Acute blood loss classification. Symptoms of acute and slow blood loss. Clinical characteristics of acute blood loss. On clinical manifestations
I. By origin (etiology):
a) traumatic;
b) Non-immature (neurotrophic).
T R A V M and T and C E C and E of Bleedings are due to the mechanical cause (operations, fractures, lighting of tissues, etc.). Bleeding should be attributed to this group, the reason for which the change in blood or atmospheric pressure was. Sudden increase in blood pressure, for example, when choking, squeezing chest, with strong cough, convulsions are manifested by hemorrhages in the connecting shell of the eye, into the mucous membranes, etc., when the atmospheric pressure decreases, the bleeding is observed, for example, when used cans in the form of point hemorrhages, bleeding from ears, nose, bronchi, in joints with fast Transition from reduced pressure To normal from working in the caissons. Bleeding can occur in the sudden closure of the gloss of the artery thrombus or an emboss with heart attacks. With sclerotic phenomena in the arteries, the increase in pressure in them often leads to breaking the wall of the vessel and blood-violations into the brain. An increase in venous pressure may cause bleeding from the veins of the rectum and trophic Yazv lower limbs.
It is determined by changes in the permeability of the vascular wall, which is based on the presence of pronounced intoxication of the body, accompanied by a pathological impulse, leading to the expansion of the vascular wall and slowing blood flow. These bleeding can be observed with some infectious diseases (Scarlatina, OSP, etc.), septic processes, toxic changes in exogenous blood vessels (benzene poisoning, phosphorus, etc.), toxic changes in endogenous vessels (autoinoxication), for example, under Uremia. In the same group, bleeding during Khabemi can be attributed, which leads to the development of hepatic insufficiency and to a sharp decrease in blood coagulation. Operational interventions against the background of the deficiency of vitamins C, K, PP groups can also be accompanied by severe bleeding. The same bleeding can be observed in hemophilia, which is characterized by a sharp decrease in blood coagulation.
II. According to the mechanism of emergence:
a) from the rupture (haemorrhagia per rhexin);
b) from corrosion - Arrosive (Haemorrhagia Per Diabrosin);
c) from leakage (Haemorrhagia Per Diapedesin).
III. By type of bleeding vessel:
a) arterial;
b) venous;
c) mixed (arteriovenous);
d) capillary;
e) parenchymal.
A rve r and a l n o e bleeding is most dangerous for the victim, because at the time of a short period of time, a large amount of blood flows from the bloodstream. Loading with assistance in such cases can lead to human death. In easier cases, the threat of a different nature occurs: the death of the limb, the delivery of blood to which due to damage to the arterial line almost completely stops. 8-10 hours is such a critical threshold tolerability by tissues of distress. If there is no help during this time, gangrene develops. For arterial bleeding Blood beats a jet, the height of which is changing with each pulse wave. Blood color is bright red due to saturation of it with oxygen. In the absence of collaterals, blood flows out of the proximal end of the damaged artery, if there are such bleeding both ends.
It is in contrast to blood bleeding, in contrast to arterial, it is characterized by continuous flowing of a jet of blood from a damaged vessel having a darker color. Venous bleeding occurs mainly from the peripheral end of the damaged vessel. If a large vein lies next to the artery, it can be observed periodically intensifying bleeding, synchronous with a pulse. When bleeding from the veins, swaying close to the heart, there is an influence of the respiratory phases: when inhalation, due to the suction effect of the chest, the bleeding decreases, and during the exhalation the blood pressure in the veins increases and the bleeding is enhanced, i.e. Acquires synchronous breathing type. At the same time, the bleeding will be from the central end of the vein. Damage to large veins of the neck and chest is dangerous due to the possibility of an air embolism. Cases of air embolism are observed and when injected venous sinuses solid cerebral shell.
K and P and L L I R N O E bleeding occurs when the skin wounds, muscles, mucous membranes, bones. It is more often mixed with bleeding from small arteries and veins. With an external inspection, the impression is that all the fabric is bleeding. Capillary bleeding, as a rule, stops independently. Its duration increases significantly with reduced blood coagulation.
Powered Bleeding is observed in damage to parenchymal organs - liver, spleen, kidney, lung. These bleeding are similar to capillary, but more dangerous of them, since the vessels of these organs do not fall as a result of them anatomical structure (associated with a stroma organ). Often these bleeding is impossible to stop mechanical methods. Therefore, biological methods or removal of the organ apply.
IV. At the place of blood outpouring:
a) external;
b) internal;
c) hidden.
N and R y N o e bleeding - blood is poured directly to the surface of the human body through the defect of its skin.
