Pathogenesis of acute blood loss. The blood loss is acute. Etiological factors of blood loss

Internal.

Bleeding occurs into internal cavities or tissues.

Hidden.

They have no characteristic manifestations. Usually occur in the abdominal organs (eg, gastrointestinal).

By volume

• Small (0.5 - 10% bcc, average - 0.5 l);
• Medium (11 – 20% of bcc, average 0.5 – 1 l);
• Large (21 – 40% of bcc, average 1–2 l);
• Massive (41 – 70% bcc, about 2–3.5 l);
• Lethal (more than 70% of the bcc, usually over 3.5 l).

According to the speed of development

• Acute (more than 7% of bcc within an hour);
• Subacute (5–7% of blood volume within an hour);
• Chronic (less than 5% of blood volume within an hour).

Causes

1. Injuries, wounds, fractures;
2. Operations;
3. Pathological changes in blood vessels (rupture of an aneurysm);
4. Menstrual irregularities, uterine bleeding, ectopic pregnancy;
5. Childbirth;
6. Gastrointestinal bleeding due to ulcerative processes;
7. Violation of the permeability of the vascular wall in the microvasculature during radiation injuries, oncological processes, and some infections;
8. Reduced blood clotting ability, which even with minor injuries can lead to heavy blood loss.

Symptoms

1. Paleness of the skin;
2. Sweating;
3. Reduced blood pressure;
4. Tachycardia (increased heart rate, the pulse is weak, difficult to palpate, low filling);
5. Decreased diuresis (urine output), oliguria and anuria;
6. Weakness, lethargy, darkening of the eyes, tinnitus, depression of consciousness up to its loss.

Diagnosis of the degree

• In case of external or surgical bleeding, the volume of blood loss can be assessed visually.
• There are also average values ​​of blood loss during various injuries or surgical procedures (example: pelvic fracture - 2-4 l, caesarean section - 0.5-0.6 l).
• In cases where the above methods are not applicable, it is very convenient to determine the severity of the condition using the Algover index, which is calculated as the ratio of the pulse rate to the systolic (upper indicator) blood pressure. Thus, the higher the pulse and lower the pressure, the more pronounced the deficit of bcc.

7753 0

Noteworthy is the recently put forward low volume hypertonic infusion concept , intended for the initial stage of ITT. We are talking about the pronounced effect of a 7.2-7.5% sodium chloride solution, injected into a vein at a rate of 4 ml/kg of body weight of the wounded (on average 300-400 ml of solution). The hemodynamic-stabilizing effect of subsequent administration of polyglucin increases markedly, which is explained by an increase in the osmotic gradient between the blood and the intercellular space. The infusion of hypertonic saline solution preceding the introduction of colloidal solutions is of great interest in the future for use during the stages of medical evacuation.

In table 1 are given approximate volumes of infusion-transfusion agents used to compensate for acute blood loss in war. Blood transfusion is required only when blood loss reaches 1.5 liters (30% of blood volume). For blood loss of up to 1.0 liters, infusion of plasma substitutes with a total volume of 2.0–2.5 liters per day is indicated. For blood loss of up to 2.0 liters, compensation for the BCC deficit is carried out using blood and plasma substitutes in a 1:2 ratio with a total volume of up to 3.5–4.0 liters per day. When blood loss exceeds 2.0 liters, the total volume of administered blood and plasma substitutes exceeds 4.0 liters.

For head injuries, the volume of saline solutions is reduced by 2 times; in case of damage to the abdominal organs, the number of blood substitutes is increased by 30–40%; in case of severe pelvic fractures, the volume of blood transfusion is increased by 20–30%,

Table 1.

If blood transfusion is not possible, the volume of administration of plasma substitutes is increased by 2 times.

In the first 6 hours, 60–70% of the daily dose of these drugs is administered.

The greater the amount of blood loss, the greater the volume of blood and red blood cell preparations that should be transfused. At the same time, from a physiological point of view, it is preferable to use fresh blood (up to 48 hours of storage), since its red blood cells immediately after transfusion begin to perform their main function - transporting gases. With long periods of storage, canned blood progressively loses its gas transport function and turns into a drug that has a mainly volemic effect. An obstacle to the widespread use of fresh blood transfusion is the possibility of transmitting dangerous infections (HIV, viral hepatitis, malaria, syphilis, etc.) and other complications, which necessitate the maximum possible limitation of the use of donor blood transfusions (freshly collected, canned). That's why Transfusion of donor blood can only be carried out for health reasons if blood components are not available in the medical institution.

Transfusion of red blood components - erythrocyte mass, erythrocyte suspension, erythrocyte concentrate(the name of the drug depends on the manufacturing method) is safer, although less effective in eliminating the consequences of acute blood loss.

Indications for transfusion of certain blood components are determined by the presence of a deficiency of the corresponding blood function in the wounded person, which is not eliminated by the body's reserve capabilities and creates a threat of death.

To carry out ITT, accepted for supply (service cards) are used blood substitutes and blood transfusion agents (Table 2).

Work on the development of “artificial blood” preparations, that is, true blood substitutes capable of carrying oxygen (a solution of polymerized hemoglobin Gelenpol, a blood substitute based on perfluorocarbon compounds Nerftoran), has not yet gone beyond the scope of clinical trials. Their use is limited by the high cost of manufacturing and the difficulty of using them in field conditions.

Table 2.

General characteristics of standard blood transfusion agents and plasma substitutes

During operations for wounds of group organs and the abdomen, surgeons often become available to large volumes of the wounded person’s own blood, which flows into large anatomical cavities of the body. Such blood must be quickly aspirated through sterile systems, heparin added, filtered through eight layers of gauze (or special filters) and returned to the wounded person into the circulation ( blood reinfusion). If there is a potential risk of bacterial contamination, a broad-spectrum antibiotic is added to the reinfused autologous blood. Hemolyzed blood and blood contaminated with intestinal contents and urine should not be reinfused.

