To begin with, I want to warn you about following all kinds of folk recipes from the Internet. If you are not sure of the reliability of the source and a person’s life depends on this information, then never trust the information received.

This kit is sold in pharmacies and travel stores, but in order to use it you need to know what you are doing and understand the responsibility that lies when using this kit. A specific set is used for traumatic painful shock; the injection is given intramuscularly.

• Dexamethasone prevents blood from leaving the vessels into the tissues
• Ketorolac tromethamine (ketanov) strong pain reliever
• Cordiamine stimulation of cardiac and respiratory activity

Mix the contents of three ampoules in a syringe and inject intramuscularly. The injection site must be chosen with unaffected vessels. Otherwise, the drug will act slowly.

And so as not to kill the victim, do not forget that the drugs should be stored in a dark, cool place, but not in a backpack under the scorching sun. If you take such a set with you, then follow temperature regime storage of drugs.

Antishock therapy is aimed at temporarily relieving pain, stimulating the heart and stopping bleeding. This injection is not the last step. After such an injection, it is necessary to organize the immediate evacuation of the victim and place him under professional medical supervision; first, the paramedics need to clarify that such support for the victim was provided.

It is also necessary to clearly determine the onset of shock. Signs of painful shock:

• Cold sweat
• pallor,
• rapid heartbeat,
• uneven shallow breathing.

Detailed signs of traumatic painful shock

Traumatic shock usually goes through two phases in its development, the so-called “erectile” phase of shock and the “torpid” phase. In patients with low compensatory capabilities of the body, the erectile phase of shock may be absent or very short (measured in minutes) and shock begins to develop immediately from the torpid phase, for example with very severe injury or injury (traumatic avulsions and crushing of limbs at the hip level, penetrating wounds of the abdominal and thoracic cavity with injury to internal organs, severe traumatic brain injury), accompanied by blood loss and crushing of soft tissues. Such injuries usually result in shock of extreme severity. In this case, the person immediately loses consciousness due to an excessively strong pain signal, which the brain is simply unable to cope with and, as it were, “turns off.”

What is important for the development of traumatic shock is not so much the absolute amount of blood loss, how much is the rate of blood loss. With rapid blood loss, the body has less time to adjust and adjust, and shock is more likely to develop. Therefore, shock is more likely when large arteries, such as the femoral artery, are injured.

Erectile shock phase: Victim on initial stage feels pain and signals it by means available to him: screaming, moaning, words, facial expressions, gestures. In the first, erectile, phase of shock, the patient is excited, scared, and anxious. Often aggressive. Resists examination and treatment attempts. He may thrash about, scream in pain, moan, cry, complain of pain, ask or demand analgesics, drugs. In this phase, the body’s compensatory capabilities have not yet been exhausted, and blood pressure often even higher than normal (as a reaction to pain and stress). At the same time, there is a spasm of skin blood vessels and pallor, which intensifies as bleeding continues and/or shock progresses. There is a rapid heartbeat (tachycardia), rapid breathing(tachypnea), fear of death, cold sticky sweat(such sweat is usually odorless), tremor (shaking) or small muscle twitching. The pupils are dilated (reaction to pain), the eyes are shiny. The look is restless, does not stop at anything. Body temperature may be slightly elevated (37-38 C) even in the absence of signs of wound infection, simply as a result of stress, the release of catecholamines and increased basal metabolism. The pulse remains satisfactory and rhythmic. There are no signs of development of disseminated intravascular coagulation syndrome, shock kidney syndrome, or shock lung syndrome. The skin is usually cold (vasospasm).

Torpid phase of shock: In this phase, the patient in most cases stops screaming, moaning, crying, thrashing about in pain, does not ask for anything, does not demand anything. He is lethargic, lethargic, apathetic, drowsy, depressed, and may lie in complete prostration or lose consciousness. Sometimes the victim may only make a faint moan. This behavior is caused by a state of shock. However, the pain does not decrease. Blood pressure decreases, sometimes to critically low numbers or is not determined at all when measured in peripheral vessels. Severe tachycardia. Pain sensitivity is absent or sharply reduced. He does not respond to any manipulation in the wound area. He either doesn’t answer questions or answers barely audibly. Convulsions may occur. Involuntary release of urine and feces often occurs.

The eyes of a patient with torpid shock dim, lose their shine, look sunken, and shadows appear under the eyes. The pupils are dilated. The gaze is motionless and directed into the distance. Body temperature can be normal, increased (wound infection) or slightly decreased to 35.0-36.0 degrees (“energy depletion” of tissues), chills even in the warm season. Noteworthy is the sharp pallor of the patients, the cyanosis (cyanotic) of the lips and other mucous membranes. Low levels of hemoglobin, hematocrit and red blood cells in the blood.

Intoxication phenomena are noted: the lips are dry, parched, the tongue is heavily coated, the patient suffers from constant extreme thirst, nausea. Vomiting may occur, which is a poor prognostic sign. The development of “shock kidney” syndrome is observed despite thirst and the medications given for it drinking plenty of fluids, the patient has little urine and it is highly concentrated and dark. In severe shock, the patient may not have any urine at all. “Shock lung” syndrome despite rapid breathing and intense work of the lungs, the supply of oxygen to tissues remains ineffective due to vasospasm and low levels of hemoglobin in the blood.

The skin of a patient with torpid shock is cold, dry (there is no longer cold sweat; there is nothing to sweat with due to the large loss of fluid during bleeding), tissue turgor (elasticity) is reduced. Sharpening facial features, smoothing nasolabial folds. Saphenous veins slept. Pulse is threadlike, more than 120 per minute. The faster and weaker the pulse, the more severe the shock.

Liver dysfunction is noted (since the liver also does not receive enough blood and experiences oxygen starvation). If a patient with traumatic shock survives, a (usually mild) icterus may appear within a few days. skin, as a result of an increase in the level of bilirubin in the blood and a violation of the bilirubin-binding function of the liver.

First aid for shock

The main first aid measure for traumatic shock is to stop bleeding. When the air temperature is low, it is also worth covering the victim to prevent hypothermia. It is necessary to ensure prompt assistance to the victim qualified medical care by calling an ambulance or taking the victim to medical institution. If the victim has no injuries or injuries, use an anti-shock position: the victim lies on his back, legs raised 15-30 centimeters.