The most diverse in nature and complex in the diagnostic and tactical relationship is a group of mixture. They are characterized by the expiration of blood in the cavity of the body, not related to the external environment, as well as in various fabrics. At the same time distinguish hidden bleeding, in which there are no obvious signs of bleeding. They can be detected by special research methods. Hidden bleeding in fabric (intra-duty, intestinal, intraosteny) or hemorrhages may heat tissues (then they speak of hemorrhagic infiltration) or to form accumulations of the washing blood in the form of hematoma. Bleeding in the cavity rarely stop independently. This is because, for example, in the cavity of the pleura there is a negative pressure, and serous cavity shells have the ability to delay blood coagulation.
V. By the time of emergence:
a) primary;
b) secondary (early, late, recurrent or repeated).
The first bleeding start immediately after injury, breaking the vessel.
It is beginning in the first hours and a day (before the development of infection in the wound) and are associated with pushing the blood cloth from the damaged vessel or relaxation of the vessel, which was previously resuming.
Later in T o p and ch is arise at any time after the development of infection in the wound and caused by purulent melting of thrombus, arrosion, melting the vascular wall.
Thus, the causes of secondary bleeding can be:
a) insufficient cessation of bleeding (ligatur scaling);
b) raising blood pressure after surgery (especially parenchymal bleeding);
c) frequent traumatic dressings (after burns, etc.);
d) a change in the chemical composition of blood (transfusion, avitaminosis, an increase in enzymatic activity, a decrease in coagulation);
e) a purulent-septic state (rotary, anaerobic infection);
e) thrombus melting under the influence of proteolytic enzymes of bacterial origin;
g) the decay of the malignant tumor.
Vi. Localization: Depending on the anatomotopographic area, which has bleeding.
VII. Clinical manifestation:
a) continued;
b) stopped.
VIII. Clinical manifestation and localization: hemochkali (haempto), bloody vomiting (haemotemesis), uterine bleeding (metrorrhagia), bleeding in the urinary stripe system (haematuria), bleeding in the gastrointestinal lumen - tar bleeding chair (Epistasis) ).
IX. By the magnitude of blood loss:
a) light (blood loss up to 20% of the volume of circulating blood);
b) middle severity (blood loss from 20% to 30% of circulating blood volume);
c) severe (blood loss over 30% of circulating blood volume). It can be compensated, decompensated and irreversible.
The reaction of the body for bleeding. Factors contributing to self-stop bleeding. Exodes of bleeding (posthemorrhagic anemia, hemorrhagic shock).
The reaction of the body to bleeding depends on:
ü volume of blood loss,
ü intensity
ü Duration of blood expiration.
When bleeding primarily reacts the control system of the aggregate state of the blood, which under conditions of bleeding provides thrombosis in damaged vessels, and also contributes to the connecting components in creating the possibility for healing damaged organs and tissues. This system includes:
a) central bodies - bone marrow, liver, spleen;
b) peripheral formations - fat cells, endothelium capillaries, blood cells;
c) local system regulators - reflexogenic zones of vessels with chemoreceptors, heart, lungs, kidneys, uterus, prostate gland, digestive organs;
d) central regulators - glands of internal secretion (adrenal glands, pituitary thyroid et al.), Vegetative nervous system, subcortical and cortical structures of the brain.
Bleeding:
ü Creating hemostatic potential - the integral properties of blood maintain a liquid state in normal and in the pathology of blood coagulation and coagulation (stop the blood flow) in certain, more often extreme states.
ü In response to bleeding, the rate of blood flow is reduced in a damaged injury or any pathological process of a blood vessel.
ü reflexive means activation of the coagulation properties of blood with the formation of a thrombus in the place of damage to the vascular wall.
ü In the future, the clutch is reduced and sealing (retraction), and then full or partial dissolution (fibrinolysis).
ü When bleeding from large arteries, the spontaneous stop of bleeding is less possible mainly due to the greater blood flow rate. The spontaneous stop of the bleeding is more often observed with complete breaks of vessels. In these cases, there is a reflex spasm of a damaged vessel, the intima octo inside the lumen and the formation of the thrombus.
ü Stopping bleeding is possible and as a result of increasing pressure in the tissues. Often, hemostasis occurs due to the compression of a damaged vessel with a hematoma, especially with a stored fascial case and a narrow sore wagon channel, the lumen of which is usually filled with blood clots.
A starting mechanism causing pathological and compensatory changes in the body as a result of bleeding is reduced by the volume of circulating blood. Blood lodge leads to the development of circulatory hypoxia. In order to compensate for the phenomena of circulatory hypoxia resulting from bleeding, the body occurs:
a) the redistribution of blood and the preservation of blood flow in vital organs by reducing the blood supply to the skin, digestive organs and muscles;
b) restoration of the volume of circulating blood as a result of the inflow of the interstitial fluid into the bloodstream;
c) an increase in cardiac output and oxygen utilization coefficient when the volume of circulating blood is restored.
