Shock develops. II. Extreme conditions, general characteristics and types Introduction. Etiology and pathogenesis

First degree shock - mild. The victim's condition is compensated, consciousness is clear, pulse is 90-100 beats per minute, maximum blood pressure is 90-100 mm Hg. Art.

Shock of the second degree - moderate severity. The victim is lethargic, the skin is pale, the pulse is frequent - up to 140 beats per minute, the filling is weak, the maximum blood pressure is reduced to 90-80 mm Hg. Art. Breathing is shallow and rapid. The prognosis is serious. To save a life, anti-shock measures are required.

Third degree shock - severe. The victim's condition is very serious. Consciousness is confused or absent altogether. The skin is pale, covered with cold sweat, and acrocyanosis is pronounced. The pulse is threadlike - 130-180 beats per minute, detected only in large arteries (carotid, femoral). The prognosis is very serious.

Fourth degree shock is a terminal condition. The victim is unconscious, gray skin, bluish lips, blood pressure below 50 mm Hg. Art., is often not determined at all. The pulse is barely noticeable in the central arteries. Breathing is shallow, rare (sobbling), pupils are dilated, there are no reflexes or reactions to painful stimulation. The prognosis is almost always unfavorable.

Emergency medical care:

If the patient is unconscious, then the patency of the upper respiratory tract should be ensured (triple Safar maneuver, insertion of an air duct, tracheal intubation);

Perform a temporary stop of external bleeding (finger pressure, pressure bandage, tourniquet, application of a hemostatic clamp);

Eliminate BCC deficiency:

Provide venous access with a needle of the largest diameter into 2 veins with their catheterization and carry out a jet infusion of blood substitutes: inject colloidal solutions (400-800 ml) into one catheter;

Inject crystalloid solutions (400-800 ml) into another catheter at a rate of 800 ml per 10 minutes if SBP stabilizes at 90 mm Hg. Art., switch to drip administration of plasma substitutes;

In case of severe shock, to stabilize hemodynamics, administer intravenous hormones from the first minutes: prednisolone 60-90 mg or hydrocortisone 125-250 mg;

For open pneumothorax, apply an occlusive dressing;

In case of charged pneumothorax, perform puncture and drainage of the pleural cavity;

Anesthesia: 2% - 1 ml of promedol (for SBP less than 60 mm Hg, damage to internal organs, TBI, the administration of narcotic analgesics is not indicated;

In case of severe combined injury, inhale nitrous oxide with oxygen in a ratio of 2:1;

If there are fractures, apply local anesthesia;

If there are wounds, apply an aseptic bandage;

Transport immobilization (for fractures) is performed only after pain relief;

In case of acute respiratory failure and apnea, perform mechanical ventilation with manual or automatic devices, oxygen therapy;

Make a rational placement of the patient on a stretcher and transport it to a specialized hospital with the foot end of the stretcher raised, warning the admissions department staff;

Monitor breathing, pulse, blood pressure.

Activities during transportation of the patient:

1. Continuation of intravenous infusion of polyglucin or gelatinol;

2. In case of multiple injuries and shock of III – IV degrees, it is advisable to transport the victim under nitrous-oxygen anesthesia;

3. In case of severe breathing disorders, tracheal intubation and artificial ventilation of the lungs with a Ruben bag are indicated.

Before transportation, it is advisable to at least partially compensate for blood loss, provide anesthesia, reliable immobilization, etc. However, if internal bleeding is suspected, hospitalization should be done as early as possible.

Activities in the hospital:

One of the main measures in the hospital is the final stop of bleeding.

1. If internal bleeding is diagnosed, immediate surgery is performed.

2. Carrying out complete pain relief: narcotic analgesics are administered after blood pressure has been restored to a minimally critical level; ketamine 6 – 10 mg/kg, calypsol 2 – 4 mg/kg. The drug of choice for rational pain relief is nitrous oxide with oxygen.

3. Replenishment of blood volume, along with infusion of crystalloid solutions, is carried out by blood transfusion

in case of shock of II – III degrees, at least 75% of blood loss;

in case of shock of III – IV degrees – up to 100% or more.

With persistent hypotension and a long (more than 30 min) period of decrease in systolic blood pressure below 70 - 80 mm Hg. Intra-arterial transfusion and administration of prednisolone (2–3 mg/kg) are indicated. The administration of pressor amines is contraindicated. Blood transfusions should be alternated with the administration of 5% glucose solution and Ringer's solution, 250–500 ml each.

In case of shock of III - IV degrees in the first 20 - 30 minutes after admission to the hospital, the rate of intravenous infusions should be high - 100 ml per minute.

