BLOOD LOSS- a pathological process that occurs as a result of damage to blood vessels and loss of part of the blood, characterized by a number of pathological and adaptive reactions.

Etiology and pathogenesis

Physiol. K. is observed during menstruation, during normal childbirth and is easily compensated by the body.

Patol. K., as a rule, requires medical intervention.

Changes in K. can be conditionally divided into several stages: initial, compensation stage and terminal. The trigger mechanism that causes compensatory and patol changes in the body as a result of blood loss is a decrease in circulating blood volume (CBV). The primary reaction to blood loss is a spasm of small arteries and arterioles, which occurs reflexively as a result of irritation of the receptor vascular zones and an increase in the tone of the sympathetic part. n. With. Thanks to this, even with large blood loss, if it occurs slowly, normal blood pressure levels can be maintained. A decrease in the lumen of small arteries and arterioles leads to an increase in total peripheral resistance, which increases in accordance with the increase in the mass of lost blood and a decrease in blood volume, which, in turn, leads to a decrease in venous flow to the heart. Reflex increase in heart rate in the initial stage of K. in response to a decrease in blood pressure and changes in chemical values. blood composition maintains cardiac output for some time, but subsequently it steadily falls (in experiments on dogs with extremely severe K., a 10-fold decrease in cardiac output was recorded with a simultaneous drop in blood pressure in large vessels to 0-5 mm Hg. ). In the compensation stage, in addition to an increase in heart rate, the strength of heart contractions increases and the amount of residual blood in the ventricles of the heart decreases. In the terminal stage, the force of heart contractions decreases, and the residual blood in the ventricles is not used.

With K. the function and state of the myocardium changes, and the maximum achievable contraction speed decreases. The reaction of coronary vessels to K. has its own characteristics. At the very beginning of K., when blood pressure decreases by a small amount, the volume of coronary blood flow does not change; As blood pressure falls, the volume of blood flow in the coronary vessels of the heart decreases, but to a lesser extent than blood pressure. Thus, when blood pressure decreased to 50% of the initial level, coronary blood flow decreased by only 30%. Coronary blood flow is maintained even when blood pressure in the carotid artery drops to 0. ECG changes reflect progressive myocardial hypoxia: at first there is an increase in the rhythm, and then, with increasing blood loss, a slowdown, a decrease in the voltage of the I wave, inversion and increase in the T wave, a decrease in the S-T segment and conduction disturbances up to the appearance of transverse blockade, blockade of the legs of the atrioventricular bundle (bundle of His), idioventricular rhythm. The latter is important for prognosis, since the degree of coordination of the heart depends on the conduction function.

There is a redistribution of blood in the organs; First of all, blood flow in the skin and muscles decreases, this ensures the maintenance of blood flow in the heart, adrenal glands, and brain. G.I. Mchedlishvili (1968) described a mechanism that makes it possible to maintain reduced blood circulation in the brain for a short time, even when blood pressure in large vessels decreases to 0. In the kidneys, blood flow is redistributed from the cortex to the brain according to the type of juxtaglomerular shunt (see Kidneys), which leads to a slowdown in blood flow, because in the medulla it is slower than in the cortex; spasm of the interlobular arteries and afferent arterioles of the glomeruli is observed. When blood pressure decreases to 50-60 mm Hg. Art. renal blood flow decreases by 30%. Significant circulatory disorders in the kidneys cause a decrease in diuresis, and a drop in blood pressure below 40 mm Hg. Art. leads to the cessation of urine formation, because the hydrostatic pressure in the capillaries becomes less than the oncotic pressure of the plasma. As a result of a drop in blood pressure, the juxtaglomerular complex of the kidneys increases the secretion of renin (see), and its content in the blood can increase up to 5 times. Under the influence of renin, angiotensin (see) is formed, which constricts blood vessels and stimulates the secretion of aldosterone (see). A decrease in renal blood flow and impaired filtration are observed for several days after undergoing K. Acute renal failure (see) can develop in severe K. in the case of delayed and incomplete replacement of lost blood. Hepatic blood flow decreases in parallel with the fall in cardiac output.

