular resistance, or with a redistribution of fluid in the body.

Manifestations of shock

The symptoms of shock are largely determined by the cause that led to its appearance, but there are common features of this pathological condition:

• violation of consciousness, which can be manifested by excitement or depression;
• decrease in blood pressure from insignificant to critical;
• an increase in heart rate, which is a manifestation of a compensatory reaction;
• centralization of blood circulation, in which there is a spasm of peripheral vessels, with the exception of the renal, cerebral and coronary;
• pallor, marbling and cyanosis of the skin;
• rapid shallow breathing that occurs with an increase in metabolic acidosis;
• a change in body temperature, usually it is low, but during the infectious process it is increased;
• pupils are usually dilated, reaction to light is slow;
• in especially severe situations, generalized convulsions, involuntary urination and defecation develop.

There are also specific manifestations of shock. For example, when exposed to an allergen, bronchospasm develops and the patient begins to choke, with blood loss, a person experiences a pronounced feeling of thirst, and with myocardial infarction, chest pain.

Degrees of shock

Depending on the severity of shock, four degrees of its manifestations are distinguished:

1. Compensated. At the same time, the patient's condition is relatively satisfactory, the function of the systems is preserved. He is conscious, systolic blood pressure is reduced, but exceeds 90 mm Hg, pulse is about 100 per minute.
2. Subcompensated. Violation is noted. The patient's reactions are inhibited, he is lethargic. The skin is pale, moist. The heart rate reaches 140-150 per minute, shallow breathing. The condition requires prompt medical attention.
3. Decompensated. The level of consciousness is reduced, the patient is severely retarded and reacts poorly to external stimuli, does not answer questions or answers in one word. In addition to pallor, there is marbling of the skin due to impaired microcirculation, as well as cyanosis of the fingertips and lips. The pulse can be determined only on the central vessels (carotid, femoral artery), it exceeds 150 per minute. Systolic blood pressure is often below 60 mmHg. There is a violation of the internal organs (kidneys, intestines).
4. Terminal (irreversible). The patient is usually unconscious, breathing is shallow, the pulse is not palpable. The usual method with the help of a tonometer often does not determine the pressure, the heart sounds are muffled. But blue spots appear on the skin in places where venous blood accumulates, similar to cadaveric ones. Reflexes, including pain, are absent, the eyes are motionless, the pupil is dilated. The prognosis is extremely unfavorable.

The Algover shock index, which is obtained by dividing heart rate by systolic blood pressure, can be used to determine the severity of the condition. Normally, it is 0.5, with 1 degree -1, with the second -1.5.

Types of shock

Depending on the immediate cause, there are several types of shock:

1. Traumatic shock resulting from external influences. In this case, there is a violation of the integrity of some tissues and the occurrence of pain.
2. Hypovolemic (hemorrhagic) shock develops when the volume of circulating blood decreases due to bleeding.
3. Cardiogenic shock is a complication of various heart diseases (tamponade, aneurysm rupture), in which the ejection fraction of the left ventricle decreases sharply, as a result of which arterial hypotension develops.
4. Infectious-toxic (septic) shock is characterized by a pronounced decrease in peripheral vascular resistance and an increase in the permeability of their walls. As a result, there is a redistribution of the liquid part of the blood, which accumulates in the interstitial space.
5. develops as an allergic reaction in response to intravenous exposure to a substance (prick, insect bite). In this case, histamine is released into the blood and vasodilation, which is accompanied by a decrease in pressure.

There are other varieties of shock that include various symptoms. For example, burn shock develops as a result of trauma and hypovolemia due to large fluid losses through the wound surface.

Help with shock

Every person should be able to provide first aid for shock, since in most situations minutes count:

1. The most important thing to do is to try to eliminate the cause that caused the pathological condition. For example, when bleeding, you need to clamp the arteries above the injury site. And with an insect bite, try to prevent the poison from spreading.
2. In all cases, with the exception of cardiogenic shock, it is advisable to raise the victim's legs above the head. This will help improve the blood supply to the brain.
3. In cases of extensive injuries and suspected spinal injury, it is not recommended to move the patient until the ambulance arrives.
4. To make up for fluid losses, you can give the patient a drink, preferably warm, water, as it will be absorbed faster in the stomach.
5. If a person has severe pain, he can take an analgesic, but it is not advisable to use sedatives, since this will change the clinical picture of the disease.

