In general, all pathological changes that develop during acute blood loss should be considered compensatory and adaptive. Their essence can be expressed in one sentence. The body, reacting to blood loss, mobilizes all organs and systems to ensure its vital functions in these conditions.
The main starting point in the chain of pathogenetic changes observed during bleeding is a decrease in blood volume (hypovolemia). Acute hypovolemia is a powerful stress for the body. It is she who triggers neurovegetative and endocrine reactions, which result in changes in the body’s main life support systems (central hemodynamics, microcirculation, external respiration, morphological composition of blood, systems for ensuring general and tissue metabolism, general nonspecific reactivity of the body and immunogenesis).
To understand the processes occurring in the body, one should remember the components of the bcc and the normal distribution of blood in the body.
80% of the blood is in the vascular bed, 20% in the parchymatous organs. Venous vessels contain 70-80% of circulating blood, 15-20% in arteries and only 5-7.5% in capillaries. 40-45% of the bcc are formed elements, 55-60% plasma.
In response to a decrease in blood volume, compensatory reactions are activated, aimed at its immediate restoration, and only after this are mechanisms correcting blood quality activated. Compensatory mechanisms are included in all functional systems body. At the beginning, the tone of the sympathetic system increases, and the secretion of catecholamines increases. As a result, changes occur in the circulatory system.
Circulatory system. In response to blood loss, the following mechanisms are activated in the circulatory system.
A decrease in BCC leads to a decrease blood pressure. Due to irritation of baro-, chemo-, and volume receptors of the heart and large vessels, vascular reflex reactions develop. At the same time, the sympatho-adrenal system is stimulated. As a result, the following processes develop.
1. Venospasm.
Initially, venous spasm develops. Veins have a well-developed motor mechanism, which allows you to quickly adapt the capacity of the venous system to a changed blood volume. As indicated, the veins contain 70-80% of the bcc. Due to venous spasm, the venous return to the heart remains the same, the central venous pressure is within normal indicators. However, if blood loss continues and reaches 10%, this compensatory mechanism no longer ensures the preservation of the value of venous return and it decreases.
2. Tachycardia.
Decreased venous return leads to decreased cardiac output. These shifts are compensated by increasing the heart rate. During this period, an increase in tachycardia is characteristic. Therefore, the cardiac output remains at the same level for a long time. A decrease in venous return to 25-30% is no longer compensated by an increase in heart rate. Low output syndrome (decreased cardiac output) develops. To maintain adequate blood flow, the following compensation mechanism begins to work—peripheral vasoconstriction.
3. Peripheral vasoconstriction.
Thanks to peripheral arteriolospasm, the pressure is maintained above the critical level. First of all, the arterioles of the skin, abdominal cavity and kidneys narrow. The cerebral and coronary arteries are not subject to vasoconstriction. The phenomenon of centralization of blood circulation is developing.” Peripheral vasoconstriction
This is a transitional stage from compensatory reactions to pathological ones.
4. Centralization of blood circulation.
By centralizing blood circulation in the brain, lungs and heart, adequate blood flow is ensured to maintain the vital functions of these organs.
In addition to the reaction of the vascular bed, other compensatory mechanisms are also triggered.
5. Influx of tissue fluid.
The consequence of compensatory restructuring of hemodynamics is a decrease in hydrostatic pressure in the capillaries. This leads to the transition of intercellular fluid into the vascular bed. Thanks to this mechanism, the bcc can increase to 10-15%. The influx of fluid leads to hemodelution. Developing hemodelution improves the rheological properties of the blood and promotes the leaching of red blood cells from the depot, increasing the number of circulating red blood cells and the oxygen capacity of the blood.
b. Oligouria.
One of the reactions to developing hypovolemia is the retention of fluid in the body. In the kidneys, the reabsorption of water and the retention of sodium and chloride ions increase. Oligouria develops.
Thus, all compensatory reactions are aimed at eliminating the discrepancy between the volume of circulating blood and the capacity of the vascular bed.
Other systems also take part in compensatory reactions.
Respiratory system. In response to blood loss, the body reacts by developing hyperventilation, which helps to increase venous return to the heart. When you inhale, the filling of the right ventricle and pulmonary vessels increases. Pulsus paradoxus may be detected, reflecting changes in hemodynamics depending on respiratory movements.
Blood system. The mechanisms of erythropoiesis are turned on. New, including insufficiently mature red blood cells enter the bloodstream. The coagulation system responds with hypercoagulation.