Blood supply to tissues and blood pressure can be maintained for some time due to the redistribution of blood within the vascular system and the transition of part of it from the low pressure system (veins, pulmonary circulation) to the high pressure system. That. a decrease in blood volume up to 10% can be compensated without changing blood pressure and heart function. As a result, venous pressure decreases slightly. This is the basis for the beneficial effect of bloodletting in cases of venous congestion and edema, including pulmonary edema.

Oxygen tension (pO 2) changes little in arterial blood and greatly in venous blood; with severe K. pO 2 drops from 46 to 23 mm Hg. Art., and in the blood of the coronary sinus from 21 to 12 mm Hg. Art. Changes in pO 2 in tissues reflect the nature of their blood supply. In the experiment, pO 2 in skeletal muscles decreases faster than blood pressure; pO 2 in the wall of the small intestine and stomach decreases parallel to the decrease in blood pressure. In the cortex and subcortical nodes of the brain, as well as in the myocardium, the decrease in pO 2 is slower than the decrease in blood pressure.

To compensate for the phenomena of circulatory hypoxia in the body, the following occurs: 1) redistribution of blood and preservation of blood flow in vital organs by reducing the blood supply to the skin, digestive organs and, possibly, muscles; 2) restoration of circulating blood volume as a result of the influx of interstitial fluid into the bloodstream; 3) an increase in cardiac output and oxygen utilization rate with restoration of circulating blood volume. The last two processes contribute to the transition of circulatory hypoxia to anemic, which poses less danger and is easier to compensate for.

Tissue hypoxia, which develops during K., leads to the accumulation of under-oxidized metabolic products in the body and to acidosis (see), which is initially compensated. As K. deepens, uncompensated acidosis develops with a decrease in pH in the venous blood to 7.0-7.05, and in the arterial blood to 7.17-7.20 and a drop in alkaline reserves. In the terminal stage of K., venous blood acidosis is combined with arterial alkalosis (see Alkalosis); at the same time, the pH in arterial blood does not change or slightly shifts to the alkaline side, but the content and tension of carbon dioxide (pCO 2) significantly decreases, which is associated both with a drop in pCO 2 in the alveolar air as a result of increased ventilation of the lungs, and with the destruction of plasma bicarbonates . In this case, the respiratory coefficient becomes greater than 1.

As a result of blood loss, blood thins; the decrease in BCC is compensated by the body by the entry of fluid into the bloodstream from the interstitial spaces and proteins dissolved in it (see Hydremia). At the same time, the pituitary gland - adrenal cortex system is activated; The secretion of aldosterone increases, which enhances sodium reabsorption in the proximal renal tubules. Sodium retention leads to increased reabsorption of water in the tubules and decreased urine formation. At the same time, the blood content of the antidiuretic hormone of the posterior lobe of the pituitary gland increases. The experiment established that after a very massive plasma volume restoration occurs quite quickly and during the first day its volume exceeds the initial value. The restoration of plasma proteins occurs in two phases: in the first phase, during the first two to three days, this occurs due to the mobilization of tissue proteins; in the second phase - as a result of increased protein synthesis in the liver; full recovery occurs in 8-10 days. The proteins that enter the bloodstream have a qualitative difference from normal whey proteins (they have increased colloid-osmotic activity, indicating their greater dispersion).

Hyperglycemia develops, the content of lactate dehydrogenase and aspartate aminotransferase in the blood increases, which indicates damage to the liver and kidneys; the concentration of the main cations and anions in blood plasma changes. With K., the titer of complement, precipitins and agglutinins decreases; the body's sensitivity to bacteria and their endotoxins increases; phagocytosis is suppressed, in particular, the phagocytic activity of Kupffer cells of the liver decreases and remains impaired for several days after restoration of blood volume. However, it has been noted that minor repeated bleeding increases the production of antibodies.