Emergency physicians in cases of shock use either solutions for intravenous infusions or vasoconstrictor drugs (dopamine, adrenaline). The choice depends on the specific situation and is determined by a combination of various factors. Medical and surgical treatment of shock depends on its type. So, in case of hemorrhagic shock, it is urgent to replenish the volume of circulating blood, and in case of anaphylactic shock, antihistamine and vasoconstrictor drugs should be administered. The victim must be urgently delivered to a specialized hospital, where treatment will be carried out under the control of vital signs.

The prognosis for shock depends on its type and degree, as well as the timeliness of assistance. With mild manifestations and adequate therapy, recovery almost always occurs, while with decompensated shock, the likelihood of death is high, despite the efforts of doctors.

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The term "shock", meaning in English and French a shock, a shock, a shock, was accidentally introduced in 1743 by the now unknown translator into English of the book of the army consultant Louis XV Le Dran to describe the condition of patients after a gunshot injury. Until now, this term has been widely used to describe the emotional state of a person when exposed to unexpected, extremely strong mental factors, without implying specific organ damage or physiological disorders. Applied to clinical medicine, shock means a critical condition, which is characterized by a sharp decrease in organ perfusion, hypoxia and metabolic disorders. This syndrome is manifested by arterial hypotension, acidosis and a rapidly progressive deterioration in the functions of the vital systems of the body. Without adequate treatment, shock quickly leads to death.

Acute short-term hemodynamic disturbances can be a transient episode in violation of vascular tone, reflexively caused by sudden pain, fright, blood type, stuffiness or overheating, as well as cardiac arrhythmia or orthostatic hypotension against anemia or hypotension. This episode is called collapse and in most cases resolves on its own without treatment. Due to a transient decrease in blood supply to the brain, it may develop fainting- short-term loss of consciousness, which is often preceded by neuro-vegetative symptoms: muscle weakness, sweating, dizziness, nausea, darkening of the eyes and tinnitus. Characterized by pallor, low blood pressure, brady or tachycardia. The same can develop in healthy people at high ambient temperatures, since heat stress leads to a significant expansion of skin vessels and a decrease in diastolic blood pressure. Longer hemodynamic disorders always pose a danger to the body.

The reasonsshock

Shock occurs when superstrong stimuli act on the body and can develop with various diseases, injuries and pathological conditions. Depending on the cause, there are hemorrhagic, traumatic, burn, cardiogenic, septic, anaphylactic, blood transfusion, neurogenic and other types of shock. There may be mixed forms of shock caused by a combination of several causes. Taking into account the pathogenesis of changes occurring in the body and requiring certain specific therapeutic measures, four main types of shock are distinguished.

hypovolemic shock occurs with a significant decrease in BCC as a result of massive bleeding or dehydration and is manifested by a sharp decrease in venous return of blood to the heart and severe peripheral vasoconstriction.

Cardiogenic shock occurs with a sharp decrease in cardiac output due to a violation of myocardial contractility or acute morphological changes in the heart valves and the interventricular septum. It develops with normal bcc and is manifested by overflow of the venous bed and the pulmonary circulation.

Redistributive shock manifested by vasodilation, a decrease in total peripheral resistance, venous return of blood to the heart and an increase in the permeability of the capillary wall.

Extracardiac obstructive shock occurs due to sudden obstruction of blood flow. Cardiac output falls sharply despite normal bcc, myocardial contractility, and vascular tone.

The pathogenesis of shock

Shock is based on generalized perfusion disorders leading to hypoxia of organs and tissues and disorders of cellular metabolism ( rice. 15.2.). Systemic circulatory disorders are the result of a decrease in cardiac output (CO) and changes in vascular resistance.

Hypovolemia, heart failure, impaired vascular tone, and obstruction of large vessels are the primary physiological disturbances that reduce effective tissue perfusion. With the acute development of these conditions, a "mediator storm" develops in the body with the activation of neurohumoral systems, the release of large amounts of hormones and pro-inflammatory cytokines into the systemic circulation, affecting vascular tone, vascular wall permeability and CO. In this case, the perfusion of organs and tissues is sharply disturbed. Acute severe hemodynamic disorders, regardless of the causes that caused them, lead to the same type of pathological picture. Serious violations of central hemodynamics, capillary circulation and a critical violation of tissue perfusion with tissue hypoxia, cell damage and organ dysfunctions develop.