It should be emphasized that the main criterion for the adequacy of the ITT should be considered not the fact of infusion of the exact volume of certain media, but, first of all, the body’s response to the therapy. Favorable signs in the dynamics of treatment include restoration of consciousness, warming and pink coloration of the integument, disappearance of cyanosis and sticky sweat, decrease in pulse rate to less than 100 beats/min, normalization of blood pressure. This clinical picture should correspond to an increase in hematocrit to a level of at least 0.28–0.30 l/l.

Gumanenko E.K.

Military field surgery

Blood loss is a common and evolutionarily oldest damage to the human body, occurring in response to blood loss from blood vessels and characterized by the development of a number of compensatory and pathological reactions.

Classification of blood loss

The state of the body that occurs after bleeding depends on the development of these adaptive and pathological reactions, the ratio of which is determined by the volume of lost blood. The increased interest in the problem of blood loss is due to the fact that almost all surgical specialists encounter it quite often. In addition, mortality rates due to blood loss remain high to this day. Blood loss of more than 30% of the circulating blood volume (CBV) in less than 2 hours is considered massive and life-threatening. The severity of blood loss is determined by its type, speed of development, volume of blood lost, degree of hypovolemia and the possible development of shock, which is most convincingly presented in the classification of P. G. Bryusov (1998), (Table 1).

Classification of blood loss

1. Traumatic, wound, operating room)

2. pathological (diseases, pathological processes)

3. artificial (exfusion, therapeutic bloodletting)

According to the speed of development

1. acute (› 7% bcc per hour)

2. subacute (5–7% of blood volume per hour)

3. chronic (‹ 5% bcc per hour)

By volume

1. Small (0.5 – 10% bcc or 0.5 l)

2. Medium (11 – 20% bcc or 0.5 – 1 l)

3. Large (21 – 40% bcc or 1–2 l)

4. Massive (41 – 70% bcc or 2–3.5 l)

5. Fatal (› 70% of blood volume or more than 3.5 l)

According to the degree of hypovolemia and the possibility of developing shock:

1. Mild (BCC deficiency 10–20%, HO deficiency less than 30%, no shock)

2. Moderate (BCC deficiency 21–30%, HO deficiency 30–45%, shock develops with prolonged hypovolemia)

3. Severe (BCC deficiency 31–40%, HO deficiency 46–60%, shock is inevitable)

4. Extremely severe (BCC deficiency over 40%, HO deficiency over 60%, shock, terminal condition).

Abroad, the most widely used classification of blood loss was proposed by the American College of Surgeons in 1982, according to which there are 4 classes of bleeding (Table 2).

Table 2.

Acute blood loss leads to the release of catecholamines by the adrenal glands, causing spasm of peripheral vessels and, accordingly, a decrease in the volume of the vascular bed, which partially compensates for the resulting deficit of bcc. Redistribution of organ blood flow (centralization of blood circulation) makes it possible to temporarily preserve blood flow in vital organs and ensure the maintenance of life in critical conditions. However, subsequently this compensatory mechanism can cause the development of severe complications of acute blood loss. A critical condition, called shock, inevitably develops with a loss of 30% of the blood volume, and the so-called “threshold of death” is determined not by the volume of bleeding, but by the number of red blood cells remaining in the circulation. For erythrocytes this reserve is 30% of the globular volume (GO), for plasma only 70%.

In other words, the body can survive the loss of 2/3 of circulating red blood cells, but will not survive the loss of 1/3 of the plasma volume. This is due to the peculiarities of compensatory mechanisms that develop in response to blood loss and are clinically manifested by hypovolemic shock. Shock is understood as a syndrome based on inadequate capillary perfusion with reduced oxygenation and impaired oxygen consumption by organs and tissues. It (shock) is based on peripheral circulatory-metabolic syndrome.

Shock is a consequence of a significant decrease in BCC (i.e., the ratio of BCC to the capacity of the vascular bed) and a deterioration in the pumping function of the heart, which can manifest with hypovolemia of any origin (sepsis, trauma, burns, etc.).

Specific causes of hypovolemic shock due to loss of whole blood may include:

1. gastrointestinal bleeding;

2. intrathoracic bleeding;

3. intra-abdominal bleeding;

4. uterine bleeding;

5. bleeding into the retroperitoneal space;

6. ruptures of aortic aneurysms;

7. injuries, etc.

Pathogenesis

Loss of blood volume impairs the performance of the heart muscle, which is determined by:

1. cardiac minute volume (MCV): MCV = CV x HR, (CV – stroke volume of the heart, HR – heart rate);

2. filling pressure of the heart cavities (preload);

3. function of heart valves;

4. total peripheral vascular resistance (TPVR) – afterload.

If the contractility of the heart muscle is insufficient, some blood remains in the cavities of the heart after each contraction, and this leads to an increase in preload. Some of the blood stagnates in the heart, which is called heart failure. In case of acute blood loss, leading to the development of BCC deficiency, the filling pressure in the cavities of the heart initially decreases, as a result of which SVR, MVR and blood pressure decrease. Since the level of blood pressure is largely determined by cardiac output (MVR) and total peripheral vascular resistance (TPVR), to maintain it at the proper level when BCC decreases, compensatory mechanisms are activated aimed at increasing heart rate and TPR. Compensatory changes that occur in response to acute blood loss include neuroendocrine changes, metabolic disorders, and changes in the cardiovascular and respiratory systems. Activation of all coagulation links makes it possible to develop disseminated intravascular coagulation (DIC syndrome). As a physiological defense, the body responds to its most frequent damage with hemodilution, which improves blood fluidity and reduces its viscosity, mobilization from the red blood cell depot, a sharp decrease in the need for both blood volume and oxygen delivery, an increase in respiratory rate, cardiac output, oxygen return and utilization in tissues.