Blood clotting during K. accelerates, despite a decrease in the number of platelets and fibrinogen content. At the same time, the fibrinolytic activity of the blood increases. Increased tone of the sympathetic part c. n. With. and the increased release of adrenaline undoubtedly contribute to the acceleration of blood clotting. Changes in the components of the coagulation system are of great importance. The adhesiveness of platelets and their ability to aggregate, prothrombin consumption, thrombin concentration, factor VIII content increase, and the content of antihemophilic globulin decreases. Tissue thromboplastin comes from the interstitial fluid, and antiheparin factor comes from destroyed red blood cells (see Blood coagulation system).

Changes in the hemostatic system persist for several days, when the total blood clotting time is already normalized. The platelet count recovers very quickly after blood loss. In the leukocyte formula (see), leukopenia with relative lymphocytosis is first detected, and then neutrophilic leukocytosis, which is initially redistributive in nature, and then caused by activation of hematopoiesis, as evidenced by a shift in the leukocyte formula to the left.

The number of red blood cells and hemoglobin content decrease depending on the volume of blood lost, with the subsequent dilution of the blood by interstitial fluid playing a major role. The minimum hemoglobin concentration required to maintain life when blood volume is restored is 3 g% (under experimental conditions). The absolute number of red blood cells continues to decrease in the posthemorrhagic period. In the first hours after blood loss, the content of erythropoietins (see) decreases, then after 5 hours. starts to increase. Their highest content is observed on the 1st and 5th days. K., and the first peak is associated with hypoxia, and the second coincides with the activation of the bone marrow. The restoration of blood composition is also facilitated by increased formation of internal Castle factor in the gastric mucosa (see Castle factors).

Nervous, endocrine and tissue factors take part in the implementation of compensatory reactions. Cardiac and vascular reactions leading to blood redistribution occur reflexively when receptor zones (sinocarotid and aorta) are irritated. Excitation of the sympathetic part c. n. With. leads to spasm of arterial vessels and tachycardia. The function of the anterior lobe of the pituitary gland and adrenal glands is enhanced. The release of catecholamines increases (see), as well as the content of aldosterone, renin, and angiotensin in the blood. Hormonal influences maintain vascular spasm, change their permeability and promote the flow of fluid into the bloodstream.

Endurance to K. varies among different animals, even of the same species. According to experimental data from the school of I.R. Petrov, painful trauma, electrical trauma, elevated ambient temperature, cooling, and ionizing radiation increase the body’s sensitivity to K.

For a person the loss is approx. 50% of blood is life-threatening, and a loss of more than 60% is absolutely fatal unless there is prompt intervention by resuscitators. The volume of lost blood does not always determine the severity of K.; in many cases, K. can be fatal even with a significantly smaller volume of blood shed, especially if the bleeding occurs when the great vessels are injured. With a very large loss of blood, especially after its rapid flow, death may occur as a result of cerebral hypoxia if the compensatory mechanisms do not have time to turn on or are insufficient. With a prolonged decrease in blood pressure, an irreversible condition may occur.

In severe cases, with K., the development of diffuse intravascular coagulation is possible, due to a combination of two factors: a slowdown in blood flow in the capillaries and an increase in the content of procoagulants in the blood. The irreversible condition as a result of prolonged K. differs in many respects from acute K. and comes close to the terminal stage of shock of another origin (see Shock). In this case, hemodynamics continuously deteriorates as a result of a vicious circle, which develops as follows. With K., oxygen transport decreases, which leads to a decrease in oxygen consumption by tissues and the accumulation of oxygen debt; as a result of hypoxia, the contractile function of the myocardium is weakened, minute volume decreases, which, in turn, further worsens oxygen transport. A vicious circle can arise in another way; as a result of a decrease in oxygen transport, the central nervous system suffers, the function of the vasomotor center is disrupted, vasomotor reflexes are weakened or distorted, the latter leads to an even greater drop in pressure and a decrease in cardiac output, which leads to further disruption of the regulatory influence of the nervous system, deterioration of hemodynamics and decrease oxygen transport. If the vicious circle is not broken, the increase in violations can lead to death.