The last two processes contribute to the transition of circulatory hypoxia into anemic, which is less danger and is easier compensated by therapeutic measures.
Chopping blood coagulation is accelerated, despite the decrease in the number of platelets and the fibrinogen content. At the same time, the fibrinolytic activity of blood increases. Improving the tone of the sympathetic part of the vegetative nervous system and the enhanced emission of adrenaline contribute to the acceleration of blood coagulation. In this case, there are changes in the components of the blood coagulation system. The adhesiveness of platelets increases and their ability to aggregation, the consumption of prothrombin, the concentration of thrombin, the content of the VIII factor (anti-emophilic globulin), but decreases the content of the antihemophilic factor in globulin. A tissue thromboplastin tissue thromboplastin comes into the blood, and an anti-fertile factor is made of destroyed erythrocytes.
In severe cases, when blood loss, the development of intravascular blood coagulation is possible, due to a combination of two factors: slowdown blood flow in capillaries and an increase in the blood content of proagulants.
Symptomatology of bleeding. Methods for determining the volume of blood loss.
Subjective symptoms: Dizziness, dry mouth, thirst, nausea, darkening in eyes, increasing weakness, noise in the ears, headache and pain in the heart area, suffocation. These patient complaints are the result of a violation of the blood supply to the internal organs and, first of all, the brain.
Objective symptoms: The pallor and humidity of the skin, the face, frequent and weak pulse, rapid breathing, in severe cases, the breath of Chein-Stokes, a decrease in venous and arterial pressure, excitement, euphoria, loss of consciousness.
However, with slow bleeding, clinical manifestations may not correspond to the amount of blood lost. It is important to determine the magnitude of bloodstures that, along with a stopping of bleeding, is crucial for the choice of therapeutic tactics. Determination of the content of erythrocytes, hemoglobin, hematocrit should be made immediately upon receipt of the patient and repeat later.
The use of subjective information, objective external signs and laboratory relative indicators can only be given indicative data on blood loss. Even the hematocritum, the relative density of blood and plasma, studied in the first hours after the start of bleeding, do not reflect the true sizes of blood loss, since the bloodstream remaining in the body is not immediately exposed, but only after a few hours and this maximum process reaches 1,5- 2 days. Therefore, if 24 hours have passed from the beginning of bleeding and more, when a significant reduction in the mass of circulating blood and its hemodilution, the amount of erythrocytes, the hemoglobin level, the hematroral number, the relative density of blood and plasma may reflect the degree of anemia and be used to determine the degree of anemia blood loss. When using the indicators of these studies and clinical data, three degrees of blood loss can be distinguished (Table 1).
The severity of blood loss (Gorbashko AI, 1982).
Blood loss called the process whose development occurs as a result bleeding. It is characterized by a combination of adaptive and pathological reactions of the organism to reduce blood volume in the body, as well as a lack of oxygen (), which was caused by a decrease in the transport of this substance with blood.
The department was founded in 1986.
The department conducts training of cadet doctors and interest doctors in three specialties: "Anesthesiology", "Children's anesthesiology", "Medicine of urgent states" at 5 clinical bases: 6th, 11th, 16th city clinical hospitals, urban clinical Hospital emergency medical care and regional children's clinical hospital. The department employs 2 professors: the laureate of the State Prize in the field of science and technology, D.M., Professor E.N. Kligunhenko and D.N. Professor Bonisar V.I., 4 associates and 3 assistants who have a scientific degree of candidate of medical sciences.
For training doctors-cadets and interests, staff members use modern techniques and simulators.
The department operates in round-the-clock access mode 2 of computer class, 2 video systems with 25 educational videos.
Cadets and Interns have the opportunity to use literature stored in the department of the department in training. The latter is equipped with copying appliances, subscription sets of magazines in three specialties, textbooks and teaching benefits (There are more than 550 literary sources in the list).
International ties of the Department are expressed in conducting with German colleagues from Bonn University of Friedrich Wilhelm (Head of Doctor of Medical Sciences Professor Yoachim Proldevka) Teaching doctors with new super-modern technologies.
So, since 2003, on the basis of the department, multidisciplinary courses (master classes) are held on the topic "Special anesthesiology, taking into account the anatomical prerequisites."
Scientific interests of the department affect issues of improving emergency care technologies and standardization of therapy, pain relief critical adults and children. Since 2004, the department proceeds to the implementation of the scientific topic "The rationale and development of organoprotective technologies of anesthesia and intensive therapy (including using HBO, plasma substitutes with a function of oxygen transfer, ozone) in patients of different age categories in critical states."