Neuroendocrine changes are realized by activation of the sympathoadrenal system in the form of increased release of catecholamines (adrenaline, norepinephrine) by the adrenal medulla. Catecholamines interact with a- and b-adrenergic receptors. Stimulation of adrenergic receptors in peripheral vessels causes vasoconstriction. Stimulation of p1-adrenergic receptors located in the myocardium has positive ionotropic and chronotropic effects, stimulation of β2-adrenergic receptors located in blood vessels causes mild dilatation of arterioles and constriction of veins. The release of catecholamines during shock leads not only to a decrease in the capacity of the vascular bed, but also to the redistribution of intravascular fluid from peripheral to central vessels, which helps maintain blood pressure. The hypothalamus-pituitary-adrenal system is activated, adrenocorticotopic and antidiuretic hormones, cortisol, aldosterone are released into the blood, resulting in an increase in the osmotic pressure of the blood plasma, leading to increased reabsorption of sodium and water, a decrease in diuresis and an increase in the volume of intravascular fluid. Metabolic disorders are observed. Developed blood flow disorders and hypoxemia lead to the accumulation of lactic and pyruvic acids. With a lack or absence of oxygen, pyruvic acid is reduced to lactic acid (anaerobic glycolysis), the accumulation of which leads to metabolic acidosis. Amino acids and free fatty acids also accumulate in tissues and aggravate acidosis. Lack of oxygen and acidosis disrupt the permeability of cell membranes, as a result of which potassium leaves the cell, and sodium and water enter the cells, causing them to swell.

Changes in the cardiovascular and respiratory systems during shock are very significant. The release of catecholamines in the early stages of shock increases peripheral vascular resistance, myocardial contractility and heart rate - the goal is centralization of blood circulation. However, the resulting tachycardia very quickly reduces the diastolic filling time of the ventricles and, consequently, coronary blood flow. Myocardial cells begin to suffer from acidosis. In cases of prolonged shock, respiratory compensation mechanisms fail. Hypoxia and acidosis lead to increased excitability of cardiomyocytes and arrhythmias. Humoral changes are manifested by the release of mediators other than catecholamines (histamine, serotonin, prostaglandins, nitric oxide, tumor necrotizing factor, interleukins, leukotrienes), which cause vasodilation and an increase in the permeability of the vascular wall with the subsequent release of the liquid part of the blood into the interstitial space and a decrease in perfusion pressure . This aggravates the lack of O2 in body tissues, caused by a decrease in its delivery due to microthrombosis and acute loss of O2 carriers - erythrocytes.

Changes that are of a phase nature develop in the microvasculature:

1. Phase 1 – ischemic anoxia or contraction of pre- and postcapillary sphincters;

2. Phase 2 – capillary stasis or expansion of precapillary venules;

3. Phase 3 – paralysis of peripheral vessels or expansion of pre- and post-capillary sphincters...

Crisis processes in the capillarone reduce the delivery of oxygen to tissues. The balance between oxygen delivery and oxygen demand is maintained as long as the necessary tissue extraction of oxygen is ensured. If there is a delay in starting intensive therapy, oxygen delivery to cardiomyocytes is disrupted, myocardial acidosis increases, which is clinically manifested by hypotension, tachycardia, and shortness of breath. A decrease in tissue perfusion develops into global ischemia with subsequent reperfusion tissue damage due to increased production of cytokines by macrophages, activation of lipid peroxidation, release of oxides by neutrophils and further microcirculation disorders. Subsequent microthrombosis leads to disruption of specific organ functions and there is a risk of developing multiple organ failure. Ischemia changes the permeability of the intestinal mucosa, which is especially sensitive to ischemia-reperfusion mediator effects, which causes the dislocation of bacteria and cytokines into the circulation system and the occurrence of such systemic processes as sepsis, respiratory distress syndrome, and multiple organ failure. Their appearance corresponds to a certain time interval or stage of shock, which can be initial, reversible (stage of reversible shock) and irreversible. To a large extent, the irreversibility of shock is determined by the number of microthrombi formed in the capillarone and the temporary factor of the microcirculation crisis. As for the dislocation of bacteria and toxins due to intestinal ischemia and impaired permeability of its wall, this situation is not so clear today and requires additional research. Yet shock can be defined as a condition in which the oxygen consumption of tissues is inadequate to their needs for the functioning of aerobic metabolism.

Clinical picture.

When hemorrhagic shock develops, there are 3 stages.

1. Compensated reversible shock. The volume of blood loss does not exceed 25% (700–1300 ml). Tachycardia is moderate, blood pressure is either unchanged or slightly reduced. The saphenous veins become empty and the central venous pressure decreases. Signs of peripheral vasoconstriction occur: coldness of the extremities. The amount of urine excreted is reduced by half (at a normal rate of 1–1.2 ml/min). Decompensated reversible shock. The volume of blood loss is 25–45% (1300–1800 ml). The pulse rate reaches 120–140 per minute. Systolic blood pressure drops below 100 mm Hg, and pulse pressure decreases. Severe shortness of breath occurs, partly compensating for metabolic acidosis through respiratory alkalosis, but can also be a sign of shock lung. Increased coldness of the extremities and acrocyanosis. Cold sweat appears. The rate of urine output is below 20 ml/h.

2. Irreversible hemorrhagic shock. Its occurrence depends on the duration of circulatory decompensation (usually with arterial hypotension over 12 hours). The volume of blood loss exceeds 50% (2000–2500 ml). The pulse exceeds 140 per minute, systolic blood pressure drops below 60 mmHg. or not determined. There is no consciousness. Oligoanuria develops.

Diagnostics

Diagnosis is based on assessment of clinical and laboratory signs. In conditions of acute blood loss, it is extremely important to determine its volume, for which it is necessary to use one of the existing methods, which are divided into three groups: clinical, empirical and laboratory. Clinical methods allow the amount of blood loss to be estimated based on clinical symptoms and hemodynamic parameters. The blood pressure level and pulse rate before the start of replacement therapy largely reflect the magnitude of the BCC deficit. The ratio of pulse rate to systolic blood pressure allows you to calculate the Algover shock index. Its value depending on the BCC deficit is presented in Table 3.

Table 3. Assessment based on the Algover shock index

The capillary refill test, or “white spot” sign, assesses capillary perfusion. It is performed by pressing on a fingernail, forehead skin or earlobe. Normally, the color is restored after 2 seconds, with a positive test - after 3 or more seconds. Central venous pressure (CVP) is an indicator of the filling pressure of the right ventricle and reflects its pumping function. Normally, the central venous pressure ranges from 6 to 12 cm of water column. A decrease in central venous pressure indicates hypovolemia. With a deficit of BCC of 1 liter, the central venous pressure decreases by 7 cm of water. Art. The dependence of the CVP value on the BCC deficit is presented in Table 4.