Pathological anatomy

Pathological changes depend on the speed and magnitude of blood loss. With recurrent relatively small bleeding (for example, from the uterus with hemorrhagic metropathy, from hemorrhoids, etc.), changes characteristic of posthemorrhagic anemia occur (see Anemia). These changes consist of increasing degeneration of parenchymal organs, increased regeneration of red bone marrow, and displacement of tubular bones by hematopoietic elements of fatty bone marrow. Protein-fatty degeneration of hepatocytes and fatty degeneration of cardiac myocytes are characteristic; at the same time, yellowish foci of myocardial dystrophy, alternating with less altered areas, create a peculiar striping, reminiscent of the colors of a tiger skin (the so-called tiger heart). In the cells of the convoluted tubules of the kidneys, proliferation of nuclei is observed without division of the cytoplasm with the formation of multinuclear symplasts, characteristic of hypoxic conditions of various etiologies.

Pathoanatomically, damage to various large arterial and venous vessels, varicose veins of the esophagus, vascular erosion of the walls of the tuberculous lung cavity, stomach ulcers, etc., as well as hemorrhages in the tissues in the area of ​​​​the damaged vessel and masses of spilled blood during internal bleeding can be detected. In gastric bleeding, the blood undergoes digestion as it moves through the intestines, turning into a tarry mass in the colon. The blood in the vessels of a corpse in the pleural and abdominal cavities partially coagulates or remains liquid due to the breakdown of fibrinogen. In pulmonary hemorrhage, the lungs, due to hemaspiration into the alveolar ducts, acquire a peculiar marbled appearance due to the alternation of light (air) and red (blood-filled) areas of the parenchyma.

Macroscopically, it is possible to correct the uneven blood supply to organs: along with anemia of the skin, muscles, and kidneys, plethora of the intestines, lungs, and brain is observed. The spleen is usually somewhat enlarged in size, flabby, congested, with copious scrapings from the cut surface. Impaired capillary permeability and changes in the blood coagulation system lead to widespread petechial hemorrhages under the serous membranes, in the mucous membranes of the gastrointestinal tract. tract, under the endocardium of the left ventricle (Minakov's spots).

Microscopically, common circulatory disorders in the microcirculation system of internal organs are detected. On the one hand, phenomena of disseminated intravascular coagulation are observed: aggregation of erythrocytes (see), the formation of fibrin and erythrocyte blood clots (see Thrombus) in arterioles and capillaries, which sharply reduces the number of functioning capillaries: on the other hand, there is a sharp focal expansion of capillaries with the formation erythrocyte stasis (see) and increased blood flow with focal congestion of the venous collectors. Electron microscopy reveals swelling of the cytoplasm of endothelial cells, clearing of the mitochondrial matrix, a decrease in the number of micropinocytotic vesicles, and expansion of intercellular junctions, which indicates a disruption in the transport of substances through the cytoplasm and increased permeability of the capillary wall. Changes in the endothelial membrane are accompanied by the formation of platelet conglomerates on its inner surface, which underlie thrombosis. Changes in the cells of parenchymal organs correspond to those during ischemia (see) and are represented by various types of dystrophies (see Dystrophy of cells and tissues). Ischemic changes in the parenchymal cells of internal organs occur first of all in the kidneys and liver.

Clinical picture

Clinical manifestations of K. do not always correspond to the amount of blood lost. With a slow flow of blood, even a significant loss of blood may not have clearly expressed both objective and subjective symptoms. Objective symptoms of significant K.: pale, moist skin with a grayish tint, pale mucous membranes, sunken face, sunken eyes, rapid and weak pulse, decreased arterial and venous pressure, rapid breathing, in very severe cases periodic, Cheyne-Stokes type (see Cheyne-Stokes breathing); subjective symptoms: dizziness, weakness, darkening of the eyes, dry mouth, severe thirst, nausea.

