Anesthesiology and resuscitation. Shock (lecture notes)

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Anesthesiology and resuscitation. Shock (lecture notes)

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Lecture No. 9. Shock

Shock is a form of a critical state of the body, manifested by multiple organ dysfunction, developing in a cascade on the basis of a generalized circulation crisis and, as a rule, ending in death without treatment.

A shock factor is any effect on the body that exceeds adaptive mechanisms in strength. In shock, the functions of respiration, the cardiovascular system, and kidneys change, the processes of microcirculation of organs and tissues and metabolic processes are disrupted.

Etiology and pathogenesis

Shock is a disease of a polyetiological nature. Depending on the etiology of occurrence, the types of shock may be different.

1. Traumatic shock:

1) with mechanical injuries - bone fractures, wounds, compression of soft tissues, etc.;

2) with burn injuries (thermal and chemical burns);

3) under the influence of low temperature - cold shock;

4) in case of electrical injuries - electric shock.

2. Hemorrhagic or hypovolemic shock:

1) develops as a result of bleeding, acute blood loss;

2) as a result of an acute violation of the water balance, dehydration of the body occurs.

3. Septic (bacterial-toxic) shock (generalized purulent processes caused by gram-negative or gram-positive microflora).

4. Anaphylactic shock.

5. Cardiogenic shock (myocardial infarction, acute heart failure). Considered in the section emergency conditions in cardiology.

In all types of shock, the main mechanism of development is vasodilation, and as a result, the capacity of the vascular bed increases, hypovolemia - the volume of circulating blood (BCC) decreases, since there are various factors: blood loss, redistribution of fluid between the blood and tissues, or a mismatch of the normal blood volume increasing vascular capacity. The resulting discrepancy between the BCC and the capacity of the vascular bed underlies the decrease in cardiac output and microcirculation disorders. The latter leads to serious changes in the body, since it is here that the main function of blood circulation is carried out - the exchange of substances and oxygen between the cell and the blood. There comes a thickening of the blood, an increase in its viscosity and intracapillary microthrombosis. Subsequently, cell functions are disrupted up to their death. In tissues, anaerobic processes begin to predominate over aerobic ones, which leads to the development of metabolic acidosis. Accumulation of metabolic products, mainly lactic acid, increases acidosis.

A feature of the pathogenesis of septic shock is a violation of blood circulation under the influence of bacterial toxins, which contributes to the opening of arteriovenous shunts, and blood begins to bypass the capillary bed and rushes from arterioles to venules. Due to a decrease in capillary blood flow and the action of bacterial toxins specifically on the cell, cell nutrition is disrupted, which leads to a decrease in the supply of oxygen to cells.

In anaphylactic shock, under the influence of histamine and other biologically active substances, capillaries and veins lose their tone, while the peripheral vascular bed expands, its capacity increases, which leads to pathological redistribution of blood. Blood begins to accumulate in the capillaries and venules, causing a violation of cardiac activity. The BCC formed at the same time does not correspond to the capacity of the vascular bed, and the minute volume of the heart (cardiac output) decreases accordingly. The resulting stagnation of blood in the microcirculatory bed leads to a breakdown in metabolism and oxygen between the cell and blood at the level of the capillary bed.

The above processes lead to ischemia of the liver tissue and disruption of its functions, which further exacerbates hypoxia in severe stages of shock development. Violated detoxification, protein-forming, glycogen-forming and other functions of the liver. The disorder of the main, regional blood flow and microcirculation in the renal tissue contributes to the disruption of both the filtration and concentration functions of the kidneys with a decrease in diuresis from oliguria to anuria, which leads to the accumulation of nitrogenous wastes in the patient's body, such as urea, creatinine, and other toxic metabolic products substances. The functions of the adrenal cortex are impaired, the synthesis of corticosteroids (glucocorticoids, mineralocorticoids, androgenic hormones) is reduced, which aggravates the ongoing processes. Circulatory disorders in the lungs explain the violation of external respiration, alveolar gas exchange decreases, blood shunting occurs, microthrombosis is formed, and as a result, the development of respiratory failure, which aggravates tissue hypoxia.