4. After stabilization of blood pressure at a level not lower than 100 mm Hg. Intravenous administration of a mixture of polyglucin or a 5% glucose solution with a 0.25% novocaine solution in equal quantities is indicated while monitoring blood pressure, pulse, diuresis and skin color (restoration of microcirculation). Typically, the dose of the polyglucin-novocaine mixture in the first day after injury varies depending on the patient’s condition from 500 to 1000 ml.

5. To correct metabolic acidosis after replacing the bcc, a 4% solution of sodium bicarbonate is administered in a dose of 200 – 600 ml (3 ml/kg), depending on the patient’s condition and the duration of the period of hypotension.

6. During the first day, intravenous administration of 6–12 g of potassium chloride is indicated, which is administered in a 20% glucose solution with insulin at the rate of no more than 1.5 g of potassium per 200 ml of solution and 1 unit of insulin per 2 g of dry glucose.

7. It is necessary to monitor the condition of the blood coagulation and anticoagulation systems. Usually, from the second day after injury, indications for the use of heparin (20 thousand units per day) and sometimes fibrinolysin appear. Anticoagulants are a powerful means of preventing pulmonary complications and, above all, “shock lung”.

Thus, the basic principles of treatment of traumatic shock are:

Early treatment, as shock lasts 12 – 24 hours;

Etiopathogenetic treatment, that is, treatment depending on the cause, severity, course of shock;

Comprehensiveness of treatment;

Differentiation of treatment, depending on the nature of the damage.

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General information

This is a serious condition where the cardiovascular system cannot keep up with the body's blood supply, usually due to low blood pressure and cell or tissue damage.

Causes of shock

Shock can be caused by a condition in the body when blood circulation is dangerously reduced, for example, with cardiovascular disease (heart attack or heart failure), with large loss of blood (severe bleeding), with dehydration, with severe allergic reactions or blood poisoning (sepsis).

Shock classification includes:

• cardiogenic shock (associated with cardiovascular problems),
• hypovolemic shock (caused by low blood volume),
• anaphylactic shock (caused by allergic reactions),
• septic shock (caused by infections),
• neurogenic shock (nervous system disorders).

Shock is a life-threatening condition and requires immediate medical treatment; emergency care is not excluded. The patient's condition in shock can quickly deteriorate; be prepared for initial resuscitation efforts.

Symptoms of shock

Symptoms of shock may include feelings of fear or agitation, bluish lips and nails, chest pain, confusion, cold clammy skin, decreased or stopped urination, dizziness, fainting, low blood pressure, paleness, excessive sweating, rapid pulse, shallow breathing, unconsciousness , weakness.

First aid for shock

Check the victim's airway and perform artificial respiration if necessary.

If the patient is conscious and has no injuries to the head, limbs, or back, lay him on his back, with his legs raised 30 cm; don't raise your head. If the patient has suffered an injury in which raised legs cause pain, then there is no need to raise them. If the patient has received severe damage to the spine, leave him in the position in which you found him, without turning him over, and provide first aid by treating wounds and cuts (if any).

The person should stay warm, loosen tight clothing, and do not give the patient anything to eat or drink. If the patient is vomiting or drooling, turn the patient's head to the side to allow the vomit to drain (only if there is no suspicion of spinal injury). If there is still a suspicion of spinal injury and the patient is vomiting, it is necessary to turn him over, fixing his neck and back.

Call an ambulance and continue to monitor vital signs (temperature, pulse, respiratory rate, blood pressure) until help arrives.

Preventive measures

Preventing shock is easier than treating it. Prompt and timely treatment of the underlying cause will reduce the risk of developing severe shock. First aid will help control the state of shock.

Shock is a syndrome complex based on inadequate capillary perfusion with reduced oxygenation and impaired metabolism of tissues and organs.

A number of pathogenetic factors are common to various shocks: first of all, low cardiac output, peripheral vasoconstriction, microcirculation disorders, and respiratory failure.

CLASSIFICATION OF SHOCKS(according to Barrett).

I - Hypovolemic shock

1 – due to blood loss

2 – due to predominant loss of plasma (burns)

3 – general dehydration (diarrhea, uncontrollable vomiting)

II – Cardiovascular shock

1 – acute cardiac dysfunction

2 – heart rhythm disorder

3 – mechanical blockage of large arterial trunks

4 – decrease in reverse venous blood flow

III – Septic shock

IV – Anaphylactic shock

V - Vascular peripheral shock

VI - Combined and rare forms of shock

Heatstroke

Traumatic shock.