Table 4. Assessment of circulating blood volume deficit based on the value of central venous pressure

Hourly diuresis reflects the level of tissue perfusion or the degree of filling of the vascular bed. Normally, 0.5–1 ml/kg of urine is excreted per hour. A decrease in diuresis of less than 0.5 ml/kg/h indicates insufficient blood supply to the kidneys due to a deficiency of blood volume.

Empirical methods for assessing the volume of blood loss are most often used in trauma and polytrauma. They use average statistical values ​​of blood loss established for a particular type of injury. In the same way, you can roughly estimate blood loss during various surgical interventions.

Average blood loss (l)

1. Hemothorax – 1.5–2.0

2. Fracture of one rib – 0.2–0.3

3. Abdominal injury – up to 2.0

4. Fracture of the pelvic bones (retroperitoneal hematoma) – 2.0–4.0

5. Hip fracture – 1.0–1.5

6. Shoulder/tibia fracture – 0.5–1.0

7. Fracture of the bones of the forearm – 0.2–0.5

8. Spinal fracture – 0.5–1.5

9. Scalped wound the size of a palm – 0.5

Surgical blood loss

1. Laparotomy – 0.5–1.0

2. Thoracotomy – 0.7–1.0

3. Amputation of the lower leg – 0.7–1.0

4. Osteosynthesis of large bones – 0.5–1.0

5. Gastric resection – 0.4–0.8

6. Gastrectomy – 0.8–1.4

7. Colon resection – 0.8–1.5

8. Caesarean section – 0.5–0.6

Laboratory methods include the determination of hematocrit number (Ht), hemoglobin concentration (Hb), relative density (p) or blood viscosity.

They are divided into:

1. calculations (application of mathematical formulas);

2. hardware (electrophysiological impedance-metric methods);

3. indicator (use of dyes, thermodilution, dextrans, radioisotopes).

Among the calculation methods, the Moore formula is most widely used:

KVP = BCCd x Htd-Htf / Htd

Where KVP is blood loss (ml);

TCVd – proper volume of circulating blood (ml).

Normally, in women, CBVd averages 60 ml/kg, in men – 70 ml/kg, in pregnant women – 75 ml/kg;

№d – proper hematocrit (in women – 42%, in men – 45%);

№f – actual hematocrit of the patient. In this formula, instead of hematocrit, you can use the hemoglobin indicator, taking 150 g/l as its proper level.

You can also use the value of blood density, but this technique is only applicable for small blood losses.

One of the first hardware methods for determining BCC was a method based on measuring the basic resistance of the body using a rheoplethysmograph (found application in the countries of the “post-Soviet space”).

Modern indicator methods provide for establishing the BCC based on changes in the concentration of substances used and are conventionally divided into several groups:

1. determination of plasma volume, and then the total blood volume through Ht;

2. determination of the volume of erythrocytes and, based on it, the total volume of blood through Ht;

3. simultaneous determination of the volume of red blood cells and blood plasma.

Evans stain (T-1824), dextrans (polyglucin), human albumin labeled with iodine (131I) or chromium chloride (51CrCl3) are used as indicators. But, unfortunately, all methods for determining blood loss give a high error (sometimes up to a liter), and therefore can only serve as a guide during treatment. However, VO2 determination should be considered the simplest diagnostic criterion for detecting shock.

The strategic principle of transfusion therapy for acute blood loss is the restoration of organ blood flow (perfusion) by achieving the required volume of blood volume. Maintaining the level of coagulation factors in quantities sufficient for hemostasis, on the one hand, and to counteract excessive disseminated coagulation, on the other. Replenishing the number of circulating red blood cells (oxygen carriers) to a level that ensures a minimum sufficient oxygen consumption in the tissues. However, most experts consider hypovolemia to be the most acute problem of blood loss, and, accordingly, the first place in treatment regimens is given to the replenishment of blood volume, which is a critical factor for maintaining stable hemodynamics. The pathogenetic role of a decrease in blood volume in the development of severe disorders of homeostasis predetermines the importance of timely and adequate correction of volumetric disorders on treatment outcomes in patients with acute massive blood loss. The ultimate goal of all efforts of the intensivist is to maintain adequate tissue oxygen consumption to maintain metabolism.

The general principles of treatment of acute blood loss are as follows:

1. Stop bleeding, fight pain.

2. Ensuring adequate gas exchange.

3. Replenishment of the BCC deficit.

4. Treatment of organ dysfunction and prevention of multiple organ failure:

Treatment of heart failure;

Prevention of kidney failure;

Correction of metabolic acidosis;

Stabilization of metabolic processes in the cell;

Treatment and prevention of DIC syndrome.

5. Early prevention of infection.

Stop bleeding and control pain.

With any bleeding, it is important to eliminate its source as soon as possible. For external bleeding - pressure on the vessel, a pressure bandage, tourniquet, ligature or clamp on the bleeding vessel. In case of internal bleeding, urgent surgical intervention is carried out in parallel with medical measures to bring the patient out of shock.

Table No. 5 presents data on the nature of infusion therapy for acute blood loss.

1. The infusion begins with crystalloids, then colloids. Blood transfusion - when Hb decreases to less than 70 g/l, Ht less than 25%.

2. Infusion rate for massive blood loss up to 500 ml/min!!! (catheterization of the second central vein, infusion of solutions under pressure).

3. Correction of volemia (stabilization of hemodynamic parameters).

4. Normalization of globular volume (Hb, Ht).

5. Correction of water-salt metabolism disorders

The fight against pain and protection from mental stress is carried out by intravenous (i.v.) administration of analgesics: 1–2 ml of a 1% solution of morphine hydrochloride, 1–2 ml of a 1–2% solution of promedol, as well as sodium hydroxybutyrate (20–40 mg /kg body weight), sibazon (5–10 mg), it is possible to use subnarcotic doses of calypsol and sedation with propofol. The dose of narcotic analgesics should be reduced by 50% due to the possible respiratory depression, nausea and vomiting that occurs with intravenous administration of these drugs. In addition, it should be remembered that their introduction is possible only after damage to internal organs has been ruled out. Ensuring adequate gas exchange is aimed at both the utilization of oxygen by tissues and the removal of carbon dioxide. All patients are shown prophylactic administration of oxygen through a nasal catheter at a rate of at least 4 l/min.