^ Lecture: Topic: Acute blood loss.
Kliguenko Elena Nikolaevna, D.M., Laureate of the State Prize in Science and Technology, Professor, Head of the Department of Anesthesiology, Intensive Therapy and Medicine of Emergency States of the FPO Dnepropetrovsk State Medical Academy
Under blood loss Understand the condition of the body that arises after the bleeding and characterized by the development of a number of adaptive and pathological reactions. Increased interest in the problem of blood loss is due to the fact that almost all surgical profile specialists meet with it quite often. In addition, the indicators of mortality with blood loss to the present remain high.
The severity of the blood loss is determined by its type, speed of development, the volume of lost blood, the degree of hypovolemia and the possible development of shock, which is most fully reflected in the classification of P.G. Brysov, widely used in our country (Table 1).
^ Table 1.
Classification of blood loss (A.G. Bryusov, 1998).
Abroad has widespread classification Bloodstocks, developed by the American College of Surgeons in 1982, on which 4th grade bleeding is distinguished (Table 2)
^ Table 2.
Classification of bleeding of the American College of Surgeons
(P. L.Marino, 1998)
Class I. - corresponds to the loss of 15% of the volume of circulating blood (BCC) or less. At the same time, clinical symptoms are missing or only orthostatic tachycardia (CSS in the transition from the horizontal position to the vertical increases by 20 or more ud. / Min.).
Class II. - Corresponds to a loss of 20 to 25% OCC. The main clinical sign is orthostatic hypotension or decrease in blood pressure during the transition from the horizontal position to vertical to 15 or more MM RT. Art. Diuresis is saved.
^ Class III - It is consistent with a loss of 30 to 40% OCC. The hypotension is manifested in the position lying on the back, Oligira (urine less than 400 ml / day).
Class IV - Loss of more than 40% OCC. It is characterized by a collapse (extremely low blood pressure) and a violation of consciousness up to coma.
Thus, shock is inevitably developing with a loss of 30% of the BCC, and the so-called "threshold of death" is determined not the volume of deadly bleeding, but the number of erythrocytes remaining in circulation. For erythrocytes, this reserve is 30% of globular volume, for plasma - only 70%. In other words, the body can survive with the loss of 2/3 of circulating erythrocytes, but will not transfer the loss of 1/3 of the plasma volume. This is due to the specifics of compensatory mechanisms developing in response to blood loss and clinically manifested by hypovolemic shock.
Under shock understand the syndromocomplex, which is based on inadequate capillary perfusion with reduced oxygenation and disturbed metabolism of tissues and organs, and under hypovolemic shock In particular, they understand the acute cardiovascular insufficiency, which developed as a result of a significant deficiency of the CCC.
Shock is a consequence of a decrease in efficient BCC (i.e., the relationship of the BCC to the capacity of the vascular bed) or the consequence of the deterioration of the pumping function of the heart, which may occur during hypovevolemia of any genesis, sepsis, injuries and burns, heart failure or reduction of sympathetic tone. The specific reason for the hypovolemic shock with the loss of solid blood can be:
gastrointestinal bleeding;
Urban bleeding;
intra-abdominal bleeding;
uterine bleeding;
bleeding into the retroperitoneal space;
aortic aneurysm rupture;
injury.
minute heart (Mos):
MOS \u003d WOS CHCS,
Where: WSA is the impact volume of the heart, and the heart rate is the frequency of heart abbreviations);
cardiac rhythm;
pressure filling of the heart cavities (preload);
cardiac valve function;
Common peripheral vascular resistance (OPS) - postload.
Under acute blood loss, the deficiency of the BCC, the filling pressure in the head cavities is initially reduced, as a result of which the WOS, Mos and blood pressure (blood pressure) are compensatory. Since the level of blood pressure is determined by cardiac emission and vascular tone (OPS), then to maintain it at the proper level, with a decrease in the BCC, compensatory mechanisms are included, aimed at an increase in heart rate and OPS. Compensatory changes arising in response to acute blood loss include: neuro-endocrine shifts, metabolic disorders, changes from cardiovascular and respiratory systems.
^ Neuro endocrine shifts the activation of the sympathetic-adrenal system in the form of increased emissions of catecholamines (adrenaline, norepinenaline) brain layer of adrenal glands. Catecholamines interact with ± - and і-adrenoreceptors. Stimulation of ± -adrenoreceptors peripheral vessels causes vasoconstriction, and their blockade is vasodilatia. Beta 1 -adrenoreceptors are localized in myocardium, і 2 -adrenoreceptors - in the wall of blood vessels. Stimulation І 1 -adrenoreceptors has a positive inotropic and chronotropic effect. Stimulation of І 2 -adrenoreceptors causes light dilatation of arterioles and veins.