Hypovolemic shock - acute cardiovascular failure, which develops as a result of a significant deficiency of blood volume. The reason for the decrease in blood volume may be loss of blood (hemorrhagic shock), plasma (burn shock). As a compensatory mechanism, the sympathetic-adrenal system is activated, the level of adrenaline and norepinephrine increases, which leads to selective narrowing of blood vessels in the skin, muscles, kidneys, and intestines, provided that cerebral blood flow is maintained (blood circulation is centralized).

The pathogenesis and clinical manifestations of hemorrhagic and traumatic shock are in many ways similar. But with traumatic shock, along with blood and plasma loss, powerful streams of pain impulses come from the damaged area, and intoxication of the body with decay products of injured tissue increases.

When examining the patient, attention is drawn to the pallor of the skin, which is cold and damp to the touch. The patient's behavior is inappropriate. Despite the severity of the condition, he may be agitated or too calm. The pulse is frequent and soft. Blood pressure and central venous pressure are reduced.

Due to compensatory reactions, even with a decrease in blood volume by 15-25%, blood pressure remains within normal limits. In such cases, you should focus on other clinical symptoms: pallor, tachycardia, oliguria. Blood pressure level can serve as an indicator only if the patient is monitored dynamically.

The erectile and torpid phases of shock are noted.

The erectile phase of shock is characterized by pronounced psychomotor agitation of the patient. Patients may be inadequate, they fuss and scream. Blood pressure may be normal, but tissue circulation is already impaired due to its centralization. The erectile phase is short-lived and rarely observed.

In the torpid phase there are 4 degrees of severity. When diagnosing them, the Aldgover shock index is informative - the ratio of pulse rate to systolic pressure.

In case of first degree shock, the patient is conscious, the skin is pale, breathing is rapid, moderate tachycardia, blood pressure is 100-90 mm Hg. Index A. is almost 0.8-1. The approximate amount of blood loss does not exceed 1 liter.

In case of shock, stage II. – the patient is lethargic, the skin is cold, pale, moist. Shallow breathing, shortness of breath. Pulse up to 130 per minute, systolic D is 85-70 mm Hg. Index A.-1-2. The approximate amount of blood loss is about 2 liters.

In case of shock, stage III. – depression of consciousness, pupils are dilated, react sluggishly to light, pulse up to 110 per minute, systolic D does not exceed 70 mm Hg. Index A. – 2 and higher. Approximate blood loss is about 3 liters.

In case of shock IU stage. – (blood loss more than 3 liters) – terminal condition, consciousness is absent, pulse and blood pressure are not determined. Breathing is shallow and uneven. The skin has a grayish tint, is cold, covered with sweat, the pupils are dilated, there is no reaction to light.

The term "shock", meaning a blow, shock, shock in English and French, was accidentally introduced in 1743 by a now unknown translator into English of a book by Louis XV's army consultant 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 damage to organs or physiological disorders. In relation to clinical medicine, shock means a critical condition characterized by a sharp decrease in organ perfusion, hypoxia and metabolic disorders. This syndrome is manifested by arterial hypotension, acidosis and rapidly progressive deterioration in the functions of vital body systems. Without adequate treatment, shock quickly leads to death.

Acute short-term hemodynamic disturbances can be a transient episode when there is a violation of vascular tone, reflexively caused by sudden pain, fear, the sight of blood, stuffiness or overheating, as well as cardiac arrhythmia or orthostatic hypotension due to 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, bradycardia or tachycardia. The same thing can develop in healthy people at high ambient temperatures, since heat stress leads to a significant dilation of skin vessels and a decrease in diastolic blood pressure. Longer hemodynamic disorders always pose a danger to the body.

Causesshock

Shock occurs when the body is exposed to super-strong irritants and can develop as a result of various diseases, injuries and pathological conditions. Depending on the cause, hemorrhagic, traumatic, burn, cardiogenic, septic, anaphylactic, blood transfusion, neurogenic and other types of shock are distinguished. There may also be mixed forms of shock caused by a combination of several reasons. 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 blood volume 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 impaired myocardial contractility or acute morphological changes in the heart valves and interventricular septum. It develops with normal bcc and is manifested by overflow of the venous bed and pulmonary circulation.

Redistribution 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 a sudden obstruction to blood flow. Cardiac output drops sharply despite normal blood volume, myocardial contractility and vascular tone.

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 a consequence of decreased cardiac output (CO) and changes in vascular resistance.