K. can be acute and chronic, of varying degrees of severity, compensated and uncompensated. The amount of blood lost, the speed and duration of its flow are of great importance for the outcome and treatment. Thus, in young healthy people, a loss of 1.5 - 2 liters of blood with a slow flow can occur without clinically significant symptoms. An important role is played by the previous condition: overwork, hypothermia or overheating, trauma, shock, concomitant diseases, etc., as well as gender and age (women are more tolerant to K. than men; newborns, infants and children are very sensitive to K. aged people).

The severity of K. can be roughly classified by the decrease in blood volume. Moderate degree - loss of less than 30% of bcc, massive - more than 30%, fatal - more than 60%.

Assessing the degree of blood loss and methods for determining it - see Bleeding.

However, the severity of the patient’s condition is determined primarily by the wedge, the picture.

Treatment

Treatment is based on strengthening the compensation mechanisms that the body has, or their imitation. The best way to eliminate both circulatory and anemic hypoxia is transfusion of compatible blood (see Blood transfusion). Along with blood, blood-substituting fluids (see) have become widespread, the use of which is based on the fact that the loss of plasma and, consequently, a decrease in blood volume is tolerated by the body much harder than the loss of red blood cells. In case of severe K., before determining the blood group, treatment should begin with an infusion of blood-substituting fluids, if necessary, even at the site of injury or during transportation. In mild cases, you can limit yourself to only blood replacement fluids. Transfusion of blood or red blood cells (see) is necessary when hemoglobin drops below 8 g% and hematocrit is less than 30. In acute K. treatment begins with a jet infusion and only after blood pressure rises above a critical level (80 mm Hg) and improvement the patient's condition changes to drip. In cases of increased bleeding and hypotension that cannot be corrected by transfusion of canned blood, direct blood transfusion from a donor is indicated, which gives a more pronounced effect even with a smaller volume of infusion.

With a prolonged decrease in blood pressure, transfusion of blood and blood-substituting fluids may be ineffective and should be supplemented with medications (cardiac drugs, corticosteroids, adrenocorticotropic hormone, antihypoxants) that normalize metabolic disorders. The administration of heparin and fibrinolysin in severe cases and with late initiation of treatment prevents the appearance of thrombohemorrhagic syndrome that develops in the case of diffuse intravascular coagulation (see Hemorrhagic diathesis). Drugs that increase vascular tone, especially pressor amines, are contraindicated until blood volume is completely restored. By increasing vascular spasm, they only worsen hypoxia.

The dose of administered blood and blood-substituting fluids depends on the patient’s condition. The ratios of blood volumes and blood-substituting fluids are approximately accepted as follows: with a blood loss of up to 1.5 liters, only plasma or blood-substituting fluids are administered, with a blood loss of up to 2.5 liters - blood and blood-substituting fluids in a ratio of 1: 1, with a blood loss of St. 3 l - blood and blood-substituting fluids in a ratio of 3:1. As a rule, the blood volume should be restored, the hematocrit should be more than 30, and the erythrocyte content should be approx. 3.5 million/µl.

Forecast

The prognosis depends on the general condition of the patient, the amount of blood lost, and especially on timely treatment. With early and vigorous treatment, even very severe K., accompanied by loss of consciousness, severe respiratory rhythm disorder, and extremely low blood pressure, ends in complete recovery. Restoration of vital functions is possible even with the onset of wedge, death (see Terminal conditions). The development of transverse heart block, impaired intraventricular conduction, the appearance of extrasystoles, and idioventricular rhythm worsens the prognosis, but does not make it hopeless (see Heart block). With timely treatment, sinus rhythm is restored. When treating significant K. after restoration of bcc, acid-base balance indicators are normalized following the restoration of hemodynamics, but the content of organic acids becomes greater than it was at the end of K., which is associated with their leaching from the tissues. Patients experience various disturbances of acid-base balance (see) for several days after the replacement of severe K., and a poor prognostic sign is the change from acidosis to alkalosis on the 2nd day. after its replacement. K., even of moderate severity, accompanied by diffuse intravascular coagulation with delayed treatment, can turn into an irreversible state. The main signs of successful treatment of K. are normalization of systolic and especially diastolic pressure, warming and pinking of the skin, and disappearance of sweating.