If respiratory failure occurs, the main goals of treatment are:

1. ensuring airway patency;

2. prevention of aspiration of gastric contents;

3. clearing the respiratory tract of mucus;

4. ventilation;

5. restoration of tissue oxygenation.

Developed hypoxemia can be caused by:

1. hypoventilation (usually in combination with hypercapnia);

2. discrepancy between ventilation of the lungs and their perfusion (disappears when breathing pure oxygen);

3. intrapulmonary shunting of blood (protected by breathing pure oxygen) caused by adult respiratory distress syndrome (PaO2 ‹ 60–70 mm Hg. FiO2 › 50%, bilateral pulmonary infiltrates, normal ventricular filling pressure), pulmonary edema, severe pneumonia ;

4. impaired diffusion of gases through the alveolo-capillary membrane (disappears when breathing pure oxygen).

Ventilation of the lungs, carried out after tracheal intubation, is carried out in specially selected modes that create conditions for optimal gas exchange and do not disturb central hemodynamics.

Replenishing the BCC deficit

First of all, in case of acute blood loss, the patient should create an improved Trendeleburg position to increase venous return. The infusion is carried out simultaneously in 2-3 peripheral or 1-2 central veins. The rate of replenishment of blood loss is determined by the value of blood pressure. As a rule, the infusion is initially carried out as a stream or rapid drip (up to 250–300 ml/min). After stabilization of blood pressure at a safe level, the infusion is carried out by drip. Infusion therapy begins with the administration of crystalloids. And in the last decade there has been a return to considering the possibility of using hypertonic NaCI solutions.

Hypertonic solutions of sodium chloride (2.5–7.5%), due to their high osmotic gradient, provide rapid mobilization of fluid from the interstitium into the bloodstream. However, their short duration of action (1–2 hours) and relatively small volumes of administration (no more than 4 ml/kg body weight) determine their primary use at the prehospital stage of treatment of acute blood loss. Colloidal solutions of anti-shock action are divided into natural (albumin, plasma) and artificial (dextrans, hydroxy-ethyl starches). Albumin and the protein fraction of plasma effectively increase the volume of intravascular fluid, because have high oncotic pressure. However, they readily penetrate the pulmonary capillary walls and glomerular basement membranes into the extracellular space, which can lead to edema of the interstitial tissue of the lungs (adult respiratory distress syndrome) or kidneys (acute renal failure). The volume of diffusion of dextrans is limited, because they cause damage to the epithelium of the renal tubules (“dextran kidney”) and adversely affect the blood coagulation system and immune cells. Therefore, today the “drugs of first choice” are solutions of hydroxyethyl starch. Hydroxyethyl starch is a natural polysaccharide obtained from amylopectin starch and consisting of high molecular weight polarized glucose residues. The starting materials for obtaining HES are starch from potato and tapioca tubers, grains of various varieties of corn, wheat, and rice.

HES from potatoes and corn, along with linear amylase chains, contains a fraction of branched amylopectin. Hydroxylation of starch prevents its rapid enzymatic breakdown, increases the ability to retain water and increase colloid osmotic pressure. In transfusion therapy, 3%, 6% and 10% HES solutions are used. The administration of HES solutions causes an isovolemic (up to 100% when administering a 6% solution) or even initially hypervolemic (up to 145% of the administered volume of a 10% solution of the drug) volume-substituting effect, which lasts for at least 4 hours.

In addition, HES solutions have the following properties that are not found in other colloidal plasma replacement drugs:

1. prevent the development of capillary hyperpermeability syndrome by closing the pores in their walls;

2. modulate the action of circulating adhesive molecules or inflammatory mediators, which, circulating in the blood during critical conditions, increase secondary tissue damage by binding to neutrophils or endothelial cells;

3. do not affect the expression of surface blood antigens, i.e. do not disrupt immune reactions;

4. do not cause activation of the complement system (consists of 9 serum proteins C1 - C9), associated with generalized inflammatory processes that disrupt the functions of many internal organs.

It should be noted that in recent years, separate randomized studies of a high level of evidence have appeared (A, B) indicating the ability of starches to cause renal dysfunction and giving preference to albumin and even gelatin preparations.

At the same time, from the late 70s of the 20th century, perfluorocarbon compounds (PFOS) began to be actively studied, which formed the basis of a new generation of plasma expanders with the function of O2 transfer, one of which is perftoran. The use of the latter in acute blood loss makes it possible to influence the reserves of three levels of O2 exchange, and the simultaneous use of oxygen therapy can also increase ventilation reserves.

Table 6. Proportion of perftoran use depending on the level of blood replacement

Clinically, the degree of reduction in hypovolemia is reflected by the following signs:

1. increased blood pressure;

2. decrease in heart rate;

3. warming and pinking of the skin; -increased pulse pressure; - diuresis over 0.5 ml/kg/hour.

Thus, summing up the above, we emphasize that the indications for blood transfusion are: - blood loss of more than 20% of the due volume, - anemia, in which the hemoglobin content is less than 75 g / l, and the hematocrit number is less than 0.25.

Treatment of organ dysfunction and prevention of multiple organ failure

One of the most important tasks is the treatment of heart failure. If the victim was healthy before the accident, then in order to normalize cardiac activity, he will usually quickly and effectively replenish the deficit of blood volume. If the victim has a history of chronic heart or vascular diseases, then hypovolemia and hypoxia aggravate the course of the underlying disease, so special treatment is carried out. First of all, it is necessary to achieve an increase in preload, which is achieved by increasing the volume of blood volume, and then increase myocardial contractility. Most often, vasoactive and inotropic agents are not prescribed, but if hypotension becomes persistent and not amenable to infusion therapy, then these drugs can be used. Moreover, their use is possible only after full compensation of the BCC. Of the vasoactive drugs, the first-line drug for maintaining the activity of the heart and kidneys is dopamine, 400 mg of which is diluted in 250 ml of isotonic solution.