Primary physiological disorders that reduce effective tissue perfusion are hypovolemia, heart failure, impaired vascular tone, and obstruction of large vessels. With the acute development of these conditions, a “mediator storm” develops in the body with the activation of neuro-humoral systems, the release into the systemic circulation of large quantities of hormones and pro-inflammatory cytokines, affecting vascular tone, vascular wall permeability and CO. In this case, the perfusion of organs and tissues is sharply disrupted. Acute severe hemodynamic disorders, regardless of the reasons that caused them, lead to the same type of pathological picture. Serious disturbances of central hemodynamics, capillary circulation and critical disruption of tissue perfusion with tissue hypoxia, cell damage and organ dysfunction develop.

Hemodynamic disorders

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

In response to a decrease in blood pressure, the activation of adaptive systems increases. First, reflex activation of the sympathetic nervous system occurs, and then the synthesis of catecholamines in the adrenal glands increases. The content of norepinephrine in plasma increases 5-10 times, and the level of adrenaline increases 50-100 times. This enhances the contractile function of the myocardium, increases cardiac activity and causes a selective narrowing of the peripheral and visceral venous and arterial beds. 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 urine volume and increases its concentration.

In shock, peripheral vasospasm 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 pallor of the intestine with weakened pulse in the mesenteric vessels visible during surgery are clear signs of peripheral vasospasm.

Constriction of the blood vessels of the heart and brain occurs to a much lesser extent compared to other zones, and these organs are provided with blood longer than others due to a sharp limitation of the blood supply to other organs and tissues. The metabolic rates of the heart and brain are high, and their reserves of energy substrates are extremely low, so these organs do not tolerate prolonged ischemia. Neuroendocrine compensation of a patient in shock is primarily aimed at providing 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 mmHg. Art.

Centralization of blood circulation- biologically appropriate compensatory reaction. In the initial period, it saves the patient’s life. It is important to remember that initial shock reactions are adaptation reactions of the body aimed at survival in critical conditions, but beyond a certain limit, they begin to be pathological in nature, leading to irreversible damage to tissues and organs. Centralization of blood circulation, which persists for several hours, along with protection of the brain and heart, is fraught with a 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 disturbances during shock includes intensive infusion therapy aimed at increasing blood volume, the use of drugs that affect vascular tone and myocardial contractility. Only in case of cardiogenic shock is massive infusion therapy 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 also removed.

The developing spasm of arterioles and precapillary sphincters during shock leads to a significant decrease in the number of functioning capillaries and a slowdown in the speed of blood flow in the perfused capillaries, ischemia and tissue 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 become overfilled with blood, and albumin and the liquid part of the blood intensively leave the vascular bed through 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, red blood cells and other formed elements of blood stick together and form large aggregates, peculiar plugs, which further worsen microcirculation until 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 blood vessels to catecholamines, preventing their vasoconstrictor effect and leads to atony of the venules. Thus, a vicious circle is closed. A 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 thrombus formation, which not only increases 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 aggravates the shock state. The resulting vicious circle can lead to a fatal outcome.

Clinical manifestations of impaired tissue perfusion are cold, moist, pale cyanotic or marbled skin, prolongation of capillary refill time over 2 seconds, temperature gradient over 3 °C, oliguria (urination less than 25 ml/hour). To determine the capillary refill time, squeeze the tip of the nail plate or the pad of the toe or hand for 2 seconds and measure the time during which the pale area regains its pink color. In healthy people this happens immediately. If microcirculation deteriorates, blanching lasts for a long time. Such microcirculation disorders are nonspecific and are a constant component of any type of shock, and the degree of 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 for all types of shock: elimination of vasoconstriction, hemodilution, anticoagulant therapy, disaggregant 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, and fat metabolism are disrupted, and the utilization of normal energy sources - glucose and fatty acids - is sharply inhibited. In this case, pronounced catabolism of muscle protein occurs.

The most important metabolic disorders during shock are the destruction of glycogen, a decrease in dephosphorylation of glucose in the cytoplasm, a decrease in energy production in mitochondria, disruption 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 that develops during shock and the suppression of insulin secretion 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. A decrease in tissue glucose utilization is almost always accompanied by hyperglycemia. In turn, hyperglycemia can lead to a decrease in oxygen transport, disruption of water-electrolyte homeostasis and glycosylation of protein molecules with a decrease in their functional activity. Significant additional damaging effects of stress hyperglycemia during shock contribute to the deepening of organ dysfunction and require timely correction while maintaining normoglycemia.

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

An important role in the pathogenesis of shock belongs to the disturbance of calcium metabolism, which intensively penetrates into the cytoplasm of cells. Elevated intracellular calcium levels increase the inflammatory response, leading to 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 survival in 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 transition 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 the rapid restoration of bcc.