Catecholamines with shock causes a decrease in the capacity of the vascular bed, the redistribution of intravascular fluid from peripheral vessels to the central, which contributes to the maintenance of blood pressure. At the same time, the hypophies-hypothalamus system is activated - adrenal glands, which is manifested by massive emission into the blood of ACTH, cortisol, aldosterone, antidiuretic hormone, resulting in an increase in the osmotic pressure of blood plasma, enhancing the reabsorption of sodium chloride and water, reducing the diurea and increasing the volume of intravascular fluid.
^ Metabolism disorders. In the conditions of normal blood flow, the cells are used glucose, which is converted into pyruvic acid in the future in ATP. When lacking or absence of oxygen, peyranograde acid is restored to dairy (anaerobic glycoliz), the accumulation of the latter leads to metabolic acidosis. Amino acids and free fatty acids, which in normal conditions are oxidized to form energy, accumulate in the tissues and aggravated with acidosis. The lack of oxygen and acidosis disrupt the function of cell membranes, as a result of which Potassium comes into extracellular space, and sodium and water come into cells, causeing their swelling.
^ Changes from cardiovascular and respiratory systems The shock is very significant. Catecholamines will release early stages Shock increases OPS, myocardial reduction and heart rate. Tachycardia reduces the time of diastolic filling of ventricles and, therefore, coronary blood flow. Myocardial cells begin to suffer from acidosis, which is initially compensated by hyperventyllation. In the case of a tightened shock respirator, compensation mechanisms are untenable. Acidosis and hypoxia lead to the oppression of the heart function, an increase in excitability of cardiomyocytes, arrhythmias.
Gumoral shifts P.pending the release of vasoactive mediators (histamine, serotonin, forebanding, nitrogen oxide, tumor necrotizing factor, interleukins, leukotrienes), which cause vasodillation and increasing the permeability of the vascular wall, followed by the fluid output of the blood in the interstitial space and a decrease in perfusion pressure. This aggravates the lack of 2 in the tissues of the body, caused by a decrease in delivery to them about 2 due to the acute loss of major carriers of 2 red blood cells.
^ Changes endothelius Kapillyarov It is manifested by the hypoxic swelling of its cells and adhesion (adhesion) to them activated polymorphic leukocytes, which launches the cascade of phase changes in blood flow in the microcirculatory line.
^ 1 phase - Ischemic anoxia or reduction of pre- and post-topillar sphincters - is completely reversible;
2 phase - the capillary state or the expansion of the prokapillary sphincters during the spasme of the postcase veul - is partially reversible;
3 phase - paralysis of peripheral vessels or expansion of pre- and post-topillar sphincters - is completely irreversible.
1 - initial;
2 - reversible shock stage;
3 - stage of irreversible shock.
The clinical picture is determined by the step of shock.
1 Stage - It is characterized by the paleness of mucous and skin. psychomotor excitation, cold limbs, minorly elevated or normal arterial pressure, rapid pulse and breathing, increased central venous pressure, preserving normal diuresis.
2 Stage - manifests itself intensity, pale-gray leather, covered with cold sticky sweat, thirst, shortness of breath, decrease in arterial and central venous pressure, tachycardia, hypothermia, oliguria.
3 Stage - characterized by Adinais, moving to whom; Pale, with an earthly tint and marble pattern, leather, progressive respiratory failure, hypotension, tachycardia, Anuria.
Diagnostics Based on the assessment of clinical and laboratory signs. In conditions acute blood loss It is extremely important to determine its value for which it is necessary to use one of the existing methods that are divided into 3 groups: clinical, empirical and laboratory. The latter can be straight and indirect.
2. Acute (within an hour).
3. Subacious (within 24 hours).
4. Chronic (within weeks, months, years).
By time occurrence.
1. Primary.
2. Secondary.
Pathoanatomic classification.
1. Bleedings arising from the mechanical destruction of vessel walls, as well as with thermal lesions.
2. Arrosion bleeding arising due to the destruction of the vessel wall by the pathological process (the collapse of the tumor, breakdown, purulent melting, etc.).
3. Diapection bleeding (with impaired permeability of blood vessels).
2. Clinic of acute blood loss
Blood performs a number of important functions in the body, which are mainly reduced to maintaining homeostasis. Thanks to the transport function of blood in the body, a constant exchange of gases, plastic and energy materials becomes possible, hormonal regulation, etc. The buffer function of blood is maintained in maintaining acid-base equilibrium, electrolyte and osmotic balances. The immune function is also aimed at maintaining homeostasis. Finally, due to the thin balance between the coagulating and anticist blood systems, its liquid state is supported.