Clinic

Hemorrhagic shock is a reaction of the body to the resulting blood loss (loss of 25-30% of BCC leads to severe shock).

In the occurrence of burn shock, the pain factor and massive plasma loss play a dominant role. Rapidly developing oliguria and anuria. The development of shock and its severity are characterized by the volume and rate of blood loss. Based on the latter, compensated hemorrhagic shock, decompensated reversible shock and decompensated irreversible shock are distinguished.

With compensated shock, pallor of the skin, cold sticky sweat, the pulse becomes small and frequent, blood pressure remains within the normal range or is slightly reduced, but slightly, urination decreases.

With uncompensated reversible shock, the skin and mucous membranes become cyanotic, the patient becomes lethargic, the pulse is small and frequent, there is a significant decrease in arterial and central venous pressure, oliguria develops, the Algover index is increased, the ECG shows a violation of myocardial oxygen supply. With an irreversible course of shock, consciousness is absent, blood pressure drops to critical numbers and may not be detected, the skin is marble-colored, anuria develops - cessation of urination. The Algover index is high.

To assess the severity of hemorrhagic shock, the determination of BCC, the volume of blood loss, is of great importance.

The shock severity analysis map and evaluation of the results obtained are shown in Table 4 and Table 5.

Table 4

Shock Severity Analysis Map

Table 5

Evaluation of results by total points

The shock index, or Algover index, is the ratio of heart rate to systolic pressure. In shock of the first degree, the Algover index does not exceed 1. In the second degree - no more than 2; with an index of more than 2, the condition is characterized as incompatible with life.

Types of shocks

Anaphylactic shock is a complex of various allergic reactions of an immediate type, reaching an extreme degree of severity.

There are the following forms of anaphylactic shock:

1) cardiovascular form, in which acute circulatory failure develops, manifested by tachycardia, often with heart rhythm disturbances, ventricular and atrial fibrillation, and a decrease in blood pressure;

2) respiratory form, accompanied by acute respiratory failure: shortness of breath, cyanosis, stridor, bubbling breathing, moist rales in the lungs. This is due to a violation of capillary circulation, swelling of the lung tissue, larynx, epiglottis;

3) cerebral form due to hypoxia, impaired microcirculation and cerebral edema.

According to the severity of the course, 4 degrees of anaphylactic shock are distinguished.

I degree (mild) is characterized by itching of the skin, the appearance of a rash, headache, dizziness, a feeling of flushing to the head.

II degree (moderate severity) - Quincke's edema, tachycardia, lowering of arterial pressure, increase of the Algover index join the previously indicated symptoms.

Grade III (severe) is manifested by loss of consciousness, acute respiratory and cardiovascular failure (shortness of breath, cyanosis, stridor breathing, small rapid pulse, a sharp decrease in blood pressure, high Algover index).

IV degree (extremely severe) is accompanied by loss of consciousness, severe cardiovascular insufficiency: the pulse is not determined, blood pressure is low.

Treatment. Treatment is carried out according to the general principles of shock treatment: restoration of hemodynamics, capillary blood flow, the use of vasoconstrictors, normalization of BCC and microcirculation.

Specific measures are aimed at inactivating the antigen in the human body (for example, penicillinase or b-lactamase in shock caused by antibiotics) or preventing the effect of the antigen on the body - antihistamines and membrane stabilizers.

1. Intravenous adrenaline infusion until hemodynamic stabilization. You can use dopmin 10-15 mcg / kg / min, and with symptoms of bronchospasm and b-adrenergic agonists: alupent, brikanil drip intravenously.

2. Infusion therapy in a volume of 2500-3000 ml with the inclusion of polyglucin and rheopolyglucin, unless the reaction is caused by these drugs. Sodium bicarbonate 4% 400 ml, glucose solutions to restore bcc and hemodynamics.