Naturally, during a tourist trip it is impossible to deliver an ambulance to the victim. In this case, it is necessary to provide evacuation routes for victims in advance, before the trip. It is advisable to instruct the group on first aid to victims before the hike.

The main goal of shock therapy is to optimize oxygen transport. This direction of treatment is implemented with the help of hemodynamic and respiratory support . Treatment of shock should include a wide range of intensive therapeutic measures acceptance, aimed at correcting the pathophysiological disorders underlying the development of shock: absolute or relative hypovolemia, disorders of the pumping function of the heart, sympathoadrenergic reaction and tissue hypoxia. Measures to prevent hypothermia and its associated consequences should be implemented in all patients.

Therapeutic actions for shock should be aimed at:

• eliminating the cause of shock;
• restoration of effective central circulation;
• increasing myocardial contractility and regulation vascular tone;
• elimination of hypoxia of organs and tissues;
• correction of disrupted metabolic processes;
• prevention and treatment of various complications.

When treating shock, the first step is to perform basic techniques cardiopulmonary resuscitation: provide passability respiratory tract, adequate ventilation and blood circulation. An important role also belongs to eliminating the cause of shock - stopping bleeding, effective pain relief, draining a purulent focus, etc. It is ideal when eliminating the cause of shock occurs simultaneously with interventions aimed at optimizing the activity of the cardiovascular system.

The foundation of treatment of all types of shock is an increase in CO and timely restoration of tissue perfusion, especially in the coronary, cerebral, renal and mesenteric vascular bed. It is possible to quickly improve blood circulation in the brain and heart with a sharp decrease in blood pressure due to the redistribution of blood from lower limbs, the vessels of which contain 15-20% of the total blood volume into the central circulation. Therefore, raising the lower extremities by 30° should be the first and immediate action as soon as a decrease in systolic blood pressure below 80 mm Hg is detected. Art. This simple and useful technique allows you to quickly increase the venous return of blood to the heart. At the same time, the patient should not be placed in a Trendelenburg position, since this may cause regurgitation of gastric contents into the airways, disrupt gas exchange in the lungs, and impair the outflow of venous blood from the brain.

When treating shock, it is recommended to maintain systolic blood pressure at least 100 mmHg. Art. , CVP - 5 - 8 cm aq. Art. , APPA - 12-15 mm Hg. Art. , SI - above 3.5 l/min/m2, oxygen saturation of mixed venous blood - above 70%, hematocrit at the level of 0.30-0.35 l/l, hemoglobin - at the level of 80-100 g/l, diuresis - at the level of 40-50 ml/hour, PaO2 - above 60 mm Hg. Art. , blood saturation - above 90%, glucose level - 4-5 mmol/l, protein - above 50 g/l, colloid-osmotic pressure of blood plasma - in the range of 20-25 mm Hg. Art. , plasma osmolarity is at the level of 280-300 mOsm/l.

Infusion therapy

Infusion therapy occupies a central place in the treatment of shock. It influences the main links in the pathogenesis of shock and allows:

• maintain an optimal level of blood volume and stabilize hemodynamics;
• improve microcirculation, oxygen delivery to cells and reduce reperfusion damage;
• restore normal distribution of fluid between water sectors, improve metabolism in cells and prevent activation of cascade systems.

An increase in blood volume is an urgent, vital measure in all forms of shock, except cardiogenic. Only under this condition is optimal blood supply to the ventricles of the heart ensured, CO increases adequately, blood pressure rises, oxygen delivery to tissues improves, and impaired metabolic processes and the patient can be brought out of a critical condition.

Replenishment of blood volume should be carried out quickly through large-diameter catheters inserted into large peripheral or central veins. If there are no signs of congestive heart failure, the first 500 ml of solution is administered as a bolus. The infusion is then continued until adequate blood pressure, central venous pressure, ventricular filling pressure, heart rate, and urine output are achieved.

Infusion solutions

Most modern specialists use a combination of crystalloid and colloid solutions when treating shock. This allows you to quickly and effectively replenish the volume of blood volume, eliminate the deficiency of extravascular fluid and help maintain normal oncotic gradients between the intravascular and interstitial spaces. Choosing the ratio of crystalloid and colloid solutions when carrying out infusion therapy in a patient with shock depends on the specific clinical situation, assessment of the degree of impairment, a clear understanding of the mechanism of action of the drug and the purpose of treatment.

Crystalloid (saline) solutions (Ringer-Locke solutions, Ringer-lactate, lactasol, saline, etc.) replenish both the intravascular blood volume and the volume and composition of the interstitial and intracellular fluid. It should be remembered that three-quarters of the volume of crystalloid solutions quickly leaves the vascular bed and increases the volume of extracellular fluid. These are potentially harmful effects crystalloid solutions are not always compensated by an increase in lymph flow, and can lead to overflow of the intercellular space. Hemodynamic stability achieved with a large volume of infusion of crystalloid solutions will always be accompanied by an increase in fluid extravasation and the formation of tissue edema. This is especially pronounced under conditions of “capillary leakage”. Generalized tissue edema impairs oxygen transport to cells and increases organ dysfunction. In this case, the lungs, heart and intestines are most affected. This is why parallel infusion of colloidal agents is necessary.

It is possible to reduce the risk of developing tissue hyperhydration when using crystalloids and quickly increase blood pressure when using hypertonic saline solution. However, there is a risk of electrolyte imbalance, hypernatremia, hyperosmotic coma and deterioration of cellular metabolism.

The use of colloidal solutions is associated with a lower risk of extravasation and the development of tissue edema; they effectively maintain the colloid-osmotic pressure of plasma and stabilize hemodynamics faster compared to crystalloid solutions. Since colloids circulate in the vascular bed for a longer time, a smaller volume of injected fluid is required to stabilize hemodynamics compared to the volume of crystalloid solutions. This significantly reduces the risk of fluid overload.

However, colloidal solutions are more expensive, can bind and reduce the ionized fraction of plasma calcium, reduce the level of circulating immunoglobulins, reduce endogenous protein production and affect the hemostatic system. Infusion of colloidal solutions increases the oncotic pressure of plasma and can lead to the movement of interstitial fluid into the vascular bed. This poses a potential risk of increasing interstitial fluid volume deficit. To prevent such disorders and maintain a normal oncotic gradient between the intravascular and interstitial spaces, it is advisable to simultaneously administer colloidal and crystalloid solutions.