Bleeding clinicit consists of local (due to the expiration of blood into the external environment or inside the tissues and organs) and the general signs of blood loss.
Symptoms of acute blood loss- This is a unifying clinical sign for all types of bleeding. The severity of these symptoms and the reaction of the body on the loss of blood depend on many factors (see below). This volume of blood loss is considered fatal when a person loses half of all circulating blood. But this is a non-absolute statement. The second important factor determining the reaction of the body on blood loss is its pace, i.e. the speed with which a person loses blood. When bleeding from a large arterial trunk, death may occur with smaller volumes of blood loss. This is due to the fact that the compensatory reactions of the body do not have time to work at the proper level, for example, in chronic blood loss in volume. General clinical manifestations of acute blood loss of the same type with all bleeding. There are complaints about dizziness, weakness, thirst, flickering flies in front of the eyes, drowsiness. Skin of pale, at a high rate of bleeding, a cold sweat can be observed. Frequently, orthostatic collapse, development of trimming states. In an objective study, tachycardia is detected, decrease in blood pressure, low-filling pulse. When developing hemorrhagic shock, the diuresis is reduced. In red blood analyzes there is a decrease in hemoglobin, hematocrit and the number of erythrocytes. But the change in these indicators is observed only with the development of hemodilution and in the first hours after blood loss, a minimophosative. The severity of clinical manifestations of blood loss depends on the pace of bleeding.
Several emissions degrees of gravity of acute blood loss.
1. With a shortage of circulating blood (BCC) 5-10%. The general condition is relatively satisfactory, the increase in the pulse is noted, but it is sufficient filling. Blood pressure (blood pressure) is normal. When studying blood hemoglobin more than 80 g / l. On capillaroscopy The condition of microcirculation is satisfactory: on a pink background, fast blood flow, not less than 3-4 loops.
2. With a BCC deficiency up to 15%. The overall state of moderate. Tachycardia is noted to 110 in 1 min. Systolic blood pressure decreases to 80 mm Hg. Art. In red blood analyzes, the reduction of hemoglobin from 80 to 60 g / l. With capillaryroscopy, fast blood flow is revealed, but on a pale background.
3. With the BCC deficiency up to 30%. The general severe condition of the patient. Pulse threaded, with a frequency of 120 in 1 min. Arterial pressure is reduced to 60 mm Hg. Art. With capillaryroscopy Pale background, slowing down blood flow, 1-2 loops.
4. With a BCC shortage of more than 30%. The patient is in very hard, often agonal state. Pulse and blood pressure on peripheral arteries are absent.
3. Clinical picture of various types of bleeding
Clearly define, from which vessel bleed, it is possible only when outdoor bleeding. As a rule, with outdoor bleeding, the diagnosis is not difficult. In case of damage to the arteries, blood is poured into an external medium with a strong pulsating jet. Scarlet blood. This is a very dangerous state, since arterial bleeding quickly leads to a critical anemization of the patient.
Venous bleedingAs a rule, it is characterized by a constant expiration of dark blood. But sometimes (when the wounded of large venous stems) may be diagnostic errors, since the transfer ripple is possible. Venous bleeding is dangerous possible by the development of an air embolism (with low central venous pressure (CVD)). For capillary bleedingthere is a constant expiration of blood from the entire surface of damaged tissue (by the type of dew). Especially severe capillary bleeding, which occur in injury to parenchymal organs (kidneys, liver, spleen, lungs). This is due to the peculiarities of the structure of the capillary network in these bodies. Bleeding in this case is very difficult to stop, and during surgery on these organs it turns into a serious problem.
3. Artificial (exfusion, medical bleeding)
For the speed of development
1. Acute (\u003e 7% OCC per hour)
2. Subacon (5-7% OCC per hour)
3. Chronic (\u003c5% OCC per hour)
In volume
1. Small (0.5 - 10% OCC or 0.5 l)
2. Average (11 - 20% OCC or 0.5 - 1 L)
3. Big (21 - 40% OCC or 1-2 L)
4. Massive (41 - 70% OCC or 2-3.5 liters)
5. Mortal (\u003e 70% OCC or more than 3.5 liters)
By the degree of hypovolemia and the possibility of developing shock:
1. Easy (BCC deficiency 10-20%, a shortage of less than 30%, no shock)
2. Moderate (BCC deficiency 21-30%, a shortage of 15-45%, shock develops with long-term hypovolemia)
3. Heavy (deficiency of the BCC 31-40%, the deficit of $ 46-60%, shock is inevitable)
4. Extremely heavy (BCC deficiency over 40%, shortage of over 60%, shock, terminal state).
Abroad, the most widespread the classification of blood loss, proposed by the American College of Surgeons in 1982, was most widely distributed, according to which 4th grade bleeding (Table 2) is distinguished.