The infusion rate is selected depending on the desired effect:

1. 2–5 mcg/kg/min (“renal” dose) dilates mesenteric and renal vessels without increasing heart rate and blood pressure;

2. 5–10 mcg/kg/min gives a pronounced ionotropic effect, mild vasodilation due to stimulation of β2-adrenergic receptors or moderate tachycardia;

3. 10–20 mcg/kg/min leads to a further increase in the ionotropic effect and pronounced tachycardia.

More than 20 mcg/kg/min – sharp tachycardia with the threat of tachyarrhythmias, narrowing of veins and arteries due to stimulation of α1_ adrenergic receptors and deterioration of tissue perfusion. As a result of arterial hypotension and shock, acute renal failure (ARF) usually develops. In order to prevent the development of the oliguric form of acute renal failure, it is necessary to monitor hourly diuresis (normally in adults it is 0.51 ml/kg/h, in children - more than 1 ml/kg/h).

Measurement of sodium and creatine concentrations in urine and plasma (in acute renal failure, plasma creatine exceeds 150 µmol/l, glomerular filtration rate is below 30 ml/min).

Dopamine infusion in a “renal” dose. Currently, there are no randomized multicenter studies in the literature indicating the effectiveness of the use of “renal doses” of sympathomimetics.

Stimulation of diuresis against the background of restoration of bcc (central venous pressure more than 30–40 cm H2O) and satisfactory cardiac output (furosemide, IV in an initial dose of 40 mg, increased if necessary by 5–6 times).

Normalization of hemodynamics and replacement of circulating blood volume (CBV) should be carried out under the control of PCWP (pulmonary capillary wedge pressure), CO (cardiac output) and TPR. During shock, the first two indicators progressively decrease and the last one increases. Methods for determining these criteria and their norms are quite well described in the literature, but, unfortunately, they are routinely used in clinics abroad and rarely in our country.

Shock is usually accompanied by severe metabolic acidosis. Under its influence, myocardial contractility decreases, cardiac output decreases, which contributes to a further decrease in blood pressure. The reactions of the heart and peripheral vessels to endo- and exogenous catecholamines are reduced. O2 inhalation, mechanical ventilation, and infusion therapy restore physiological compensatory mechanisms and, in most cases, eliminate acidosis. Sodium bicarbonate is administered in case of severe metabolic acidosis (venous blood pH below 7.25), calculated according to the generally accepted formula, after determining acid-base balance indicators.

A bolus of 44–88 mEq (50–100 ml of 7.5% HCO3) can be administered immediately, with the remaining amount over the next 4–36 hours. It should be remembered that excessive administration of sodium bicarbonate creates the prerequisites for the development of metabolic alkalosis, hypokalemia, and arrhythmias. A sharp increase in plasma osmolarity is possible, up to the development of hyperosmolar coma. In case of shock, accompanied by a critical deterioration in hemodynamics, stabilization of metabolic processes in the cell is necessary. Treatment and prevention of DIC syndrome, as well as early prevention of infections, are carried out according to generally accepted schemes.

Justified, from our point of view, is a pathophysiological approach to solving the problem of indications for blood transfusions, based on an assessment of oxygen transport and consumption. Oxygen transport is a derivative of cardiac output and blood oxygen capacity. Oxygen consumption depends on the delivery and ability of the tissue to take oxygen from the blood.

When hypovolemia is replenished with colloid and crystalloid solutions, the number of red blood cells is reduced and the oxygen capacity of the blood is reduced. Due to the activation of the sympathetic nervous system, cardiac output compensatory increases (sometimes exceeding normal values ​​by 1.5–2 times), microcirculation “opens” and the affinity of hemoglobin for oxygen decreases, tissues take relatively more oxygen from the blood (oxygen extraction coefficient increases). This allows you to maintain normal oxygen consumption when the oxygen capacity of the blood is low.

In healthy people, normovolemic hemodilution with a hemoglobin level of 30 g/l and a hematocrit of 17%, although accompanied by a decrease in oxygen transport, does not reduce oxygen consumption by tissues, and the level of blood lactate does not increase, which confirms the sufficiency of oxygen supply to the body and the maintenance of metabolic processes at sufficient level. In acute isovolemic anemia up to hemoglobin (50 g/l), in patients at rest, tissue hypoxia is not observed before surgery. Oxygen consumption does not decrease, and even increases slightly, and blood lactate levels do not increase. In normovolemia, oxygen consumption does not suffer at a delivery level of 330 ml/min/m2; at lower delivery levels, there is a dependence of consumption on oxygen delivery, which corresponds approximately to a hemoglobin level of 45 g/l with normal cardiac output.

Increasing the oxygen capacity of blood by transfusion of preserved blood and its components has its negative aspects. Firstly, an increase in hematocrit leads to an increase in blood viscosity and deterioration of microcirculation, creating additional stress on the myocardium. Secondly, the low content of 2,3-DPG in erythrocytes of donor blood is accompanied by an increase in the affinity of oxygen for hemoglobin, a shift of the oxyhemoglobin dissociation curve to the left and, as a result, a deterioration in tissue oxygenation. Thirdly, transfused blood always contains microclots, which can “clog” the capillaries of the lungs and sharply increase the pulmonary shunt, impairing blood oxygenation. In addition, transfused red blood cells begin to fully participate in oxygen transport only 12-24 hours after blood transfusion.

Our analysis of the literature showed that the choice of means for correcting blood loss and posthemorrhagic anemia is not a resolved issue. This is mainly due to the lack of informative criteria for assessing the optimality of certain methods of compensating for transport and oxygen consumption. The current trend towards reducing blood transfusions is due, first of all, to the possibility of complications associated with blood transfusions, restrictions on donation, and patients’ refusal to undergo blood transfusions for any reason. At the same time, the number of critical conditions associated with blood loss of various origins is increasing. This fact dictates the need for further development of methods and means of replacement therapy.

An integral indicator that allows you to objectively assess the adequacy of tissue oxygenation is the saturation of hemoglobin with oxygen in mixed venous blood (SvO2). A decrease in this indicator by less than 60% over a short period of time leads to the appearance of metabolic signs of tissue oxygen debt (lactic acidosis, etc.). Consequently, an increase in lactate content in the blood can be a biochemical marker of the degree of activation of anaerobic metabolism and characterize the effectiveness of the therapy.