Not all colloidal solutions in equally meet modern requirements for the treatment of shock. Traditionally, fresh frozen plasma is still used as a source of colloids. But today, plasma transfusion poses quite a great danger to the recipient, since it can be contaminated with hepatitis and human immunodeficiency viruses. Allergic and anaphylactic reactions, possible acute lesions lungs and kidneys, immunodeficiency and other conditions complete the picture. Therefore, the use of plasma as a colloidal blood substitute is not currently recommended. Excessive use of albumin preparations in the treatment of shock should also be limited. Studies have shown that the use of albumin in critical conditions increases the mortality of patients. It has been established that the increase in plasma colloid osmotic pressure after the administration of albumin is short-term, and then it extravasates into the interstitial space. Therefore, the administration of albumin to correct hypoalbuminemia is called “a major metabolic misunderstanding.” A reasonable alternative to albumin preparations are solutions of hydroxyethyl starch and dextrans.

Solutions of hydroxyethyl starch reduce the permeability of the endothelial wall of capillary vessels, improve the rheological properties of blood, they are distinguished by a persistent volemic effect, rapid metabolism, and also have a significantly smaller effect on kidney function. Elimination of acute hypovolemia with solutions of hydroxyethyl starch leads to a rapid improvement in central hemodynamics, microcirculation and oxygen transport, which ultimately restores bioenergetic processes at the cellular level. Unlike other colloidal solutions, hydroxyethyl starch preparations do not block protein synthesis and do not have side effect on the functions of the immune and lymphoid systems. Starch particles help reduce endothelial cell activation and reduce capillary leakage.

Clinical results indicate that starch preparations for shock have significant advantages compared to albumin solutions:

• increase fluid content in the lungs to a lesser extent;
• disrupt gas exchange in the lungs to a lesser extent;
• can be used without particular risk in patients with respiratory
• distress syndrome;
• do not interfere with myocardial contractility;
• reduce swelling and damage to brain tissue.

An analysis of extensive long-term clinical experience revealed the features and advantages of colloidal solutions based on hydroxyethyl starch, especially their second generation. First of all, this concerns the safety of use and the exceptionally low incidence of adverse reactions compared to other colloidal infusion solutions. This is due to the structural similarity of hydroxyethyl starch to glycogen. The experience accumulated to date in the use of colloidal solutions allows us to recommend the use of second-generation hydroxyethylated starch solutions as first-choice drugs for BCC replacement in patients with shock.

Fighting hypoxia

The main thing in case of shock is to eliminate tissue hypoxia, since this is the central link in the pathogenesis of this pathological condition. Oxygen consumption depends on metabolic needs and is difficult to adjust. The body's need for oxygen can be reduced only by eliminating hyperthermia or eliminating the activity of the muscles involved in breathing and assigning their function to a mechanical ventilation device.

The delivery of oxygen to tissues is determined mainly by the value of CO and the oxygen capacity of the blood. Optimal level Blood oxygen saturation (above 90%) and tissue oxygenation can be maintained using various methods of oxygen therapy - oxygen inhalation through a face mask or nasal catheters. If respiratory failure persists during oxygen inhalation, mechanical ventilation should be performed, which can be done through a wide mask or endotracheal tube. Endotracheal intubation is preferable in cases of obstruction and damage to the airways, as well as when long-term mechanical ventilation is required. Indications for the use of mechanical ventilation: severe tachypnea (respiratory rate more than 35 per minute), cyanosis of the skin and mucous membranes, participation of auxiliary muscles in the act of breathing, changes mental status patient, a decrease in oxygen tension in arterial blood below 70 mm Hg. Art. and an increase in carbon dioxide tension above 50 mm Hg. Art. when breathing oxygen.

Increased myocardial contractility and regulation of vascular tone

The basis of the treatment strategy for all forms of shock is the regulation of the volume of blood volume, the level of general vascular resistance and myocardial contractility. Initially, the BCC value is usually corrected. If there is no positive effect of infusion therapy, immediate use of adrenergic drugs is necessary.

Adrenergic drugs

Drugs that affect vascular tone and myocardial contractility differ in varying degrees of impact on alpha- and beta-adrenergic and dopaminergic receptors, have different chronotropic effects and effects on myocardial oxygen consumption. These include dopamine, dobutamine, epinephrine, norepinephrine and other drugs. The first-line drug for shock is dopamine.

Dopamine- endogenous sympathetic amine, is a biosynthetic precursor of adrenaline and acts as a central and peripheral neurotransmitter. In low doses (1-3 mg/kg/min) it stimulates dopaminergic receptors and causes selective dilatation of renal and mesenteric arterioles. At the same time, renal blood flow, diuresis and sodium excretion increase, as well as intestinal perfusion improves, its ischemia is eliminated and the barrier function of the intestinal mucosa is restored. In moderate doses (5 mg/kg/min), stimulation of cardiac beta receptors occurs, which leads to increased myocardial contractility and increased CO. At the same time, heart rate and blood pressure change little. With increasing doses (from 5 to 10 mg/kg/min), beta-adrenergic effects still predominate, but further increases in CO are accompanied by increases in heart rate and blood pressure. With more high doses(over 10 mg/kg/min), preferential stimulation of alpha-adrenergic receptors occurs and pronounced peripheral vasoconstriction develops, which leads to a significant increase in vascular resistance and blood pressure.

Dobutamine is a synthetic catecholamine that is used primarily for beta-adrenergic effects. Compared to dopamine, it causes peripheral vasoconstriction and a weaker chronotropic response to a lesser extent. Therefore, dobutamine is preferable to use in situations where the goal of treatment is to increase CO without significantly increasing blood pressure.

Norepinephrine has a predominantly alpha-adrenergic effect, leading to constriction of peripheral vessels, and to a lesser extent - a positive chrono- and inotropic effect on the myocardium. Norepinephrine increases blood pressure and improves renal function without the use of low doses of dopamine and furosemide.