Table 2.
Acute blood loss leads to the emission of the adrenal glands of catecholamines, causing the spasm of peripheral vessels and, accordingly, a decrease in the volume of the vascular channel, which partially compensates for the resulting BCC deficiency. The redistribution of organ blood flow (blood circulation centralization) allows you to temporarily maintain blood flow in vital organs and ensure the maintenance of life in critical states. However, subsequently, this compensatory mechanism may cause the development of severe complications of acute blood loss. A critical condition called shock is inevitably developing with a loss of 30% of the BCC, and the so-called "threshold of death" is determined not the volume of bleeding, but the number of erythrocytes remaining in circulation. For erythrocytes, this reserve is 30% of globular volume (GO), for plasma only 70%.
In other words, the body can survive with a loss of 2/3 of circulating erythrocytes, but will not transfer the loss of 1/3 of the plasma volume. This is due to the peculiarities of compensatory mechanisms developing in response to blood loss and clinically manifested by hypovolemic shock. The shock is understood as syndrome, which is based on inadequate capillary perfusion with reduced oxygenation and impaired oxygen consumption by organs and tissues. Its at the heart (shock) is the peripheral circulatory-metabolic syndrome.
Shock is a consequence of a significant reduction in the BCC (i.e., the relationship of the BCC to the capacity of the vascular bed) and the deterioration of the pumping function of the heart, which can manifest with hypovolemia of any genesis (sepsis, injuries, burns, etc.).
The specific reason for the hypovolemic shock due to the loss of solid blood can be:
1. Gastrointestinal bleeding;
2. Intragretic bleeding;
3. intra-abdominal bleeding;
5. Bleeding into the retroperitoneal space;
6. Rales of aortic aneurysms;
7. Injuries and others.
Pathogenesis
The loss of the OCC disrupts the performance of the heart muscle, which is determined by:
1. minute heart rate (Mos): Mos \u003d WSS XHS, (WOS - impact volume of the heart, heart rate - cardiac frequency);
2. Pressure filling the cavities of the heart (preload);
3. The function of cardiac valves;
4. Common peripheral vascular resistance (OPS) - post-load.
With an insufficient contractile ability of the heart muscle in the cavities of the heart after each reduction, a part of blood remains, and this leads to an increase in preload. Part of the blood is stood in the heart, which is called heart failure. Under acute blood loss, leading to the development of the BCC deficiency, the filling pressure in the head cavities is initially reduced, as a result of which the WOS, Mos and Hell decrease. Since the level of blood pressure is largely determined by the minutes of the heart (MOS) and the total peripheral vascular resistance (OPS), then to maintain it at the proper level, with a decrease in the BCC, compensatory mechanisms are included, aimed at an increase in heart rate and OPS. Compensatory changes arising in response to acute blood loss include neuroendocrine shifts, metabolic disorders, changes from cardiovascular and respiratory systems. Activation of all coagulation links causes the possibility of developing disseminated intravascular blood coagulation (DVS syndrome). In the order of physiological protection at its most frequent damage, the body corresponds to hemodilution that improves blood flow and the viscosity reduces its mobilization of erythrocyte depots, a sharp decrease in the need for ECC and in the delivery of oxygen, an increase in the respiratory rate, cardiac output, recoil and recycling of oxygen in tissues.
Neuroendocrine shifts are implemented by activation of the sympatholic system in the form of increased emissions of catecholamines (adrenaline, norepinephrine) brain layer of adrenal glands. Catecholamines interact with A- and B - adrenoreceptors. Stimulation of peripheral vessels adrenoreceptors causes vasoconstriction. Stimulation of P1 - adrenoreceptors localized in myocardium has positive ionotropic and chronotropic effects, stimulation of P2-adrenoreceptors located in blood vessels, causes light dilatation of arterioles and veins. The emission of catecholamines with shock leads not only to a decrease in the capacity of the vascular bed, but also the redistribution of intravascular fluid from peripheral vessels to the central, which contributes to the maintenance of blood pressure. The hypothalamus system is activated - adrenocortic and antidieretic hormones, cortisol, aldosterone are emitted into the blood, cortisol, aldosterone, which is an increase in the osmotic pressure plasma pressure, leading to an increase in sodium and water reabsorption, reducing the diurer and an increase in the volume of intravascular fluid. There are disorders of metabolism. Developed bleeding and hypoxemia disorders lead to the accumulation of dairy and peer-grade acids. With a lack or absence of oxygen, peyranograde acid is restored to dairy (anaerobic glycoliz), the accumulation of which leads to metabolic acidosis. Amino acids and free fatty acids also accumulate in tissues and aggravate acidosis. The lack of oxygen and acidosis disrupt the permeability of cell membranes, as a result of which potassium leaves the cell, and sodium and water come into cells, caused their swelling.