Ongoing bleeding cannot be compensated indefinitely due to the adaptive reactions of the body. Increasing blood loss leads to the progression of hypovolemia, decreased cardiac output, disruption of the rheological properties of blood, and its sequestration. A vicious hypovolemic circle is formed.
Decentralization of blood circulation.
Centralization of blood circulation leads to a decrease in blood flow in many organs (liver, kidneys, etc.). As a result, acidosis develops in the tissues, which leads to the expansion of capillaries and sequestration of blood in them. Sequestration leads to a decrease in BCC by
10% or more, which leads to loss of effective blood volume and uncontrollable hypotension.
Violation of the rheological properties of blood.
Microcirculation disorders in tissues are accompanied by local hemoconcentration, blood stasis, and intravascular aggregation of formed elements (“sludge” of formed elements). These disorders lead to blockage of capillaries, which increases blood sequestration.
Metabolic disorders.
Pathological changes in hemodynamics, microcirculation and rheological properties of blood lead to impaired perfusion and tissue hypoxia. Metabolism in tissues becomes anaerobic. Metabolic acidosis develops, which in turn aggravates microcirculation disorders and organ function. Changes affect all organs and systems, and multiple organ failure develops.
Hemorrhagic shock
Massive blood loss in the later stages leads to the development of hemorrhagic shock. Hemorrhagic shock is multiple organ failure resulting from unreimbursed or untimely compensated blood loss. It is customary to distinguish three stages of hemorrhagic shock:
Stage 1 – compensated reversible shock
Stage 2 – decompensated reversible shock
Stage 3 – irreversible shock.
Compensated, shock - the volume of blood loss is compensated by changes in cardiovascular activity of a functional nature.
Uncompensated shock – there are deep circulatory disorders, reactions of cardio-vascular system functional nature cannot maintain central hemodynamics and blood pressure, decentralization of blood flow develops.
Irreversible hemorrhagic shock - there are deeper circulatory disorders that are irreversible, and multiple organ failure is aggravated.
Or anemia is a syndrome caused by a decrease in red blood cells and hemoglobin in a unit of circulating blood. True anemia, which must be distinguished from hemodilution caused by massive transfusion of blood substitutes, is accompanied by either an absolute decrease in the number of circulating red blood cells or a decrease in the content of hemoglobin in them.
The acute anemia syndrome, with the exception of some features, is of the same type: euphoria or depression of consciousness, pallor skin, tachycardia - initial manifestations of hemorrhagic shock; dizziness, flashing “spots” before the eyes, decreased vision, tinnitus; shortness of breath, palpitations; Auscultation - a “blowing” systolic murmur at the apex. As anemia increases and compensatory reactions decrease, blood pressure progressively decreases; tachycardia increases. According to the classification of I.A. Kassirsky distinguishes 3 types of anemia: 1) posthemorrhagic; 2) hemic - due to impaired blood formation; 3) hemolytic - due to the destruction of red blood cells. In addition, they distinguish: acute, chronic and acute against the background of chronic anemia.
Classification of blood loss
By volume, blood loss is divided into 3 degrees, which determine its severity: I - up to 15% of the bcc - mild; II - from 15 to 50% severe; III, blood loss of more than 50% is considered prohibitive, since with such blood loss, even with its immediate replacement, irreversible changes are formed in the homeostasis system.
Symptoms of blood loss
To the heaviness clinical manifestations and the outcome of blood loss is influenced by many factors. The most important are:
1) the age of the patient - children, due to imperfect compensation mechanisms, and elderly people, due to their exhaustion, endure even small blood loss very hard;
2) the rate of blood loss is greater, the more powerful the bleeding, the faster the compensation mechanisms are depleted, therefore arterial bleeding is classified as the most dangerous; 3) place of blood effusion - intracranial hematomas, hemopericardium, pulmonary hemorrhages do not cause large blood loss, but are the most dangerous due to severe functional disorders; 4) the person’s condition before bleeding - anemic conditions, vitamin deficiency, chronic diseases lead to rapid functional decompensation even with low blood loss.
The circulatory system makes up 0.6 body weight, i.e. 4-6 l. Its distribution in the body is uneven. Up to 70% of the bcc is contained in the veins, in the arteries - up to 15%, capillaries include up to 12% of the blood and only 3% is in the chambers of the heart. Hence, the venous system has the maximum compensatory capacity for blood loss. We will consider the compensatory reaction in a person who was healthy before hemorrhage.