Epinephrine, an endogenous catecholamine released by the adrenal glands in response to stress, has a wide range of negative systemic effects, including vasoconstrictor effects on renal vessels, arrhythmogenic effects on the heart, and increased myocardial oxygen demand. Therefore, the use of epinephrine is limited to cases of complete refractoriness to other catecholamines and anaphylactic shock.

Use of adrenergic medicines in order to increase blood pressure, it is indicated for true cardiogenic and anaphylactic shock, as well as for shock that is refractory to intensive infusion therapy.

Vasodilators

Elimination of peripheral vascular spasm significantly reduces the load on the heart, increases CO and improves tissue perfusion. But vasodilators(sodium nitroprusside, nitroglycerin, etc.) can be administered only after correction of blood volume and treatment of cardiac depression, when systolic blood pressure exceeds 90 mm Hg. Art. The main indication is prolonged vasoconstriction with oliguria, high central venous pressure or pulmonary edema and pulmonary edema. It must be emphasized that vasodilators in shock can only be used according to strict indications and with full hemodynamic control, because sudden vasodilation in patients with hypovolemia or dehydration can be accompanied by a catastrophic drop in blood pressure. These drugs should be administered only in small doses intravenously or in infusions and only until urination is normalized, the extremities become warm and pink, and the veins are dilated and well filled.

Sodium nitroprusside- a balanced vasodilator that acts directly on the smooth muscles of the walls of arteries and veins. A decrease in resistance to blood expulsion leads to an increase in CO, and a decrease in venous return of blood to the heart reduces venous pressure in the pulmonary circulation and central venous pressure. Nitroprusside acts quickly, but short-term. The duration of its action is from 1 to 3 minutes, so a continuous dosed infusion of the drug is necessary. Since sodium nitroprusside contains cyanide, its continuous use for more than 72 hours at administration rates exceeding 3 mg/kg/min can lead to intoxication.

Nitroglycerine and bound organic nitrates, unlike sodium nitroprusside, act predominantly on the venous part of the bloodstream, reducing the return of blood to the heart, and thereby reducing the load on the myocardium in heart failure.

Correction of metabolic disorders

If necessary, carry out emergency correction electrolyte disturbances, especially potassium and calcium levels, as well as hyperglycemia. After initial stabilization of patients, glucose levels are maintained below 8.3 mmol/L. A continuous infusion of insulin and glucose is used. Until glucose levels stabilize, monitoring is required every 30-60 minutes; thereafter, monitoring should be performed every 4 hours.

Although metabolic acidosis reduces the effectiveness of vasopressor drugs, its correction with sodium bicarbonate solution should be carried out only when the blood pH is below 7.2. Unjustified administration of sodium bicarbonate leads to a decrease in the supply of oxygen to the tissues and increases acidosis in the central nervous system.

For almost all types of shock, small doses of glucocorticoids are used, and for signs of adrenal insufficiency and low cortisol levels, their use is mandatory. Broad-spectrum antibiotics for shock are prescribed empirically for open or potentially infected wounds, multiple organ injuries abdominal cavity and in cases where sepsis is suspected. To prevent deep vein thrombosis, low doses of unfractionated or low molecular weight heparins, elastic compression and intermittent pneumatic compression of the lower extremities.

With shock, there is often a need for treatment of other pathological syndromes. Most frequent consequences shock are acute cardiac, renal and liver failure, respiratory distress syndrome, disseminated intravascular coagulation syndrome and secondary gastrointestinal bleeding from acute erosions.

Organ dysfunctions during shock and principles of their treatment

The organs that suffer most from shock from impaired perfusion are usually called “shock organs,” or target organs. First of all, these are the lungs and kidneys, damage to which is the most characteristic feature of any shock. A weak link is also an organ that is damaged before the development of shock. Basic diagnostic criteria dysfunctions of organs and systems are given in table 15.3.

Kidneys

The kidneys are one of the first to suffer in shock. Vasoconstriction of the renal vessels develops in early stages this pathological condition, which leads to a sharp decrease in renal filtration and urination up to anuria. Prerenal acute renal failure develops. Autoregulatory mechanisms are able to maintain constant renal blood flow only when systemic blood pressure is above 80 mmHg. Art. A prolonged decrease in renal perfusion leads to damage to the tubular epithelium, death of some nephrons and impairment of the excretory function of the kidneys. With prolonged compression syndrome and blood transfusion shock, obstruction of the renal tubules by falling protein precipitates also occurs. The outcome is acute renal failure.

The possibility of reverse development of renal disorders when shock is eliminated remains only in the first hours. If the decrease in blood pressure is not a short-term episode, but continues for a long time long time, then even normalization of hemodynamics is not able to stop the chain of pathological changes and prevent necrosis of the tubular epithelium. Degenerative changes in the renal tubules most often result in the death of the patient.

Impaired renal function in shock manifests itself sharp decline the volume of urine excreted up to anuria, an increase in the concentration of creatinine, urea, potassium in the blood, metabolic acidosis. When treating shock, you should strive to ensure that hourly diuresis is at least 40 ml/hour. Against the background of ongoing infusion therapy and restored bcc, furosemide and small doses of dopamine can be used to stimulate diuresis, improving renal blood circulation and thereby reducing the risk of developing acute renal failure. If there is no effect from diuretics and dopamine, hemodialysis is used.

Lungs

The lungs are always damaged during shock. Respiratory system reacts as standard direct damage lungs (aspiration of gastric contents, lung contusion, pneumothorax, hydrothorax), and for shock and others pathological factors. Endotoxins and liposaccharides have a direct damaging effect on pulmonary endothelial cells, increasing their permeability. Other active mediators, such as platelet activating factor, tumor necrosis factor, leukotrienes, thromboxane A2, activated neutrophils, also have pathological effects on the lungs.

Aggressive metabolites, inflammatory mediators and blood cell aggregates formed during shock enter the systemic circulation, damage the alveolo-capillary membrane and lead to a pathological increase in the permeability of pulmonary capillaries. Moreover, even in the absence of increased capillary hydrostatic or decreased oncotic pressure, not only water, but also plasma protein intensively penetrates through the wall of the pulmonary capillaries. This leads to overflow of the interstitial space with fluid, sedimentation of protein in the epithelium of the alveoli and the endothelium of the pulmonary capillaries. Changes in the lungs progress especially quickly during inadequate infusion-transfusion therapy. These disorders lead to non-cardiogenic pulmonary edema, loss of surfactant and alveolar collapse, development of intrapulmonary shunting and perfusion of poorly ventilated and unventilated alveoli with subsequent hypoxia. The lungs become “hard” and poorly extensible. These pathological changes are not immediately and not always determined radiographically. Chest x-rays may initially be relatively normal, and x-ray findings often lag the actual changes in the lungs by 24 hours or more.