3. Membrane stabilizers intravenously: prednisolone up to 600 mg, ascorbic acid 500 mg, troxevasin 5 ml, sodium etamsylate 750 mg, cytochrome C 30 mg (daily doses are indicated).

4. Bronchodilators: eufillin 240-480 mg, noshpa 2 ml, alupent (brikanil) 0,5 mg drip.

5. Antihistamines: diphenhydramine 40 mg (suprastin 60 mg, tavegil 6 ml), cimetidine 200-400 mg intravenously (daily doses are indicated).

6. Protease inhibitors: trasylol 400 thousand U, contrical 100 thousand U.

Traumatic shock is a pathological and critical condition of the body that has arisen in response to an injury, in which the functions of vital systems and organs are impaired and inhibited. During trauma shock, torpid and erectile phases are distinguished.

By the time of occurrence, shock can be primary (1-2 hours) and secondary (more than 2 hours after injury).

Erectile stage or phase of occurrence. Consciousness remains, the patient is pale, restless, euphoric, inadequate, can scream, run somewhere, escape, etc. In this stage, adrenaline is released, due to which pressure and pulse can remain normal for some time. The duration of this phase is from several minutes and hours to several days. But in most cases it is short.

The torpid phase replaces the erectile one, when the patient becomes lethargic and adynamic, blood pressure decreases and tachycardia appears. Injury severity estimates are shown in Table 6.

Table 6

Assessment of the extent of injury severity

After calculating the points, the resulting number is multiplied by the coefficient.

Notes

1. In the presence of injuries that are not specified in the list of the volume and severity of the injury, the number of points is awarded according to the type of injury, according to the severity corresponding to one of the listed ones.

2. In the presence of somatic diseases that reduce the adaptive functions of the body, the found sum of points is multiplied by a coefficient from 1,2 to 2,0.

3. At the age of 50-60 years, the sum of points is multiplied by a factor of 1,2, older - by 1,5.

Treatment. The main directions in treatment.

1. Elimination of the action of the traumatic agent.

2. Elimination of hypovolemia.

3. Elimination of hypoxia.

Anesthesia is carried out by the introduction of analgesics and drugs, the implementation of blockades. Oxygen therapy, if necessary, tracheal intubation. Compensation for blood loss and BCC (plasma, blood, rheopolyglucin, polyglucin, erythromass). Normalization of metabolism, as metabolic acidosis develops, calcium chloride 10% - 10 ml, sodium chloride 10% - 20 ml, glucose 40% - 100 ml are introduced. Fight against vitamin deficiency (vitamins of group B, vitamin C).

Hormone therapy with glucocorticosteroids - prednisolone intravenously once 90 ml, and subsequently 60 ml every 10 hours.

Stimulation of vascular tone (mezaton, norepinephrine), but only with a replenished volume of circulating blood. Antihistamines (diphenhydramine, sibazon) are also involved in anti-shock therapy.

Hemorrhagic shock is a condition of acute cardiovascular insufficiency that develops after a significant amount of blood loss and leads to a decrease in perfusion of vital organs.

Etiology: injuries with damage to large vessels, acute gastric and duodenal ulcers, rupture of an aortic aneurysm, hemorrhagic pancreatitis, rupture of the spleen or liver, rupture of the tube or ectopic pregnancy, the presence of placental lobules in the uterus, etc.

According to clinical data and the magnitude of the deficiency of blood volume, the following degrees of severity are distinguished.

1. Not expressed - there are no clinical data, the level of blood pressure is normal. The volume of blood loss is up to 10% (500 ml).

2. Weak - minimal tachycardia, slight decrease in blood pressure, some signs of peripheral vasoconstriction (cold hands and feet). The volume of blood loss is from 15 to 25% (750-1200 ml).

3. Moderate - tachycardia up to 100-120 beats per minute, decrease in pulse pressure, systolic pressure 1-90 mm Hg. Art., anxiety, sweating, pallor, oliguria. The volume of blood loss is from 100 to 25% (35-1250 ml).