Blood loss of up to 500 ml is easily and immediately compensated by minor venous spasm, without causing functional disorders (therefore, donation is absolutely safe).
Blood loss causes irritation of volume receptors, which leads to their persistent and total spasm. Hemodynamic disorders do not develop in this case. Blood loss in 2-3 days is compensated by activating one’s own hematopoiesis. Therefore, unless there are special reasons for this, it makes no sense to interfere with the bloodstream by transfusion of solutions and additionally stimulate hematopoiesis.
When blood loss exceeds a liter, in addition to irritating the volume receptors of the veins, the alpha receptors of the arteries are irritated, which are present in all arteries, with the exception of the central ones, which provide blood flow to vital organs: the heart, lungs, and brain. The sympathetic is excited. nervous system, the function of the adrenal glands is stimulated (neurohumoral reaction) and the adrenal cortex releases a huge amount of catecholamines into the blood: adrenaline - 50-100 times higher than normal, norepinephrine 5-10 times. As blood loss increases, this first causes a spasm of the capillaries, then mflkus and increasingly larger ones, except for those where there are no alpha receptors. The contractile function of the myocardium is stimulated with the development of tachycardia, the liver also contracts with the release of blood from the depot, and arteriovenous shunts open in the lungs. All this is collectively defined as the development of circulatory centralization syndrome. This compensatory reaction allows you to maintain normal blood pressure and hemoglobin levels for some time. They begin to decrease only 2-3 hours after blood loss. This time is most optimal for stopping bleeding and correcting blood loss.
If this does not happen, hypovolemia and hemorrhagic shock develop, the severity of which is determined: by the level of blood pressure, pulse; diuresis and the content of hemoglobin and blood hematocrit. This is explained by the depletion of neuro-reflex compensation mechanisms: vasospasm is replaced by vasodilation with a decrease in blood flow in vessels of all levels with stasis of erythrocytes, impaired tissue metabolism and the development of metabolic acidosis. Stasis of red blood cells in the capillaries further increases blood loss by 12%.
The adrenal cortex increases the production of ketosteroids by 3.5 times, which activate the pituitary gland with an increase in the production of aldosterone. As a result of this, not only spasm of the renal vessels occurs, but also bypass arteriovenous shunts open, turning off the juxtoglomerular apparatus with a sharp decrease in diuresis, up to complete anuria. The kidneys are the first to indicate the presence and severity of blood loss, and the restoration of diuresis is used to judge the effectiveness of blood loss compensation. Hormonal changes block the exit of plasma from the bloodstream into the interstitium, which, with disruption of microcirculation, further complicates tissue metabolism, aggravates acidosis and multiple organ failure.
The developing adaptation syndrome in response to blood loss does not stop even with immediate restoration of blood volume. After replenishing blood loss: blood pressure remains reduced for another 3-6 hours, blood flow in the kidneys - 3-9 hours, in the lungs - 1-2 hours, and microcirculation is restored only on the 4-7th day. The complete elimination of all violations occurs only after many days and weeks.
Treatment of blood loss
Correction of acute blood loss begins only after temporary or final stop bleeding. Blood loss of up to 500 ml is considered physiological, and restoration of circulating blood volume (CBV) occurs independently.
With blood loss of up to a liter, this issue is approached differently. If the patient maintains blood pressure, tachycardia does not exceed 100 per minute, diuresis is normal - it is better not to interfere with the bloodstream and the homeostasis system, so as not to disrupt the compensatory-adaptive reaction. Only the development of anemia and hemorrhagic shock is an indication for intensive care.
In such cases, correction begins at the scene of the incident and during transportation. In addition to assessing the general condition, it is necessary to take into account blood pressure and pulse indicators. If blood pressure is kept within 100 mm Hg. Art. There is no need for transfusion of antishock drugs. When blood pressure drops below 90 mm Hg. drip transfusion of colloidal blood substitutes. Decrease in blood pressure below 70 mm Hg. Art. is an indication for jet transfusion of solutions. Their volume during transportation should not exceed one liter (otherwise it will be difficult for the resuscitator to navigate the volume of blood loss). It is advisable to use autotransfusion of blood by lifting it up lower limbs, since they contain up to 18% bcc.