Such changes in the lungs were originally referred to as “shock lung” and are now referred to as “acute lung injury syndrome” (ALI) and “acute respiratory distress syndrome” (ARDS). These syndromes differ from each other only in the degree of severity of respiratory failure. In surgical practice, they most often develop in patients with septic, traumatic and pancreatogenic shock, as well as with fat embolism, severe pneumonia, after extensive surgical interventions and massive blood transfusions, with aspiration of gastric contents and the use of inhalations of concentrated oxygen. Acute respiratory distress syndrome is characterized by the following symptoms:

• severe respiratory failure with severe hypoxemia even with inhalation of a mixture with a high concentration of oxygen (paO2 below 50 mm Hg);
• diffuse or focal infiltrates without cardiomegaly and increased vascular pattern on chest x-ray;
• decreased lung compliance;
• extracardiac pulmonary edema.

For acute respiratory syndromes it is necessary to identify and treat the underlying disease and provide respiratory support aimed at effective oxygenation of the blood and provision of oxygen to tissues.

Diuretics and limiting the volume of fluid administered in patients with acute respiratory distress syndrome do not have any effect on the degree of pulmonary edema and do not provide a positive effect. In conditions of pathological permeability of pulmonary capillaries, the introduction of colloidal solutions such as albumin also does not effectively reduce extravascular water in the lungs. The incidence of acute lung injury did not change with the use of anti-inflammatory drugs (ibuprofen) and anti-cytokine therapy (IL-1 receptor antagonists and monoclonal antibodies to tumor necrosis factor).

Pathological changes in the lungs can be reduced if a minimum level of pulmonary capillary pressure is maintained, sufficient only to maintain adequate CO, and the BCC is replenished with starch preparations, which reduce “capillary leakage”. At the same time, the level of hemoglobin in the blood must remain at least 100 g/l to ensure the required delivery of oxygen to the tissues.

Artificial pulmonary ventilation (ALV) with moderate positive end-expiratory pressure allows maintaining the PaO 2 level above 65 mm Hg. Art. when the oxygen concentration in the inhaled mixture is below 50%. Inhalation through an endotracheal tube is more high concentrations oxygen can lead to the displacement of nitrogen from the alveoli and cause their collapse and atelectasis. It can cause oxygen toxicity to the lungs, impair oxygenation, and lead to the formation of diffuse pulmonary infiltrates. Positive expiratory pressure prevents the collapse of bronchioles and alveoli and increases alveolar ventilation.

Mortality in acute respiratory distress syndrome is extremely high and exceeds an average of 60%, and in septic shock - 90%. At favorable outcome perhaps as full recovery, and the formation of pulmonary fibrosis with the development of progressive chronic pulmonary insufficiency. If patients manage to survive acute period damage to the lungs, a secondary pulmonary infection becomes a serious threat for them. In patients with acute respiratory distress syndrome, it is difficult to diagnose associated pneumonia. Therefore, if clinical and radiological findings suggest pneumonia, active antimicrobial therapy is indicated.

Gastrointestinal tract

Redistribution of blood flow caused by shock leads to ischemia of the gastric mucosa and destruction of the protective barrier that protects it from the effects of hydrochloric acid. Reverse diffusion of hydrogen ions into the gastric mucosa leads to ulceration and is often accompanied by secondary gastric bleeding. To prevent bleeding, it is necessary to stop the destruction of the protective barrier of the mucous membrane by treating shock and improving the delivery of oxygen to the tissues. In addition, the pH of the stomach contents should be increased. A level of this indicator above 4 effectively prevents stomach bleeding, and at pH above 5 they almost never occur. For this purpose, histamine H2 receptor blockers and proton pump inhibitors are prescribed.

The integrity of the mucous membrane, without changing the acidity of the stomach contents, is maintained by cytoprotectors. A suspension of sucralfate (1 g of the drug is dissolved in 10-20 ml of sterile water) is administered into the stomach through a nasogastric tube every 6-8 hours. Sucralfate is comparable in effectiveness to H2-blockers and antacids; at the same time, the drug does not affect the bactericidal activity of gastric juice, which depends on the pH value. Tube enteral nutrition plays a major role in preventing the formation of stress ulcers in the stomach, especially when drugs are administered directly into the intestine.

Ischemia of the digestive tract leads to damage to enterocytes and functional intestinal failure. The consequence of suppressed motility is impaired evacuation and accumulation in the intestinal lumen. large quantities liquids and gases. The slowdown in the passage of chyme is accompanied by a sharp change in composition intestinal microflora and intensive formation of toxic products. Overstretching of the intestinal wall aggravates disorders caused by ischemia of enterocytes and is accompanied by increased intestinal permeability, translocation of bacteria and toxins through the glycocalyx membrane into the blood and lymph. In addition, the deposition of fluid in the intestinal lumen leads to a decrease in blood volume, exacerbating hemodynamic disturbances characteristic of shock. Thus, the intestine plays a particularly important role in the pathogenesis of the development of multiple organ dysfunction and failure in patients with shock.

The main function of the intestine - absorption of nutrients - is impaired in severe cases up to complete absence. Under these conditions, enteral nutrition not only does not lead to the entry of necessary substances into the blood, but aggravates overstretching of the intestinal wall and its hypoxia.

Basic principles of treatment of functional intestinal failure:

• normalization of water and electrolyte balance;
• drug stimulation intestinal motility;
• enterosorption;
• parenteral nutrition;
• if there is a threat of generalization of the intestinal flora - selective decontamination of the intestine.