Blood loss in forensic medicine

To the medical court In practice, they usually encounter the consequences of acute K., edges being the main cause of death in injuries accompanied by massive external or internal bleeding. In such cases, forensic medical. the examination establishes the occurrence of death from acute K., the presence and nature of the connection between the damage and the cause of death, and also (if necessary) determines the amount of blood shed. When examining the corpse, a picture of acute anemia is revealed. The pallor of the skin is noteworthy, the cadaveric spots are poorly expressed, the internal organs and muscles are anemic and pale. Under the endocardium of the left ventricle of the heart, hemorrhages characteristic of death from K. are observed in the form of thin spots and stripes, the diagnostic value of which was first established in 1902 by P. A. Minakov. Usually Minakov's spots are dark red in color, well contoured, diameter. 0.5 cm or more. More often they are localized in the area of ​​the interventricular septum, less often - on the papillary muscles near the fibrous ring. Their pathogenesis has not been fully elucidated. P. A. Minakov associated their formation with a significant increase in negative diastolic pressure in the cavity of the left ventricle with massive blood loss. Other authors explain their occurrence by irritation of c. n. With. under the influence of hypoxia. Minakov's spots occur in more than half of cases of death from acute K., so they are assessed in conjunction with other changes. In cases where death from K. occurs quickly due to acute bleeding from large blood vessels (aorta, carotid artery, femoral artery) or from the heart, morphol, the picture of acute anemia is not expressed, while the organs have an almost normal color.

To the medical court In practice, great importance is attached to determining the amount of blood shed both during internal and external bleeding. When large blood vessels are injured, death is possible with a rapid loss of approx. 1 liter of blood, which is associated not so much with general bleeding as with a sharp drop in blood pressure and anemia of the brain. The amount of blood shed during external bleeding is determined by determining the dry residue of blood and then converting it to liquid. The dry residue is determined either by comparing the weight of areas of the blood stain and the carrier object of equal area, or by extracting blood from the stain with an alkaline solution. Conversion of dry residue to liquid blood is carried out based on the fact that 1000 ml of liquid blood on average corresponds to 211 g of dry residue. This method allows determination only with a certain degree of accuracy.

In case of bleeding, the degree of saturation of the damaged soft tissues is also taken into account to decide the question of the victim’s life expectancy.

During expert assessment, one should be aware of the possibility of bleeding as a result of disorders in the blood coagulation system (checked by collecting detailed anamnestic data from relatives of the deceased).

Bibliography: Avdeev M.I. Forensic medical examination of a corpse, M., 1976, bibliogr.; Wagner E. A. and Tavrovsky V. M. Transfusion therapy for acute blood loss, M., 1977, bibliogr.; Weil M. G. and Shubin G. Diagnosis and treatment of shock, trans. from English, M., 1971, bibliogr.; Kulagin V.K. Pathological physiology of trauma and shock, L., 1978; Pathological physiology of extreme conditions, ed. P. D. Gorizontova and N. N. Sirotinina, p. 160, M., 1973; Petrov I. R. and Vasadze G. Sh. Irreversible changes in shock and blood loss, L., 1972, bibliogr.; Soloviev G. M. and Radzivil G. G. Blood loss and regulation of blood circulation in surgery, M., 1973, bibliogr.; Progress in surgery, ed. by M. Allgower a. o., v. 14, Basel, 1975; Sandri ter W. a. L a s with h H. G. Pathological aspects of schock, Meth. Achiev. exp. Path., v. 3, p. 86, 1967, bibliogr.

V. B. Koziner; N. K. Permyakov (pat. an.); V.V. Tomilin (court).

Blood loss, severity of blood loss

Blood loss in the body is compensated due to spasm of peripheral vessels, redistribution of blood (mobilization from the “depot” - spleen, liver, intestinal vessels), saturation of blood with oxygen, increased and deepening of breathing, increased release of young red blood cells from the bone marrow and intense influx of fluid from tissues into vessels to restore blood volume.