When a patient is admitted to the hospital, it is impossible to urgently determine the true volume of blood loss. Therefore, paraclinical methods are used to approximate blood loss; since they largely reflect the state of the homeostasis system. A comprehensive assessment is based on the following indicators: blood pressure, pulse, central venous pressure (CVP), hourly diuresis, hematocrit, hemoglobin content, red blood cells.
Correction of the syndrome of acute anemia and hemorrhagic shock also falls within the competence of resuscitators. It is pointless to start it without stopping the bleeding; moreover, the intensity of the bleeding may increase.
The main criteria for replenishing blood loss are: stable blood pressure at 110/70 mm Hg. Art.; pulse - within 90 per minute; Central venous pressure at the level of 4-6 cm of water. Art.; blood hemoglobin at 110 g/l; diuresis over 60 ml per hour: In this case, diuresis is the most important. indicator of bcc recovery. By any means of stimulation: adequate infusion therapy, stimulation with aminophylline and lasix - urination should be restored within 12 hours. Otherwise, necrosis of the renal tubules occurs with the development of irreversible renal failure. Anemic syndrome is accompanied by hypoxia, forming the hemic form of hypoxic syndrome.
The article was prepared and edited by: surgeonBlood loss - a pathological process that occurs as a result of bleeding and is characterized by a complex set of pathological disorders and compensatory reactions to a decrease in the volume of circulating blood and hypoxia caused by a decrease in the respiratory function of the blood.
Etiological factors of blood loss:
Violation of the integrity of blood vessels (wound, damage by a pathological process).
Increased vascular wall permeability (VWP).
Decreased blood clotting (hemorrhagic syndrome).
There are 3 stages in the pathogenesis of blood loss: initial, compensatory, terminal.
Initial. BCC decreases - simple hypovolemia, cardiac output decreases, blood pressure drops, and circulatory hypoxia develops.
Compensatory. A complex of protective and adaptive reactions is activated, aimed at restoring bcc, normalizing hemodynamics, and oxygen supply to the body.
Terminal stage blood loss can occur due to insufficiency of adaptive reactions associated with serious diseases, under the influence of unfavorable exogenous and endogenous factors, extensive trauma, acute massive blood loss exceeding 50-60% of the blood volume and the absence of therapeutic measures.
In the compensatory stage, the following phases are distinguished: vascular reflex, hydremic, protein, bone marrow.
Vascular reflex phase lasts 8–12 hours from the onset of blood loss and is characterized by spasm of peripheral vessels due to the release of catecholamines by the adrenal glands, which leads to a decrease in the volume of the vascular bed (“centralization” of blood circulation) and helps maintain blood flow in vital important organs. Due to the activation of the renin-angiotensin-aldosterone system, the processes of sodium and water reabsorption in the proximal tubules of the kidneys are activated, which is accompanied by a decrease in diuresis and water retention in the body. During this period, as a result of an equivalent loss of blood plasma and formed elements, a compensatory flow of deposited blood into the vascular bed, the content of red blood cells and hemoglobin per unit volume of blood and the hematocrit value remain close to the original (“hidden” anemia). Early signs acute blood loss are leukopenia and thrombocytopenia. In some cases, an increase in the total number of leukocytes is possible.
Hydremic phase develops on the 1st–2nd day after blood loss. Manifested by the mobilization of tissue fluid and its entry into bloodstream, which leads to restoration of plasma volume. “Dilution” of blood is accompanied by a progressive decrease in the number of red blood cells and hemoglobin per unit volume of blood. Anemia is normochromic, normocytic in nature.
Bone marrow phase develops on the 4th–5th day after blood loss. It is determined by the intensification of erythropoiesis processes in the bone marrow as a result of overproduction by the cells of the juxtaglomerular apparatus of the kidneys, in response to hypoxia, of erythropoietin, which stimulates the activity of the committed (unipotent) erythropoiesis precursor cell - CFU-E. The criterion for sufficient regenerative capacity of the bone marrow (regenerative anemia) is an increase in the content of young forms of erythrocytes (reticulocytes, polychromatophils) in the blood, which is accompanied by a change in the size of erythrocytes (macrocytosis) and cell shape (poikilocytosis). It is possible that red blood cells with basophilic granularity may appear, and sometimes single normoblasts in the blood. Due to increased hematopoietic function of the bone marrow, moderate leukocytosis develops (up to 12×10 9 /l) with a shift to the left to metamyelocytes (less often to myelocytes), the number of platelets increases (up to 500×10 9 /l or more).