Liver

Ischemic damage to hepatocytes during shock leads to cytolysis, a sign of which is an increase in the activity of indicator enzymes - lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase. Septic shock is also characterized by toxic damage to liver cells. Bilirubin metabolism is disrupted, detoxification function deteriorates, and the synthesis of albumin, ceruloplasmin, cholinesterase, and blood clotting factors decreases. This leads to jaundice, increased intoxication, hypoproteinemia and coagulopathy. As a result of the action of toxins that are not neutralized by the liver, encephalopathy develops up to coma. Acute liver failure during shock most often develops in the presence of previous liver diseases, against the background of which ischemia quickly leads to the death of hepatocytes and the formation of foci of necrosis in the liver parenchyma.

Basic principles of treatment of liver failure:

• prescription of hepatoprotectors and antioxidants;
• decreased absorption of toxic products from the intestine - eubiotics, lactulose, selective decontamination; in case of gastrointestinal bleeding, it is necessary to free the intestines from spilled blood using a cleansing enema;
• use of filtration methods of detoxification.

Blood

Blood as tissue is also damaged by shock. Its transport, buffer and immune functions are disrupted, and the coagulation and fibrinolysis systems are affected. In shock, hypercoagulation always develops and intensive formation of intravascular blood clots, formed predominantly in the microvasculature. In this case, a number of blood clotting factors are consumed (platelet, fibrinogen, factor V, factor VIII, prothrombin) and their content in the blood decreases, which leads to a significant slowdown in blood clotting. Simultaneously with this process, the enzymatic process of fibrinogen breakdown begins in already formed clots with the formation of fibrinogen degradation products (FDP), which have a powerful fibrinolytic effect. The blood completely stops clotting, which can cause significant bleeding from puncture sites, wound edges and the mucous membrane of the gastrointestinal tract.

An important role in hemocoagulation disorders is played by a decrease in the concentration of antithrombin III and protein C, so correction of their deficiency is advisable. Coagulopathy is corrected by administration of fresh frozen plasma or individual factors coagulation. Thrombocytopenia (less than 50 x 109/L) requires platelet transfusion.

A progressive decrease in the content of fibrinogen and platelets in combination with an increase in the level of fibrinogen degradation products and soluble fibrin monomers, as well as corresponding clinical symptoms, should be the basis for the diagnosis of disseminated intravascular coagulation syndrome (DIC) and the initiation of special therapy. DIC syndrome is very difficult to eliminate and more than 50% of patients die from ongoing bleeding. The high mortality rate from this phenomenon makes it necessary to carry out preventive anticoagulant therapy in patients with shock. The principles of treatment of DIC syndrome are outlined in a separate chapter.

Central nervous system.

In all patients with severe shock, damage to the functions of the central nervous system is noted - disturbances of consciousness varying degrees, damage to the center of thermoregulation, respiration, vasomotor and other autonomic centers. The main criterion for brain dysfunction is a level of consciousness on the Glasgow scale of less than 14 points. Treatment uses drugs that increase the resistance of brain cells to hypoxia.

Heart

In shock, the heart is one of the organs that increased load to compensate for developing violations. An increase in the intensity of cardiac activity requires an increase in coronary blood flow and oxygen delivery to the myocardium itself. Meanwhile, prolonged hypotension and severe tachycardia always lead to a deterioration in the perfusion of the coronary arteries; this, in combination with metabolic acidosis and the release of specific cardiac depressants, worsens myocardial contractility and causes a further decrease in the pumping function of the heart and the development of irreversible shock. This develops more quickly in patients with concomitant coronary heart disease. The development of heart failure requires the use of inotropic support.

Multiple organ failure syndrome

Most often, with shock, a serious dysfunction of not one “target organ” occurs, but several at once. The syndrome that develops when two or more vital organs are damaged is called multiple organ failure syndrome. This term refers to a dysfunction of vital organs, in which it is impossible to independently maintain homeostasis without medication correction. Its clinical and laboratory manifestations are represented by a combination of signs of damage to individual organs described above. However, multiple organ failure is not a simple sum of insufficiency various organs. Disturbances in the activity of individual organs and systems aggravate each other, forming new “vicious circles” and accelerating decompensation. Disturbances of homeostasis in multiple organ failure very quickly become irreversible, so the development of this syndrome is always a sign terminal stage any kind of shock.

The critical reserves of individual organs are different. The patient survives with 15% normal function liver, 25% kidney function, 35% red blood cell count and only 45% lung tissue. A person is very sensitive to the loss of plasma: a loss of more than 30% of its initial volume leads to death. Therefore, fluid infusion is especially important early in the treatment of shock.

Anaphylaxis is classified as a reaction immediate type, if avoided, incurable pathologies may arise or death. To alleviate the patient’s condition before the doctors arrive, drugs and devices from a specially designed anti-shock first aid kit are used. In our article we will consider in detail the composition of the anti-shock first aid kit, the placement of auxiliary equipment and the first actions when an acute condition appears.

Anaphylaxis is acute reaction the body, which occurs due to a single or repeated interaction with an allergen. The risk of developing anaphylaxis increases significantly if at least one family member has such a reaction. The extreme, that is, the worst manifestation of anaphylaxis is anaphylactic shock.

Pay attention! A severe reaction usually appears within 15-30 minutes after contact with the allergen or within a few seconds if the allergen was injected.

Causes and symptoms of pathology development

Signs of anaphylaxis include:

• itching sensations, burning of the skin;
• cough and runny nose;
• profuse lacrimation;
• rashes;
• difficulty breathing, suffocation;
• wheezing, feeling of heaviness in the chest;
• increase in the size of the tongue;
• acceleration or deceleration of heart rate;
• state of shock;
• dizziness and even fainting;
• redness of the skin due to a sudden rush of blood.

An anaphylactic reaction occurs due to human exposure to allergens such as: all kinds of food (milk, cheese, garlic, peanuts, shellfish), latex, medications, pollen. Also, a serious condition occurs after insect bites.

Important! Anaphylaxis occurs only if a person is initially diagnosed with an allergy to at least one of the above allergens.

Rules for the composition of an anti-shock first aid kit

For lately the number of cases of anaphylaxis has almost tripled. In this regard, the Ministry of Health of the Russian Federation has developed an order that describes an algorithm for providing urgent treatment and preventive care to victims, a clear sequence of treatment measures for secondary medical care, and also approved the composition of a universal anti-shock first aid kit.