Hemodynamic disorders

Low CO is an early feature of many types of shock, except for redistributive shock, in which cardiac output may even be increased in the initial stages. CO depends on the strength and frequency of myocardial contractions, venous blood return (preload) and peripheral vascular resistance (afterload). The main reasons for the decrease in CO during shock are hypovolemia, deterioration of the pumping function of the heart, and increased tone of the arterioles. The physiological characteristics of various types of shock are presented in tab. 15.2.

In response to a decrease in blood pressure, the activation of adaptive systems increases. First, there is a reflex activation of the sympathetic nervous system, and then the synthesis of catecholamines in the adrenal glands also increases. The content of norepinephrine in plasma increases by 5-10 times, and the level of adrenaline increases by 50-100 times. This enhances the contractile function of the myocardium, increases the rate of cardiac activity and causes a selective narrowing of the peripheral and visceral venous and arterial bed. The subsequent activation of the renin-angiotensin mechanism leads to even more pronounced vasoconstriction and the release of aldosterone, which retains salt and water. The release of antidiuretic hormone reduces the volume of urine and increases its concentration.

In shock, peripheral angiospasm develops unevenly and is especially pronounced in the skin, abdominal organs and kidneys, where the most pronounced decrease in blood flow occurs. Pale and cool skin observed during examination, and blanching of the intestine with a weakened pulse in the mesenteric vessels, visible during surgery, are clear signs of peripheral angiospasm.

The narrowing of the vessels of the heart and brain occurs to a much lesser extent compared to other areas, and these organs are provided with blood longer than others due to a sharp restriction of the blood supply to other organs and tissues. The metabolic levels of the heart and brain are high and their stores of energy substrates are extremely low, so these organs do not tolerate prolonged ischemia. Neuroendocrine compensation of the patient in shock is primarily aimed at meeting the immediate needs of vital organs - the brain and heart. Sufficient blood flow in these organs is maintained by additional autoregulatory mechanisms, as long as blood pressure exceeds 70 mm Hg. Art.

Centralization of blood circulation- biologically expedient compensatory reaction. In the initial period, she saves the life of the patient. It is important to remember that the initial shock reactions are adaptation reactions of the organism aimed at survival in critical conditions, but passing a certain limit, they begin to be pathological in nature, leading to irreversible damage to tissues and organs. The centralization of blood circulation, which persists for several hours, along with the protection of the brain and heart, is fraught with mortal danger, although more distant. This danger lies in the deterioration of microcirculation, hypoxia and metabolic disorders in organs and tissues.

Correction of central hemodynamic disorders in shock includes intensive infusion therapy aimed at increasing the BCC, the use of drugs that affect vascular tone and myocardial contractility. Only in cardiogenic shock, massive infusion therapy is contraindicated.

Violations mmicrocirculation and tissue perfusion

The microvasculature (arterioles, capillaries and venules) is the most important link in the circulatory system in the pathophysiology of shock. It is at this level that nutrients and oxygen are delivered to organs and tissues, and metabolic products are removed.

The developing spasm of arterioles and precapillary sphincters in shock leads to a significant decrease in the number of functioning capillaries and slowing down the blood flow velocity in the perfused capillaries, tissue ischemia and hypoxia. Further deterioration of tissue perfusion may be associated with secondary capillary pathology. The accumulation of hydrogen ions, lactate and other products of anaerobic metabolism leads to a decrease in the tone of arterioles and precapillary sphincters and an even greater decrease in systemic blood pressure. In this case, the venules remain narrowed. Under these conditions, the capillaries overflow with blood, and albumin and the liquid part of the blood intensively leave the vascular bed through the pores in the walls of the capillaries (“capillary leak syndrome”). Thickening of blood in the microcirculatory bed leads to an increase in blood viscosity, while the adhesion of activated leukocytes to endothelial cells increases, erythrocytes and other blood cells stick together and form large aggregates, kind of plugs, which further worsen microcirculation up to the development of sludge syndrome.

Vessels blocked by the accumulation of blood cells are switched off from the bloodstream. The so-called “pathological deposition” develops, which further reduces the BCC and its oxygen capacity and reduces the venous return of blood to the heart and, as a result, causes a drop in CO and a further deterioration in tissue perfusion. Acidosis, in addition, reduces the sensitivity of vessels to catecholamines, preventing their vasoconstrictive action and leads to atony of the venules. Thus, a vicious circle is closed. The change in the ratio of the tone of the precapillary sphincters and venules is considered a decisive factor in the development of the irreversible phase of shock.