Protein compensation is realized due to the activation of proteosynthesis in the liver and is detected within a few hours after bleeding. Subsequently, signs of increased protein synthesis are recorded within 1.5-3 weeks.
Types of blood loss:
According to the type of damaged vessel or chamber of the heart:
arterial, venous, mixed.
By volume of lost blood (from bcc):
light (up to 20-25%), moderate (25-35%), severe (more than 35-40%).
According to the time of onset of bleeding after injury to the heart or vessel:
Primary – bleeding begins immediately after injury.
Secondary – bleeding is delayed in time from the moment of injury.
According to the place of bleeding:
External – hemorrhage into the external environment.
Internal - hemorrhage in the body cavity or organs.
The outcome of bleeding is also determined by the state of the body's reactivity - the perfection of adaptation systems, gender, age, concomitant diseases, etc. Children, especially newborns and infants, endure blood loss much more severely than adults.
A sudden loss of 50% of blood volume is fatal. Slow (over several days) blood loss of the same volume of blood is less life-threatening, since it is compensated by adaptation mechanisms. Acute blood loss up to 25–50% of the bcc is considered life-threatening due to the possibility of developing hemorrhagic shock. In this case, bleeding from the arteries is especially dangerous.
Restoration of erythrocyte mass occurs within 1–2 months, depending on the amount of blood loss. At the same time, the reserve fund of iron in the body is consumed, which can cause iron deficiency. Anemia in this case acquires a hypochromic, microcytic character.
The main dysfunctions of organs and systems during acute blood loss are presented in Fig. 1
Figure 1. – Main dysfunctions of organs and systems during acute blood loss (according to V.N. Shabalin, N.I. Kochetygov)
Continued bleeding leads to depletion of the body's adaptive systems involved in the fight against hypovolemia - develops hemorrhagic shock. In this case, the protective reflexes of the macrocirculatory system are no longer sufficient to ensure adequate cardiac output, as a result of which systolic pressure quickly drops to critical figures (50-40 mm Hg). The blood supply to the organs and systems of the body is disrupted, oxygen starvation develops and death occurs due to paralysis of the respiratory center and cardiac arrest.
The main link in the pathogenesis of the irreversible stage of hemorrhagic shock is decompensation of blood circulation in the microvasculature. Disruption of the microcirculation system already occurs at early stages development of hypovolemia. Prolonged spasm of capacitive and arterial vessels, aggravated by a progressive decrease in blood pressure with incessant bleeding, sooner or later leads to a complete stop of microcirculation. Stasis sets in, and aggregates of red blood cells form in the spasmed capillaries. The decrease and slowdown in blood flow that occurs in the dynamics of blood loss is accompanied by an increase in the concentration of fibrinogen and globulins in the blood plasma, which increases its viscosity and promotes the aggregation of red blood cells. As a result, the level of toxic metabolic products increases rapidly and becomes anaerobic. Metabolic acidosis is compensated to a certain extent by respiratory alkalosis, which develops as a result of reflexively occurring hyperventilation. Severe disturbances in vascular microcirculation and the entry into the blood of under-oxidized metabolic products can lead to irreversible changes in the liver and kidneys, and also have a detrimental effect on the functioning of the heart muscle even during a period of compensated hypovolemia.
Measures for blood loss
Treatment for blood loss is based on etiotropic, pathogenetic and symptomatic principles.
Anemia
Anemia(literally – anemia, or general anemia) is a clinical and hematological syndrome characterized by a decrease in hemoglobin content and/or the number of red blood cells per unit volume of blood. Normally, the content of erythrocytes in peripheral blood in men averages 4.0-5.0 × 10 12 / l, in women - 3.7- 4.7 × 10 12 / l; hemoglobin level is 130-160 g/l and 120-140 g/l, respectively.
Etiology: acute and chronic bleeding, infections, inflammation, intoxication (salts of heavy metals), helminthic infestations, malignant neoplasms, vitamin deficiencies, diseases of the endocrine system, kidneys, liver, stomach, pancreas. Anemia often develops with leukemia, especially in its acute forms, and with radiation sickness. In addition, pathological heredity and disorders of the body’s immunological reactivity play a role.