Inflammatory mediators produced during cellular damage contribute to further disruption of perfusion, which further damages cells within the microvasculature. Thus, a vicious circle is completed - impaired perfusion leads to cell damage with the development of 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, multiple organ failure syndrome develops.

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

Persistence or progression of shock may result from either ongoing perfusion defects, cellular damage, or a combination of both. 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 tissue perfusion and 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 interrelation of these disorders can lead to the formation of a vicious circle with complete depletion of the body’s adaptive capabilities. Preventing the development of this vicious circle and restoring the body's autoregulatory mechanisms is the main task of intensive care for patients with shock.

Stages of shock

Shock is a dynamic process that begins with the action of the aggression factor, which leads to systemic circulatory disorders, and, as the disorders progress, ends with irreversible damage to organs and death of the patient. The effectiveness of compensatory mechanisms, the degree of clinical manifestations and the reversibility of the changes that occur 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 normal (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 cellular metabolism remains aerobic. If the influence of the aggression factor ceases, 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 mmHg. Art. , severe tachycardia, shortness of breath, oliguria and cold clammy skin. At this stage, compensatory mechanisms are independently unable to maintain adequate CO and satisfy 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 developed disorders under the influence of adequate therapy.

Intermediate (progressive) stage of shock

This is a life-threatening critical situation with a systolic blood pressure level below 80 mmHg. Art. and pronounced but reversible organ dysfunction with immediate intensive treatment. This requires artificial pulmonary 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 on 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 multiorgan dysfunction usually leads to irreversible organ damage and death.

Diagnostic tests and monitoring for shock

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

Diagnostic tests for shock also include a clinical blood test, determination of electrolytes, creatinine, blood clotting parameters, blood group and Rh factor, arterial blood gases, electrocardiography, echocardiography, and chest radiography. Only carefully collected and correctly interpreted data helps 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 monitor the effectiveness of shock treatment, monitoring of hemodynamic parameters, heart, lung and kidney activity is indicated. The number of controlled parameters must be reasonable. Monitoring for shock must necessarily include recording of the following indicators:

• Blood pressure, 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 unknown cause of shock;
• diuresis;
• blood gases and plasma electrolytes.

To approximate 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 per minute to the value of systolic blood pressure. And the higher this indicator, the greater the danger to the patient’s life. The inability to monitor any of the listed indicators makes the correct choice of therapy difficult and increases the risk of developing iatrogenic complications.

Central venous pressure

Low central venous pressure is an indirect criterion of absolute or indirect hypovolemia, and its rise above 12 cm of water. Art. indicates heart failure. Measuring central venous pressure and assessing its response to a low fluid load helps to select a fluid therapy regimen and determine the appropriateness of inotropic support. Initially, the patient is given a test dose of liquid over 10 minutes: 200 ml at an initial CVP below 8 cm aq. Art. ; 100 ml - with a central venous pressure within 8-10 cm aq. Art. ; 50 ml - with a central venous pressure above 10 cm aq. Art. The reaction is assessed based on the rule “5 and 2 cm aq. Art. ": if the central venous pressure increases 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 of the Frank-Starling contractility regulation mechanism and indicates heart failure. If the increase in central venous pressure is less than 2 cm water. Art. - this indicates hypovolemia and is an indication for further intensive fluid resuscitation without the need for inotropic therapy. Increase in central venous pressure 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 condition of the right ventricle, which may differ from the condition of the left. More objective and broader information about the condition of the heart and lungs is provided by monitoring hemodynamics in the pulmonary circulation. Without its use, the hemodynamic profile of a patient with shock is incorrectly assessed in more than a third of cases. The main indication for catheterization of the pulmonary artery in shock is an increase in central venous pressure 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. "

Hemodynamic monitoring in the pulmonary circulation

Invasive monitoring of blood circulation in the pulmonary circulation 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 pulmonary artery, which reflects the filling pressure of the left ventricle;
• SV by thermodilution method;
• partial pressure of oxygen and oxygen saturation of hemoglobin in mixed venous blood.

Determination of these parameters significantly expands the possibilities of monitoring and assessing the effectiveness of hemodynamic therapy. The resulting indicators allow:

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

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

Diuresis

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

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

1. Hypovolemic shock:

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

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

3. Septic shock:

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

4. Anaphylactic shock.

Mechanisms of shock development

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

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

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

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

Clinical manifestations of shock

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

Stages of diagnostic search

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

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

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

Clinical criteria for the main forms of shock

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Diagnosis of shock

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

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

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

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

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

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

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

Prognosis and treatment of shock

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

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

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

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

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

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

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

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

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

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

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

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