An inevitable consequence of slowing capillary blood flow is the development of hypercoagulation syndrome. This leads to disseminated intravascular thrombosis, which not only enhances capillary circulation disorders, but also causes the development of focal necrosis and multiple organ failure.

Ischemic damage to vital tissues consistently leads to secondary damage that maintains and exacerbates the state of shock. The resulting vicious circle can lead to a fatal outcome.

Clinical manifestations of impaired tissue perfusion - cold, moist, pale cyanotic or marbled skin, prolongation of capillary filling time over 2 seconds, temperature gradient over 3 °C, oliguria (urination less than 25 ml/hour). To determine the capillary filling time, squeeze the tip of the nail plate or the ball of the toe or hand for 2 seconds and measure the time during which the pale area restores the pink color. In healthy people, this happens immediately. In case of deterioration of microcirculation, blanching lasts for a long time. Such microcirculation disorders are nonspecific and are a constant component of any type of shock, and their severity determines the severity and prognosis of shock. The principles of treatment of microcirculation disorders are also not specific and practically do not differ in all types of shock: elimination of vasoconstriction, hemodilution, anticoagulant therapy, antiplatelet therapy.

Metabolic disorders

Under conditions of reduced perfusion of the capillary bed, adequate delivery of nutrients to tissues is not ensured, which leads to metabolic disorders, dysfunction of cell membranes, and cell damage. Carbohydrate, protein, fat metabolism is disturbed, the utilization of normal energy sources - glucose and fatty acids - is sharply inhibited. In this case, a pronounced catabolism of muscle protein occurs.

The most important metabolic disorders in shock are the destruction of glycogen, a decrease in glucose dephosphorylation in the cytoplasm, a decrease in energy production in mitochondria, a malfunction of the sodium-potassium pump of the cell membrane with the development of hyperkalemia, which can cause atrial fibrillation and cardiac arrest.

The increase in plasma levels of adrenaline, cortisol, glucagon and the suppression of insulin secretion that develops during shock affect the metabolism in the cell by changes in the use of substrates and protein synthesis. These effects include increased metabolic rate, increased glycogenolysis and gluconeogenesis. Reduced glucose utilization by tissues is almost always accompanied by hyperglycemia. In turn, hyperglycemia can lead to a decrease in oxygen transport, disruption of water and electrolyte homeostasis, and glycosylation of protein molecules with a decrease in their functional activity. A significant additional damaging effect of stress hyperglycemia during shock contributes to the deepening of organ dysfunction and requires timely correction with the maintenance of normoglycemia.

Against the background of increasing hypoxia, the processes of oxidation in tissues are disrupted, their metabolism proceeds along the anaerobic pathway. At the same time, acidic metabolic products are formed in a significant amount, and metabolic acidosis develops. The criterion for metabolic dysfunction is the blood pH level below 7.3, base deficiency in excess of 5.0 mEq/l, and an increase in the concentration of lactic acid in the blood over 2 mEq/l.

An important role in the pathogenesis of shock belongs to a violation of calcium metabolism, which intensively penetrates into the cytoplasm of cells. Elevated intracellular calcium levels increase the inflammatory response, leading to an intense synthesis of potent mediators of the systemic inflammatory response (SIR). Inflammatory mediators play a significant role in the clinical manifestations and progression of shock, as well as in the development of subsequent complications. Increased production and systemic distribution of these mediators can lead to irreversible cell damage and high mortality. The use of calcium channel blockers improves the survival of patients with various types of shock.

The action of pro-inflammatory cytokines is accompanied by the release of lysosomal enzymes and free peroxide radicals, which cause further damage - "sick cell syndrome". Hyperglycemia and an increase in the concentration of soluble products of glycolysis, lipolysis and proteolysis lead to the development of hyperosmolarity of the interstitial fluid, which causes the transfer of intracellular fluid into the interstitial space, dehydration of cells and further deterioration of their functioning. Thus, cell membrane dysfunction may represent a common pathophysiological pathway for various causes of shock. And although the exact mechanisms of cell membrane dysfunction are unclear, the best way to eliminate metabolic disorders and prevent the irreversibility of shock is to quickly restore BCC.