General symptoms: pallor of the skin and mucous membranes, shortness of breath, palpitations, as well as complaints of dizziness, headaches, tinnitus, discomfort in the heart area, severe general weakness and fatigue. In mild cases of anemia, general symptoms may be absent, since compensatory mechanisms (increased erythropoiesis, activation of the functions of the cardiovascular and respiratory systems) provide the physiological need of tissues for oxygen.
Classification. The existing classifications of anemia are based on their pathogenetic characteristics, taking into account the characteristics of the etiology, data on the content of hemoglobin and red blood cells in the blood, the morphology of red blood cells, the type of erythropoiesis and the ability of bone marrow to regenerate.
Table 1. Classification of anemia
|
Criteria |
Types of anemia |
|
I. For reason |
Primary Secondary |
|
II. By pathogenesis |
Posthemorrhagic Hemolytic Dyserythropoietic |
|
III. By type of hematopoiesis |
Erythroblastic Megaloblastic |
|
IV. According to the ability of the bone marrow to regenerate (by the number of reticulocytes) |
Regenerative 0.2-1% reticulocytes Aregenerative (aplastic) 0% reticulocytes Hyporegenerative< 0,2 % ретикулоцитов Hyperregenerative > 1% reticulocytes |
|
V. By color index |
normochromic 0.85-1.05 hyperchromic >1.05 hypochromic< 0,85 |
|
VI. By red blood cell size |
Normocytic 7.2 - 8.3 µm Microcytic:< 7,2 мкм Macrocytic: > 8.3 - 12 µm Megalocytic: > 12-15 µm |
|
VII. According to the severity of development |
|
Acute blood loss- the severity of the condition depends on the amount of blood lost, the rate of blood loss in the initial state of the body, age, gender, function of the cardiovascular system and other factors. Blood loss leads to hemodynamic disorders, microcirculation, anemia, hypoxemia and hypoxia.
Acute blood loss may be due to internal bleeding (with a disturbed ectopic pregnancy, rupture of the liver, spleen, into the lumen gastrointestinal tract etc.), external (in case of injuries to large vessels, open bone fractures and soft tissue injuries), as well as due to hematomas during closed fractures(pelvis, thighs, lower legs, etc.).
With multiple fractures of the pelvic bones, blood loss can reach 1500-2000 ml, hip fractures - 800-1200 ml, tibia - 350-650 ml.
Symptoms. Sharp progressive pallor of the skin and visible mucous membranes. The face is haggard, the features are pointed. Complaints of weakness, tinnitus, thirst, weakened vision, flickering and darkening in the eyes. Breathing initially becomes more frequent, and then its rhythm may be disrupted. The pulse is frequent, the filling is weak, and arterial and venous pressure decreases. A threatening symptom is the appearance of yawning (a sign of oxygen starvation). In the terminal period, loss of consciousness and disappearance of the pulse are observed, then the pupils dilate, and convulsions are possible.
Diagnosis. It is established based on the patient’s history and complaints, external examination data, pulse rate and SBP value.
Rice. 1. Points of finger pressure of arteries:
1 - temporal; 2 - mandibular; 3 - sleepy; 4 - subclavian; 5 - elbow; 6 - radial; 7 - shoulder; 8 - axillary; 9 - femoral; 10 - popliteal; 11 - dorsum of the foot; 12 - posterior tibial
The fact that the SBP as a result of bleeding is below 100 mm Hg. Art., indicates hemorrhagic shock. The classification of hemorrhagic shock by degree is similar to the degree classification traumatic shock according to Kiss (Keith) (see).
Urgent Care
. For external bleeding, depending on its nature, a temporary stop of bleeding is indicated by using a pressure bandage (for venous bleeding), pressing the vessel at certain points (Fig. 1), applying an elastic bandage or tourniquet (for damage to large vessels). A tourniquet is applied to the limb above the bleeding site for a period of no more than 2 hours in summer and 1 hour in winter. The tourniquet should not be applied directly to the surface of the body, but on top of a soft pad (napkins, towels, etc.) with a force sufficient to compress arterial vessel, however, without excessive, damaging soft fabrics efforts. A tourniquet that is not applied tightly enough only compresses the veins, without compressing the damaged artery, and thereby increases bleeding.
Internal bleeding in cases of damage to the abdominal organs and pelvic bones can be slowed down by applying a special inflatable anti-shock (pneumatic) suit. However, the final stop of bleeding is possible only surgically in a hospital setting. In this regard, victims, even with suspected internal bleeding, need urgent delivery to surgery department to completely stop bleeding.