The set consists of both medicines and special tools. In a dental, surgical office, as well as in medical posts that are located in small and large enterprises, there should be mandatory be an anti-shock first aid kit. This kit contains all the necessary medications that can quickly relieve the symptoms of anaphylaxis. You should regularly inspect your first aid kit, replacing medications that have expired.

Anti-shock installation: what is included, where and how to store the components?

According to the standards of the Ministry of Health of the Russian Federation, the anti-shock first aid kit is equipped with the following medications:

• Ethanol.
• Antihistamines (“Suprastin” and/or “Tavegil”).
• "Diphenhydramine."
• Glucose solution 5%.
• "Adrenalin".
• "Cordiamin" 25% in ampoules.
• "Strofanthin-K" in ampoules 0.05%.
• Atropine solution.
• "Prednisolone."
• Sodium chloride solution.
• "Eufilin."

In addition, the first aid kit should include the following items:

1. Tourniquet.
2. Scalpel.
3. Mouth retractor and tongue holder.
4. Sterile gauze, cotton wool and bandage.
5. Catheter (allows access to a vein for immediate administration of anti-shock solutions).
6. Adhesive plaster or medical plaster.
7. Oxygen cushion.
8. Syringes with a volume of 2 and 10 ml.

Additional first aid kit items

Depending on how the attack progresses, assistive tools may be useful. Of course, the emergency doctor has them, but it is also worth stocking up on them at home, because an attack of anaphylaxis most often overtakes the patient suddenly. The anti-shock kit may additionally include:

• Transfusion system for blood transfusion.
• Oxygen mask.
• Tweezers.
• Snorkel.
• Disposable gloves.

Packing such devices into an anti-shock set is important in cases where acute conditions have already recurred more than once.

Algorithm for providing first aid for anaphylaxis

Providing the first treatment measures should begin with calling medical service, whose doctors have everything with them necessary tools and drugs. In telephone mode, the condition of the “emergency” patient is described in as much detail as possible, a list of medications is given that were taken, and the cause of the occurrence is also indicated. anaphylactic shock, type of allergen.

Next you should provide emergency assistance to the patient. In this situation, there is no need to panic, as it is important to correctly identify the allergen and remove it from the victim. Before the ambulance arrives, it is important to carry out anti-shock therapy:

1. If possible, you should ask the patient about what could have caused the acute allergic reaction. If the reaction is caused by an insect bite, doctors advise lubricating the area with an antiseptic. You can also cool the bite site and apply a tourniquet over the wound.
2. It is worth immediately giving the patient antihistamines, which are available in the anti-shock medicine cabinet. You can also administer an intramuscular injection of Adrenaline.
3. The patient is placed in a horizontal position, on a flat, non-soft surface. The legs should be only slightly higher than the head, which is slightly tilted to the side.

In the process of providing anti-shock ambulance, it is recommended to measure the pulse and monitor breathing. It is also necessary to determine the exact time when the reaction began.

Who and where should have an anti-shock first aid kit?

An anti-shock kit should be available to people suffering from food allergies, asthma, and those who have previously experienced anaphylaxis. A serious condition occurs mainly when a person is at home and only in 25% of cases - in places general nutrition, in 15% of cases - in educational institutions or at work.

How to prevent anaphylaxis?

Of course, the most important rule is to identify and eliminate a trigger, such as food or medication. Since serious conditions appear unexpectedly, it is important that the patient’s family members are aware of how to properly and quickly provide first aid in emergency situations.

Patients who frequently experience symptoms of anaphylactic shock are advised to carry an epinephrine inhaler or an epinephrine dose syringe with them at all times. This can be explained by the fact that the substance itself, when it enters the body, acts as an antihistamine, due to which the victim’s condition can quickly return to normal.

Should there be an anti-shock kit in the treatment room and why?

An anti-shock first aid kit should be fully stocked in those medical, cosmetology and treatment rooms where procedures are performed on a regular basis, during which the integrity of the skin is compromised. For example, in a cosmetology office, where the procedure for applying tattoos, tattoos and microblading is carried out, where the procedure for mesotherapy and biorevitalization is performed.

/. Elimination of violations of the central nervous system(neuroleptanalgesia (NLA), central analgesics, diazepines, etc.

2. Oxygen therapy.

3. Artificial ventilation, indirect massage hearts.

4. Elimination tissue hypoxia: (hyperbaric oxygenation (HBO) according to
possibilities), anabolic hormones, aspartic acid, glutamic
acid, etc.

5. Plasma substitutes (according to indications).

6. Administration of erythromass (indications).

7. Magnification contractile function myocardium (cardiac glycosides, nitrates,
kortiko steroid s).

8. Improving the rheological properties of blood (anticoagulants, antiplatelet agents,
rheopolyglucins, etc.).

9. Elimination of acidosis and normalization of water and electrolyte balance (soda
solutions, solutions of potassium, calcium, glucose-insulin, hemodialysis, etc.).

10. Detoxification measures (forced diuresis, hemosorption,
peritoneal dialysis).

11. Treatment of hepatic and renal failure.

12. Hourly diuresis.

Test questions for the lecture.

1. What is included in the concept of “shock”?

2. List the main reasons leading to shock states.

3. Describe the clinical signs of anaphylactic shock, variants of its course.

4. What is the sequence of therapeutic measures for this shock?

5. Give clinical picture traumatic shock.

6. What should be the scope of assistance for severe mechanical damage with
the purpose of preventing the development of a state of shock?

7. What position should be given to the patient in an unconscious state during
transportation?

8. Yours therapeutic tactics at cardiogenic shock?

9. Depending on the trigger mechanism, what types of shock conditions do you experience?

Homework.

1.V. A. Mikhelson pp. 139-149. + reference book.

2.Reference book emergency care, sections: cardiogenic, anaphylactic,

burn and traumatic shocks.

3. “Patient care”, techniques for carrying out the following activities:

technique of noniroleptanalgesia, technique of applying arterial and

venous tourniquets, catheterization.

Self-control tasks:

1. The erectile phase of traumatic shock is characterized by:
A). A sharp drop in blood pressure.

b). Motor excitement. V). Lethargy. G). Speech excitement.