Etiology and pathogenesis. Acute blood loss can be primarily of traumatic origin when vessels of more or less large caliber are injured. It may also depend on the destruction of the vessel by one or another pathological process: rupture of the tube during ectopic pregnancy, bleeding from a stomach or duodenal ulcer, from varicose veins of the lower segment of the esophagus in atrophic cirrhosis of the liver, from varicose hemorrhoidal veins. Pulmonary bleeding in a patient with tuberculosis, intestinal bleeding in typhoid fever can also be very profuse and sudden and cause more or less anemia.

A simple listing of blood losses of various etiologies suggests that the clinical picture, course, and therapy will be different depending on the general condition of the patient before the onset of bleeding: a healthy person who was injured, a previously healthy woman after a tube rupture during an ectopic pregnancy , a patient with a stomach ulcer, who did not know about his illness before, will react similarly to sudden gastric bleeding. Otherwise, patients with cirrhosis, typhoid fever or tuberculosis will suffer blood loss. The underlying disease determines the background on which the further course of anemia largely depends.

Acute blood loss of up to 0.5 liters in a healthy, middle-aged person causes short-term, mild symptoms: slight weakness, dizziness. The daily experience of blood transfusion institutes - the donation of blood by donors - confirms this observation. Loss of 700 ml of blood or more causes more pronounced symptoms. It is believed that blood loss exceeding 50-65% of blood, or more than 4-4.5% of body weight, is definitely fatal.

With acute blood loss, death occurs even with smaller amounts of blood shed. In any case, acute loss of more than a third of the blood causes fainting, collapse and even death.

The speed of blood flow matters. The loss of even 2 liters of blood occurring over 24 hours is still compatible with life (according to Ferrata).

The degree of anemia and the speed of restoration of normal blood composition depend not only on the amount of blood loss, but also on the nature of the injury and the presence or absence of infection. In cases of anaerobic infection, the most pronounced and persistent anemia is observed in the wounded, since anemia from blood loss is accompanied by increased hemolysis caused by anaerobic infection. These wounded people have particularly high reticulocytosis and yellowness of the integument.

Observations during the war on the course of acute anemia in the wounded clarified our knowledge about the pathogenesis of the main symptoms of acute anemia and the compensatory mechanisms developing during this process.

Bleeding from a damaged vessel stops as a result of the convergence of the edges of the wounded vessel due to its reflex contraction, due to the formation of a blood clot in the affected area. N.I. Pirogov drew attention to important factors that help stop bleeding: the “pressure” of blood in the artery, blood supply and blood pressure in the wounded vessel decrease, the direction of the blood stream changes. The blood is sent along other, “bypass” routes.

As a result of the depletion of blood plasma in proteins and a drop in the number of cellular elements, the viscosity of the blood decreases and its turnover accelerates. Due to the decrease in the amount of blood, the arteries and veins contract. The permeability of vascular membranes increases, which enhances the flow of fluid from the tissues into the vessels. This is accompanied by the supply of blood from blood depots (liver, spleen, etc.). All these mechanisms improve blood circulation and oxygen supply to tissues.

In acute anemia, the mass of circulating blood decreases. The blood becomes depleted of red blood cells, oxygen carriers. The minute volume of blood decreases. Oxygen starvation of the body occurs as a result of a decrease in the oxygen capacity of the blood and often acutely developing circulatory failure.

Severe condition and death in acute bleeding depend mainly not on the loss of a large number of oxygen carriers - red blood cells, but on weakening of blood circulation due to depletion of the vascular system with blood. Oxygen starvation during acute blood loss is of the hematogenous-circulatory type.

One of the factors compensating for the effects of anemia is also an increase in the coefficient of oxygen utilization by tissues.

V.V. Pashutin and his students also studied gas exchange in acute anemia. M. F. Kandaratsky already showed in his dissertation in 1888 that at high degrees of anemia, gas exchange does not change.

According to M.F. Kandaratsky, 27% of the total amount of blood is sufficient for minimal life manifestations. The normally available amount of blood allows the body to satisfy the need for maximum work.

As I.R. Petrov showed, with large blood losses, the cells of the cerebral cortex and cerebellum are especially sensitive to the lack of oxygen. Oxygen starvation explains the initial excitation and subsequent inhibition of the functions of the cerebral hemispheres.

In the development of the entire clinical picture of anemia and the body’s compensatory and adaptive reactions, the nervous system is of great importance.

Even N.I. Pirogov drew attention to the influence of emotional unrest on the strength of bleeding: “The fear that brings bleeding to a wounded person also prevents the bleeding from stopping and often serves to bring it back.” From this, Pirogov concluded and pointed out that “the doctor must first of all morally reassure the patient.”

At the clinic we had to observe a patient whose regeneration was inhibited after a nervous shock.

Under the influence of blood loss, the bone marrow is activated. With large blood losses, the yellow bone marrow of the long bones temporarily turns into active - red. The foci of erythropoiesis sharply increase in it. Bone marrow puncture reveals large accumulations of erythroblasts. The number of erythroblasts in the bone marrow reaches enormous sizes. Erythropoiesis in it often prevails over leukopoiesis.

In some cases, blood regeneration after blood loss may be delayed due to a number of reasons, of which malnutrition must be highlighted.

Pathological anatomy. On section, when the patient dies early, we find pallor of the organs, low filling of the heart and blood vessels with blood. The spleen is small. The heart muscle is pale (turbid swelling, fatty infiltration). There are small hemorrhages under the endocardium and epicardium.

Symptoms. With acute massive blood loss, the patient becomes pale as a sheet, as if in mortal fright. Insurmountable muscle weakness sets in. In severe cases, complete or partial loss of consciousness occurs, shortness of breath with deep breathing movements, muscle twitching, nausea, vomiting, yawning (cerebral anemia), and sometimes hiccups. Cold sweat usually appears. The pulse is frequent, barely perceptible, blood pressure is sharply reduced. There is a complete clinical picture of shock.