Inflammatory mediators produced by cellular damage contribute to further disruption of perfusion, which further damages cells within the microvasculature. Thus, a vicious circle closes - a violation of perfusion leads to cell damage with the development of a systemic inflammatory response syndrome, which in turn further worsens tissue perfusion and cell metabolism. When these excessive systemic responses persist for a long time, become autonomous and cannot be reversed, the syndrome of multiple organ failure develops.

In the development of these changes, the leading role belongs to the tumor necrosis factor (TNF), interleukins (IL-1, IL-6, IL-8), platelet activating factor (PAF), leukotrienes (B4, C4, D4, E4), thromboxane A2, prostaglandins (E2, E12), prostacyclin, gamma-interferon. Simultaneous and multidirectional action of etiological factors and activated mediators in shock leads to endothelial damage, impaired vascular tone, vascular permeability, and organ dysfunction.

Persistence or progression of shock may result from either a continuing perfusion defect or cellular damage, or a combination of the two. Since oxygen is the most labile vital substrate, its inadequate delivery by the circulatory system forms the basis of the pathogenesis of shock, and timely restoration of perfusion and tissue oxygenation often completely stops the progression of shock.

Thus, the pathogenesis of shock is based on deep and progressive disorders of hemodynamics, oxygen transport, humoral regulation and metabolism. The relationship of these disorders can lead to the formation of a vicious circle with the complete depletion of the body's adaptive capabilities. Preventing the development of this vicious circle and restoring the autoregulatory mechanisms of the body is the main task of intensive care for patients with shock.

Stages of shock

Shock is a dynamic process, starting from the moment of action of the factor of aggression, which leads to systemic circulatory disorders, and with the progression of disorders ending in irreversible organ damage and death of the patient. The effectiveness of compensatory mechanisms, the degree of clinical manifestations and the reversibility of the resulting changes make it possible to distinguish a number of successive stages in the development of shock.

Preshock stage

Shock is usually preceded by a moderate decrease in systolic blood pressure, not exceeding 20 mm Hg. Art. from the norm (or 40 mm Hg if the patient has arterial hypertension), which stimulates the baroreceptors of the carotid sinus and aortic arch and activates the compensatory mechanisms of the circulatory system. Tissue perfusion is not significantly affected and cell metabolism remains aerobic. If at the same time the influence of the factor of aggression stops, then compensatory mechanisms can restore homeostasis without any therapeutic measures.

Early (reversible) stage of shock

This stage of shock is characterized by a decrease in systolic blood pressure below 90 mm Hg. Art. , severe tachycardia, shortness of breath, oliguria and cold clammy skin. At this stage, compensatory mechanisms alone are not able to maintain adequate CO and meet the oxygen needs of organs and tissues. Metabolism becomes anaerobic, tissue acidosis develops, and signs of organ dysfunction appear. An important criterion for this phase of shock is the reversibility of the resulting changes in hemodynamics, metabolism and organ functions and a fairly rapid regression of the developed disorders under the influence of adequate therapy.

Intermediate (progressive) stage of shock

This is a life-threatening emergency with systolic blood pressure below 80 mmHg. Art. and severe, but reversible dysfunction of organs with immediate intensive treatment. This requires artificial lung ventilation (ALV) and the use of adrenergic drugs to correct hemodynamic disorders and eliminate organ hypoxia. Prolonged deep hypotension leads to generalized cellular hypoxia and critical disruption of biochemical processes, which quickly become irreversible. It is from the effectiveness of therapy during the first so-called "golden hour" the patient's life depends.

Refractory (irreversible) stage of shock

This stage is characterized by severe disorders of central and peripheral hemodynamics, cell death and multiple organ failure. Intensive therapy is ineffective, even if the etiological causes are eliminated and blood pressure temporarily increases. Progressive multiple organ dysfunction usually leads to permanent organ damage and death.

Diagnostic studies and monitoring in shock

Shock does not leave time for orderly collection of information and clarification of the diagnosis before treatment. Systolic blood pressure in shock is most often below 80 mm Hg. Art. , but shock is sometimes diagnosed with higher systolic blood pressure if there are clinical signs of a sharp deterioration in organ perfusion: cold skin covered with sticky sweat, mental status change from confusion to coma, oligo- or anuria, and insufficient filling of skin capillaries. Fast breathing during shock usually indicates hypoxia, metabolic acidosis and hyperthermia, and hypoventilation - depression of the respiratory center or increased intracranial pressure.

Diagnostic studies for shock also include a clinical blood test, determination of electrolytes, creatinine, blood coagulation, blood group and Rh factor, arterial blood gases, electrocardiography, echocardiography, chest x-ray. Only carefully collected and correctly interpreted data helps to make the right decisions.