Blood loss up to 500 ml is considered small, up to 1000 ml - moderate, up to 1500 ml - large, over 1500 ml massive. Children and elderly people are most sensitive to blood loss.

The human body is more sensitive to plasma loss. Death occurs from a loss of 30% of plasma, while death from a decrease in red blood cells is over 70%.

The body compensates for the loss of 400-500 ml of blood on its own, without therapeutic measures. A sudden loss of 2-2.5 liters of blood is fatal, and a loss of 1-1.5 liters leads to the development of acute anemia.

V.P. Dyadichkin

"Blood loss, severity of blood loss" article from the section

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

The average amount of blood in the body of an adult is 6-8% of the total mass, or 65-80 ml of blood per 1 kg of body weight, and in the body of a child - 8-9%. That is, the average blood volume in an adult male is 5000-6000 ml. A decrease in the total blood volume is called hypovolemia, an increase in blood volume compared to the norm is hypervolemia

Acute blood loss develops when a large vessel is damaged, when a very rapid drop in blood pressure occurs to almost zero. This condition is observed with a complete transverse rupture of the aorta, superior or inferior veins, or pulmonary trunk. The volume of blood loss is insignificant (250–300 ml), but due to a sharp, almost instantaneous drop in blood pressure, anoxia of the brain and myocardium develops, which leads to death. The morphological picture consists of signs of acute death, a small amount of blood in the body cavities, damage to a large vessel and a specific sign - Minakov's spots. In acute blood loss, bleeding of internal organs is not observed. With massive blood loss, there is a relatively slow flow of blood from damaged vessels. In this case, the body loses about 50–60% of the available blood. Over several tens of minutes, a gradual drop in blood pressure occurs. The morphological picture is quite specific. “Marbled” skin, pale, limited, island-shaped cadaveric spots that appear at a later date than in other types of acute death. Internal organs are pale, dull, dry. A large amount of spilled blood in the form of clots (up to 1500–2500 ml) is found in the body cavities or at the scene of the incident. During internal bleeding, sufficiently large volumes of blood are needed to saturate the soft tissue around the injury.

The clinical picture of blood loss does not always correspond to the amount of blood lost. With slow bleeding, the clinical picture may be blurry, and some symptoms may be completely absent. The severity of the condition is determined primarily on the basis of the clinical picture. With very large blood loss, and especially with rapid blood flow, compensatory mechanisms may be insufficient or may not have time to turn on. In this case, hemodynamics progressively worsen as a result of a vicious circle. Blood loss reduces oxygen transport, which leads to a decrease in oxygen consumption by tissues and the accumulation of oxygen debt; as a result of oxygen starvation of the central nervous system, the contractile function of the myocardium is weakened, IOC decreases, which, in turn, further worsens oxygen transport. If this vicious circle is not broken, then increasing violations lead to death. Sensitivity to blood loss is increased by overwork, hypothermia or overheating, time of year (in the hot season, blood loss is less tolerated), trauma, shock, ionizing radiation, and concomitant diseases. Gender and age matter: women are more tolerant of blood loss than men; Newborns, infants and the elderly are very sensitive to blood loss.

Blood loss is a deficiency of circulating blood volume. There are only two types of blood loss - hidden and massive. Hidden blood loss is a deficiency of red blood cells and hemoglobin; the plasma deficiency is compensated by the body as a result of the phenomenon of hemodilution. Massive blood loss is a deficiency in circulating blood volume, leading to dysfunction of the cardiovascular system. The terms “hidden and massive blood loss” are not clinical (related to the patient), these are academic (physiology and pathophysiology of blood circulation) study terms. Clinical terms: (diagnosis) posthemorrhagic iron deficiency anemia corresponds to hidden blood loss, and the diagnosis hemorrhagic shock - massive blood loss. As a result of chronic hidden blood loss, you can lose up to 70% of red blood cells and hemoglobin and save your life. As a result of acute massive blood loss, you can die, losing only 10% (0.5 l) of your blood volume. 20% (1l) often leads to death. 30% (1.5 l) of blood volume is an absolutely fatal blood loss if it is not compensated. Massive blood loss is any blood loss exceeding 5% of the blood volume. The volume of blood that is taken from the donor is the boundary between hidden and massive blood loss, that is, between that to which the body does not respond and that which can cause collapse and shock.