2. Torpid phase:

A). Sharp pallor of the skin. b). Sudden loss of consciousness, c). Progressive drop in blood pressure. G). Lethargy.

d). Progressive increase in heart rate, thread-like pulse. 2. Sequence of first aid for traumatic shock: a). Place the patient to bed, b). Anesthesia, c). Stop bleeding. G). Improve oxygen access. d). Cardiac glycosides.

e). Replenishment of circulating blood volume (CBV). and). Transport immobilization. h). Vasoconstrictor and vascular drugs. And). Give ammonia.

Task No. 1.

A 30-year-old man was injured in a car accident. There is no consciousness. Pulse on carotid arteries not palpable. There is no breathing. The victim has a wide leather belt at waist level. What actions need to be taken?

1. Immediately begin artificial ventilation of the lungs, indirect
heart massage without wasting time removing the belt.

2. Carry out artificial ventilation and chest compressions after
release from the belt to avoid rupture of the liver and spleen.

3. Turn the victim onto his right side.

4, Do not touch the victim until the traffic police arrive.

Task No. 2.

You work at a medical center. A 38-year-old woman, K., contacted you; her surgeon recommended a course of penicillin intramuscularly for a boil on the left shoulder. After the injection of penicillin, the patient felt a sharp general weakness, itching, a feeling of heat throughout the body, chills, anxiety, agitation, headache, difficulty breathing, then loss of consciousness, and convulsions appeared.

1. What happened to the patient?

2. What is the emergency care of a paramedic?

3. What do you think was the paramedic’s mistake in this situation?

4. Further tactics for the paramedic? Forecast?

Topic 8; Intensive therapy for acute poisoning.

Purpose of studying the topic:

Know the clinical manifestations of acute poisoning and the principles of treatment
emergency care, taking into account the table of poisons and antidotes;

Be able to provide first aid in case of acute poisoning.

Plan.

1. Basics of toxicology: definition of this branch of medicine, types of poisoning, nature of the action of poisons, ways of penetration of poisons into the body, diagnosis of acute poisoning. The main clinical symptoms observed in acute poisoning. Table of poisons and antidotes.

Shock- hypocirculation syndrome with impaired tissue perfusion that occurs in response to mechanical damage and other pathological influences, as well as their immediate complications, leading to decompensation of vital functions.

The volume and nature of anti-shock measures when providing various types of medical care.

In case of shockogenic trauma, active antishock therapy should be started even in the absence of pronounced clinical manifestations of shock in the first hours.

In some cases, pathogenetic and symptomatic therapy is combined (for example, intravenous infusions for correction of blood volume and administration of vasopressors when blood pressure drops below a critical level).

Stop bleeding.

Continued bleeding leads to an alarming increase in the deficit of blood volume, which cannot be replenished without complete hemostasis. When providing each type of medical care, within the available capabilities, hemostatic measures must be performed as quickly and fully as possible, without which all anti-shock therapy cannot be effective.

Anesthesia.

Afferent pain impulses are one of the most important links in the pathogenesis of shock development. Adequate pain relief, eliminating one of the main causes of shock, creates the prerequisites for successful correction of homeostasis in case of developed shock, and performed in early dates after damage - for its prevention.

Immobilization of injuries.

Maintaining mobility in the area of ​​damage leads to an increase in both pain syndrome, and bleeding from damaged tissues, which, of course, can cause shock or aggravate its course. In addition to direct fixation of the damaged area, the purpose of immobilization is also careful transportation during the evacuation of victims.

Maintaining respiratory and cardiac function.

Correction of disturbed homeostasis during shock requires some time, but a critical drop in blood pressure and depression of respiratory function, characteristic of decompensated shock, can quickly lead to death. And therapy directly aimed at maintaining breathing and cardiac activity, being essentially symptomatic, allows you to gain time for pathogenetic treatment.

Elimination of the direct impact of the shockogenic factor.

This group of measures includes the release of victims from the rubble, extinguishing the flames, stopping the impact electric current and other similar actions that do not require separate decoding and justification of their necessity.

However, with massive injuries and destruction of the limbs, blood circulation often cannot be normalized until the crushed segment is amputated, the wound is treated, the bleeding is stopped, and a protective aseptic bandage and immobilizing splint are applied to the treated wound.

Toxic amines (histamine, serotonin), polypeptides (bradykinin, kallidin), prostaglandins, lysosomal enzymes, tissue metabolites (lactic acid, electrolytes, adenyl compounds, ferritin) were found in substances circulating in the blood that have intoxicating properties. All of these substances have a direct inhibitory effect on hemodynamics and gas exchange and thereby aggravate the clinical manifestations of shock.

They violate antimicrobial barriers and contribute to the formation of irreversible consequences of shock. Considering this circumstance, indications for amputation of a limb in some cases are set, despite the presence of shock, and are considered as an element of anti-shock measures.

Therapy aimed at normalizing blood volume and correcting metabolic disorders:

Infusion-transfusion therapy.

Modern transfusiology is characterized by scientifically based restriction of blood transfusion. In order to correct BCC, crystalloid and colloid solutions, as well as blood components, are widely used, in large quantities available in the arsenal modern medicine. In this case, the goal is not only to compensate for the volume of blood volume, but also to combat generalized tissue dehydration and correct disturbed water and electrolyte balances.

In conditions of decompensation, it is usually necessary to control the acid-base state of the blood (pH and alkaline reserve), since instead of the expected metabolic acidosis Metabolic symptoms are common in shock alkalosis, especially 6-8 hours after injury. In this case, alkalosis occurs more often, the later the BCC deficiency is replenished.

Correction of vascular tone.

The need to correct vascular tone is due to the fact that its value largely determines not only the parameters of the systemic circulation (for example, cardiac output and blood pressure), but also the distribution of blood flows along the nutritional and shunt pathways, which significantly changes the degree of tissue oxygenation.

With prolonged spasm of peripheral vessels and the introduction of significant volumes of fluid, the use of drugs that actively reduce total peripheral resistance, reduce the return of venous blood to the heart and thereby facilitate its work is indicated.

Hormone therapy.

The administration of large doses (hydrocortisone - 500-1000 mg) of glucocorticoids, especially in the first minutes of treatment, has a positive inotropic effect on the heart, reduces renal vascular spasm and capillary permeability; eliminates adhesive properties shaped elements blood; restores reduced osmolarity of intra- and extracellular fluid spaces.