Monitoring is a system for monitoring the vital functions of the body, capable of quickly notifying about the occurrence of threatening situations. This allows you to start treatment on time and prevent the development of complications. To control the effectiveness of shock treatment, monitoring of hemodynamic parameters, activity of the heart, lungs and kidneys is indicated. The number of controlled parameters should be reasonable. Monitoring during shock should necessarily include the registration of the following indicators:

• BP, using intra-arterial measurement if necessary;
• heart rate (HR);
• intensity and depth of breathing;
• central venous pressure (CVP);
• pulmonary artery wedge pressure (PAWP) in severe shock and unclear cause of shock;
• diuresis;
• blood gases and plasma electrolytes.

For an approximate assessment of the severity of shock, you can calculate the Algover-Burri index, or, as it is also called, the shock index - the ratio of the pulse rate in 1 minute to the value of systolic blood pressure. And the higher this indicator, the greater the danger threatens the life of the patient. The inability to monitor any of these indicators makes it difficult to choose the right therapy and increases the risk of iatrogenic complications.

Central venous pressure

Low CVP is an indirect criterion for absolute or indirect hypovolemia, and its rise is above 12 cm of water. Art. indicates heart failure. Measurement of CVP with an assessment of its response to a small fluid load helps to choose an infusion therapy regimen and determine the appropriateness of inotropic support. Initially, the patient is administered a test dose of liquid for 10 minutes: 200 ml with an initial CVP below 8 cm aq. Art. ; 100 ml - with CVP within 8-10 cm aq. Art. ; 50 ml - with CVP above 10 cm aq. Art. The reaction is evaluated based on the rule “5 and 2 cm aq. Art. »: if the CVP has increased by more than 5 cm, the infusion is stopped and the question of the advisability of inotropic support is decided, since such an increase indicates a breakdown in the Frank-Starling contractility regulation mechanism and indicates heart failure. If the increase in CVP is less than 2 cm of water. Art. - this indicates hypovolemia and is an indication for further intensive fluid therapy without the need for inotropic therapy. An increase in CVP in the range of 2 and 5 cm aq. Art. requires further infusion therapy under the control of hemodynamic parameters.

It must be emphasized that CVP is an unreliable indicator of left ventricular function, since it depends primarily on the state of the right ventricle, which may differ from the state of the left. More objective and broader information about the state of the heart and lungs is provided by hemodynamic monitoring in the pulmonary circulation. Without its use, in more than a third of cases, the hemodynamic profile of a patient with shock is incorrectly assessed. The main indication for pulmonary artery catheterization in shock is an increase in CVP during infusion therapy. The response to the introduction of a small volume of fluid when monitoring hemodynamics in the pulmonary circulation is assessed according to the rule “7 and 3 mm Hg. Art. ".

Monitoring of hemodynamics in the pulmonary circulation

Invasive monitoring of blood circulation in a small circle is performed using a catheter installed in the pulmonary artery. For this purpose, a catheter with a floating balloon at the end (Swan-Gans) is usually used, which allows you to measure a number of parameters:

• pressure in the right atrium, right ventricle, pulmonary artery and PAWP, which reflects the filling pressure of the left ventricle;
• SW by thermodilution method;
• partial pressure of oxygen and saturation of hemoglobin with oxygen in mixed venous blood.

The determination of these parameters greatly expands the possibilities of monitoring and evaluating the effectiveness of hemodynamic therapy. The resulting indicators allow:

• differentiate cardiogenic and non-cardiogenic pulmonary edema, detect pulmonary embolism and rupture of the mitral valve leaflets;
• evaluate BCC and the state of the cardiovascular system in cases where empirical treatment is ineffective or is associated with an increased risk;
• to adjust the volume and rate of fluid infusion, the dose of inotropic and vasodilator drugs, the value of positive end-expiratory pressure during mechanical ventilation.

Decreased venous mixed oxygen saturation is always an early indicator of cardiac output inadequacy.

Diuresis

A decrease in diuresis is the first objective sign of a decrease in BCC. Patients with shock must install a permanent urinary catheter to control the volume and rate of urination. When carrying out infusion therapy, diuresis should be at least 50 ml / hour. With alcohol intoxication, shock can occur without oliguria, since ethanol inhibits the secretion of antidiuretic hormone.