Main therapeutic measures on prehospital stage for patients with acute blood loss, temporary stoppage of bleeding and replacement of blood loss are indicated. The latter is indicated when the pulse rate is over 100 beats per minute and the SBP falls below 90 mm Hg. Art. To replenish blood loss, colloidal and crystalloid solutions are used.
The administration of vasoactive agents (norepinephrine, dopamine) is permissible only in critical situations when infusion therapy fails to raise SOD above critical (70 mm Hg) and ensure satisfactory blood supply to vital organs (see).
With ongoing internal bleeding, to maintain blood pressure at a subcritical level (70 mm Hg. Art.), intravenous infusion plasma-substituting solutions at a rate of 80-120 drops per minute simultaneously with rapid delivery of the victim to the hospital in a position with the head end down. The use of hypertensive drugs in this case is contraindicated.
Hospitalization: urgent to the surgical hospital in a lying position on a stretcher.
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 severe complications 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.).
The specific cause of hypovolemic shock due to loss whole blood can be:
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, sharp decline the need for both bcc and oxygen delivery, an increase in respiratory rate, cardiac output, return and utilization of oxygen 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-adrenoreceptors localized in the myocardium has positive ionotropic and chronotropic effects, stimulation of p2-adrenoreceptors 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 osmotic pressure blood plasma, leading to increased reabsorption of sodium and water, decreased diuresis and increased intravascular fluid volume. 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 impair permeability 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 soon reduces the time of diastolic filling 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 increased permeability vascular wall with 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, 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 one to estimate the amount of blood loss 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, evaluates 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. C-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, 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.
General principles Treatments for 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 metabolic processes in a cage;
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.
| Minimum | Average | Means. | Heavy. | Arrays | |
| BP sys. | 100–90 | 90–70 | 70–60 | ‹60 | ‹60 |
| Heart rate | 100–110 | 110–130 | 130–140 | ›140 | ›140 |
| Algover Index | 1–1,5 | 1,5–2,0 | 2,0–2,5 | ›2.5 | ›2.5 |
| Volume of blood flow.ml. | Up to 500 | 500–1000 | 1000–1500 | 1500–2500 | ›2500 ml |
| V bloody (ml/kg) | 8–10 | 10–20 | 20–30 | 30–35 | ›35 |
| % loss of bcc | <10 | 10–20 | 20–40 | ›40 | >50 |
| V infusion (% of loss) | 100 | 130 | 150 | 200 | 250 |
| Hemotr. (% of V infusion) | - | 50–60 | 30–40 | 35–40 | 35–40 |
| Colloids (% V inf.) | 50 | 20–25 | 30–35 | 30 | 30 |
| Crystalloids (% V infusion) | 50 | 20–25 | 30–55 | 30 | 30 |
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
Fight with pain syndrome, defence from mental stress carried out by intravenous (i.v.) administration of analgesics: 1–2 ml of 1% solution of morphine hydrochloride, 1–2 ml of 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 sub-narcotic doses of calypsol and sedation with propofol. The dose of narcotic analgesics should be reduced by 50% due to possible respiratory depression, nausea and vomiting that may occur during intravenous administration 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 both at the utilization of oxygen by tissues and at 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.
Whenever respiratory failure The main goals of treatment are:
1. ensuring cross-country ability respiratory tract;
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 during breathing pure oxygen);
3. intrapulmonary blood shunting (protected by breathing pure oxygen) caused by adult respiratory distress syndrome (PaO2 ‹ 60–70 mm Hg. FiO2 › 50%, bilateral pulmonary infiltrates, normal pressure ventricular filling), 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 protein fraction plasma effectively increases 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 last years There were separate randomized studies of a high level of evidence (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
| Blood replacement level | Amount of blood loss | Total volume of transfusion (% of blood loss) | Perftoran dose |
| I | To 10 | 200–300 | Not shown |
| II | 11–20 | 200 | 2–4 ml/kg body weight |
| III | 21–40 | 180 | 4–7 ml/kg body weight |
| IV | 41–70 | 170 | 7–10 ml/kg body weight |
| V | 71–100 | 150 | 10–15 ml/kg body weight |
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 for severe metabolic acidosis (pH venous blood below 7.25), calculating it using the generally accepted formula, after determining the 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.
U 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 a 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 own negative sides. 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 settled 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 donations, 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.