4. Severe - tachycardia more than 120 beats per minute, systolic pressure below 60 mm Hg. Art., often not determined by the tonometer, stupor, extreme pallor, cold extremities, anuria. The volume of blood loss is more than 35% (more than 1750 ml). Laboratory in the general analysis of blood, a decrease in the level of hemoglobin, erythrocytes and hematocrit. The ECG shows nonspecific changes in the ST segment and the T wave, which are due to insufficient coronary circulation.

Treatment of hemorrhagic shock includes stopping bleeding, the use of infusion therapy to restore BCC, the use of vasoconstrictors or vasodilators, depending on the situation. Infusion therapy involves intravenous administration of fluid and electrolytes in a volume of 4 liters (saline, glucose, albumin, polyglucin). In case of bleeding, transfusion of single-group blood and plasma is indicated in a total volume of at least 4 doses (1 dose is 250 ml). The introduction of hormonal drugs, such as membrane stabilizers (prednisolone 90-120 mg), is shown. Depending on the etiology, specific therapy is carried out.

Septic shock is the penetration of an infectious agent from its initial focus into the blood system and its spread throughout the body. The causative agents can be: staphylococcal, streptococcal, pneumococcal, meningococcal and enterococcal bacteria, as well as Escherichia, Salmonella and Pseudomonas aeruginosa, etc. Septic shock is accompanied by a dysfunction of the pulmonary, hepatic and renal systems, a violation of the blood coagulation system, which leads to thrombohemorrhagic syndrome ( Machabeli syndrome), which develops in all cases of sepsis. The course of sepsis is affected by the type of pathogen, this is especially important with modern methods of treatment. Laboratory progressing anemia is noted (due to hemolysis and oppression of hematopoiesis). Leukocytosis up to 12 109 / l, however, in severe cases, as a sharp depression of the hematopoietic organs is formed, leukopenia can also be observed.

Clinical symptoms of bacterial shock: chills, high fever, hypotension, dry warm skin - at first, and later - cold and wet, pallor, cyanosis, mental status disorder, vomiting, diarrhea, oliguria. Characterized by neutrophilia with a shift of the leukocyte formula to the left up to myelocytes; ESR increases to 30-60 mm/h or more. The level of blood bilirubin is increased (up to 35-85 µmol/l), which also applies to the content of residual nitrogen in the blood. Blood coagulation and prothrombin index are lowered (up to 50-70%), the content of calcium and chlorides is reduced. The total blood protein is reduced, which is due to albumin, and the level of globulins (alpha-globulins and b-globulins) increases. In the urine, protein, leukocytes, erythrocytes and cylinders. The level of chlorides in the urine is reduced, and urea and uric acid are elevated.

Treatment is primarily etiological in nature, therefore, before prescribing antibiotic therapy, it is necessary to determine the pathogen and its sensitivity to antibiotics. Antimicrobial agents should be used at maximum doses. For the treatment of septic shock, it is necessary to use antibiotics that cover the entire spectrum of gram-negative microorganisms. The most rational is the combination of ceftazidime and impinem, which have proven effective against Pseudomonas aeruginosa. Drugs such as clindamycin, metronidazole, ticarcillin, or imipinem are the drugs of choice when a resistant pathogen occurs. If staphylococci are sown from the blood, it is necessary to begin treatment with drugs of the penicillin group. Treatment of hypotension is at the first stage of treatment in the adequacy of the volume of intravascular fluid. Use crystalloid solutions (isotonic sodium chloride solution, Ringer's lactate) or colloids (albumin, dextran, polyvinylpyrrolidone). The advantage of colloids is that when they are introduced, the required filling pressures are reached most quickly and remain so for a long time. If there is no effect, then inotropic support and (or) vasoactive drugs are used. Dopamine is the drug of choice because it is a cardioselective β-agonist. Corticosteroids reduce the overall response to endotoxins, help to reduce fever and give a positive hemodynamic effect. Prednisolone at a dose of 60 to 90 mg per day.

Author: Kolesnikova M.A.

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