If the patient recovers from shock, if he does not die from heavy blood loss, then, upon regaining consciousness, he complains of thirst. He drinks if given to him to drink, and again falls into oblivion. The general condition gradually improves, a pulse appears, and blood pressure rises.

The life of the body and its blood circulation are possible only with a certain amount of fluid in the bloodstream. Following the loss of blood, the blood reservoirs (spleen, skin and other red blood cell depots) are immediately emptied, and fluid from the tissues and lymph enter the blood. This explains the main symptom - thirst.

The temperature after acute bleeding usually does not increase. Small increases for 1-2 days are sometimes observed after bleeding into the gastrointestinal tract (for example, with bleeding from a stomach and duodenal ulcer). Temperature increases to higher numbers occur with hemorrhage in the muscles and serous cavities (pleura, peritoneum).

The pallor of the integument depends on a decrease in the amount of blood - oligemia - and on the contraction of skin vessels, which occurs reflexively and reduces the capacity of the bloodstream. It is clear that at the first moment after blood loss, blood of more or less the same composition will flow through the reduced channel; oligemia is observed in the literal sense of the word. When examining blood during this period, the number of red blood cells, hemoglobin and the usual color indicator for the patient before blood loss are detected. These indicators can be even greater than before blood loss: on the one hand, with the indicated decrease in the bloodstream, the blood can thicken, on the other hand, blood richer in formed elements enters the vessels from the released blood vessels. In addition, as indicated above, when the vessels contract, more plasma is squeezed out of them than formed elements (the latter occupy the central part of the “blood cylinder”).

Anemia stimulates the functions of the hematopoietic organs, so the bone marrow begins to produce red blood cells with greater energy and release them into the blood. In this regard, in the subsequent period the composition of erythrocytes changes. With increased production and release into the blood of red blood cells that are inferior in terms of hemoglobin saturation, the latter are paler than normal (oligochromia), of different sizes (anisocytosis) and of different shapes (poikilocytosis). The size of red blood cells after bleeding increases slightly (shift of the Price-Jones curve to the right). In the peripheral blood, younger red blood cells that have not yet completely lost basophilia, polychromatophils, appear. The percentage of reticulocytes rises significantly. As a rule, polychromatophilia and an increase in the number of reticulocytes develop in parallel, being an expression of enhanced regeneration and increased entry of young red blood cells into the peripheral blood. The resistance of erythrocytes to hypotonic solutions of table salt first decreases for a short time, and then increases due to the release of younger elements into the peripheral blood. Erythroblasts may appear. The color index decreases during this period.

The speed of restoration of normal blood composition depends on the amount of blood lost, on whether bleeding continues or not, on the age of the patient, on his state of health before blood loss, on the underlying suffering that caused the blood loss, and, most importantly, on the timeliness and appropriateness of therapy.

The normal number of red blood cells is restored most quickly. The amount of hemoglobin increases more slowly. The color indicator gradually returns to normal.

After a large loss of blood in a previously healthy person, the normal number of red blood cells is restored in 30-40 days, hemoglobin in 40-55 days.

In case of anemia from blood loss, especially after injuries, it is important to establish the period that has passed since the injury and blood loss. Thus, according to Yu. I. Dymshits, 1-2 days after a penetrating wound of the chest, accompanied by hemorrhage into the pleural cavity, in 2/3 of cases less than 3.5 million red blood cells are determined per 1 mm3. Anemia is hypochromic in nature: in 2/3 of cases the color index is less than 0.7. But after 6 days, the number of red blood cells below 3.5 million per 1 mm3 is observed in less than 1/6 of the cases (in 13 out of 69 examined).

Following bleeding, moderate neutrophilic leukocytosis usually occurs (12,000-15,000 leukocytes per 1 mm3), as well as an increase in the number of blood platelets and increased blood clotting within 10 minutes).

The percentage of reticulocytes in the bone marrow increases significantly. Forcel believed that the degree of reticulocytosis is the most subtle indicator of the regenerative ability of the bone marrow.

Treatment. In case of acute anemia, therapeutic intervention should be urgent. The body suffers from a lack of blood and fluid, which must be replenished immediately. It is clear that the most effective remedy, if blood loss is significant, is a blood transfusion.

Blood transfusion achieves replenishment of fluid and nutritional material lost by the body, irritation of the bone marrow, strengthening of its functions, hemostatic effect, introduction of full-fledged red blood cells and fibrin enzyme. Usually 200-250 ml of blood or larger doses are transfused. If bleeding continues, the dose of re-transfused blood is reduced to 150-200 ml.

In conditions of combat trauma and shock with blood loss, 500 ml of blood is infused. If necessary, this dose is increased to 1-1.5 liters. Before blood transfusion, all measures are taken to stop bleeding.

In case of bleeding, transfusion of fresh and canned blood gives the same result. If necessary, it facilitates further surgical intervention (for stomach ulcers, ectopic pregnancy). Blood transfusion is indicated for bleeding from a typhoid ulcer and is contraindicated if the bleeding is caused by a ruptured aortic aneurysm. For bleeding from the lungs in patients with tuberculosis, blood transfusion does not give clear results and is usually not used. To stop bleeding, infusion of blood plasma into a vein is successfully used.

According to L.G. Bogomolova, you can use dry plasma obtained by drying at a low temperature and dissolved in distilled sterile water before infusion.

The physiological sodium chloride solution (0.9%) and various mixtures of salt solutions used are not blood substitutes. Significantly better results are obtained by injecting salt mixtures into a vein, to which colloids related to the given organism are added.

The introduction of blood replacement fluids and blood into the vein must be done slowly. The required infusion rate is 400 ml over 15 minutes with a healthy heart and healthy vascular system. In case of circulatory disorders, it is necessary to use the drip method of administration. Failure to comply with these rules may result in adverse reactions to infusion and complications.

In later stages, the main method of treatment is the use of iron. Arsenic is a good help.

In addition, bed rest, good nutrition with a sufficient content of vitamins, in particular vitamin C, are required. As observations show, for rapid restoration of blood in donors, it is necessary to contain at least 50-60 mg of ascorbic acid in the daily ration.

Of interest are the methods of stopping bleeding that were used in the past by Russian folk medicine. It was recommended to drink raw carrot and radish juice when