• Minor blood loss (less than 0.5 l) 0.5-10% of bcc. Such blood loss is tolerated by a healthy body without consequences or manifestation of any clinical symptoms. There is no hypovolemia, blood pressure is not reduced, pulse is within normal limits, slight fatigue, skin is warm and moist, has a normal shade, consciousness is clear.
• Average (0.5-1.0 l) 11-20% bcc. Mild degree of hypovolemia, blood pressure reduced by 10%, moderate tachycardia, pale skin, cold extremities, pulse slightly increased, breathing rapid without rhythm disturbance, nausea, dizziness, dry mouth, possible fainting, twitching of individual muscles, severe weakness, adynamia, slow reaction to others.
• Large (1.0-2.0 l) 21-40% bcc. Moderate severity of hypovolemia, blood pressure reduced to 100-90 mm Hg. Art., pronounced tachycardia up to 120 beats/min, breathing is very rapid (tachypnea
) with rhythm disturbances, sharp progressive pallor of the skin and visible mucous membranes, lips and nasolabial triangle are cyanotic, pointed nose, cold sticky sweat, acrocyanosis, oliguria, darkened consciousness, painful thirst, nausea and vomiting, apathy, indifference, pathological drowsiness, yawning (a sign of oxygen starvation), pulse - frequent, small filling, weakened vision, flickering spots and darkening in the eyes, clouding of the cornea, hand tremors.
• Massive (2.0-3.5 l) 41-70% bcc. Severe degree of hypovolemia, blood pressure reduced to 60 mm Hg, sharp tachycardia up to 140-160 beats/min, thread-like pulse up to 150 beats/min, not palpable in peripheral vessels, detected much longer in the main arteries, absolute indifference of the patient to the environment environment, delirium, consciousness is absent or confused, severe deathly pallor, sometimes a bluish-gray skin tone, “goose bumps”, cold sweat, anuria, Cheyne-Stokes type breathing, convulsions may be observed, a haggard face, pointed features, sunken dull eyes , an indifferent look.
• Fatal (more than 3.5 l) more than 70% of the bcc. Such blood loss is fatal for a person. Terminal state (preagonia or agony), coma, blood pressure below 60 mm Hg. Art., may not be detected at all, bradycardia from 2 to 10 beats/min, agonal breathing, superficial, barely noticeable, dry, cold skin, characteristic “marbling” of the skin, disappearance of pulse, convulsions, involuntary release of urine and feces, dilated pupils , then agony and death develop.

Question 4: basic requirements when performing blood transfusions

The main task in the treatment of hemorrhagic shock is to eliminate hypovolemia and improve microcirculation. From the first stages of treatment, it is necessary to establish a jet transfusion of fluids (saline solution, 5% glucose solution) to prevent reflex cardiac arrest - empty heart syndrome.

Immediate stopping of bleeding is possible only when the source of bleeding is accessible without anesthesia and everything that accompanies a more or less extensive operation. In most cases, patients with hemorrhagic shock have to be prepared for surgery by infusing various plasma-substituting solutions and even blood transfusions into a vein, and continue this treatment during and after surgery and stop the bleeding.

Infusion therapy aimed at eliminating hypovolemia is carried out under the control of central venous pressure, blood pressure, cardiac output, total peripheral vascular resistance and hourly diuresis. For replacement therapy in the treatment of blood loss, combinations of plasma substitutes and preserved blood products are used, based on the volume of blood loss.

To correct hypovolemia, blood substitutes with hemodynamic action are widely used: dextran preparations (reopolyglucin

Polyglucin), gelatin solutions (gelatinol), hydroxyethyl starch (refortan

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, the speed of development, the volume of blood lost, the 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 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, the volume of blood volume 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.