Changes from cardiovascular and respiratory systems at shock are very significant. The emission of catecholamines in the early stages of shock increases the OPS, the reduction of myocardium and heart rate is the goal of the centralization of blood circulation. However, the resulting tachycardia very soon reduces the time of diastolic filling of ventricles and, consequently, coronary blood flow. Myocardial cells begin to suffer from acidosis. In the case of a tightened shock, respiratory compensation mechanisms are untenable. Hypoxia and acidosis lead to an increase in excitability of cardiomyocytes, arrhythmias. Humoral shifts are manifested by the release and other, except for catecholamines, mediators (histamine, serotonin, prostaglandins, nitrogen oxide, tumornecking factor, interleukins, leukotrienes), which cause vasodilation and an increase in the permeability of the vascular wall, followed by a fluid part of the blood in an interstitial space and a decrease in perfusion pressure. . This aggravates the lack of O2 in the tissues of the body, caused by a decrease in its delivery due to microtromotic formation and the acute loss of O2-erythrocyte carriers.
In the microcirculatory bed, changes are developing phase character:
1. 1 phase - ischemic anoxia or reduction of pre- and post-patellular sphincters;
2. 2 phase - capillary state or extension of breastpillary veul;
3. 3 Phase - paralysis of peripheral vessels or expansion of pre- and post-patellular sphincters ...
Crisis processes in capillary reduce the delivery of oxygen to the tissues. The balance between the delivery of oxygen and the need for it is maintained as long as the necessary tissue extraction of oxygen is provided. When delaying with the beginning of the intensive therapy, the delivery of oxygen to cardiomyocytes is disturbed, the amidosis of myocardium is increasing, which is clinically manifested by hypotension, tachycardia, shortness of breath. The decrease in tissue perfusion converts into global ischemia, followed by reperfusion damage to tissues due to increased production of cytokine macrophages, activation of re-oxidation of lipids, release neutrophils of oxides and further microcirculation disorders. The subsequent microtromotic formation forms a violation of the specific functions of the organs and the risk of developing polyorgan failure arises. Ischemia changes the permeability of the intestinal mucosa, especially sensitive to the ischemic-reperfusion-mediator, which causes the dislocation of bacteria and cytokines into the circulation system and the occurrence of such system processes as sepsis, respiratory distress - syndrome, polyorgan deficiency. Their appearance corresponds to a specific time interval or stage of shock, which can be the initial, reversible (reversible shock stage) and irreversible. To a large extent, the irreversibility of the shock is determined by the number of microtrombov formed in the capalial and temporary factor in the crisis of microcirculation. As for the dislocation of bacteria and toxins due to the ischemia of the intestine and the impact of the permeability of its wall, this provision is currently not so unambiguous and requires additional research. And yet the shock can be defined as a condition in which the oxygen consumption by tissues inadequately their needs for the functioning of aerobic metabolism.
Clinical picture.
In the development of hemorrhagic shock, 3 stages are distinguished.
1. Compensated reversible shock. The volume of blood loss does not exceed 25% (700-1300 ml). Moderate tachycardia, blood pressure or not changed, or slightly lowered. Entry subcutaneous veins, decreases CVD. There are signs of peripheral vasoconstrictions: cooling limbs. The amount of urine isolated is reduced by half (at a rate of 1-1.2 ml / min). Decompensated reversible shock. The volume of blood loss is 25-45% (1300-1800 ml). Pulse frequency reaches 120-140 per minute. Systolic blood pressure is reduced below 100 mm Hg, the magnitude of the pulse pressure decreases. There is a pronounced shortness of breath, partly compensating metabolic acidosis by respiratory alkalosis, but can also be a sign of a shock lung. Strengthen the cooling limbs, acricyanosis. Cold sweat appears. Urine release rate is below 20 ml / h.
2. irreversible hemorrhagic shock. Its occurrence depends on the duration of the decompensation of blood circulation (usually in the arterial hypotension of 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 mm.rt. or not determined. Consciousness is absent. Oligoanuria is developing.
Diagnostics
Diagnostics is based on the 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 that are divided into three groups: clinical, empirical and laboratory. Clinical methods allow to assess the volume of blood loss based on clinical symptoms and hemodynamic parameters. The level of blood pressure and the pulse frequency before the start of the pricilla therapy largely reflect the magnitude of the BCC deficiency. The ratio of the pulse rate to the systolic blood pressure allows you to calculate the Alg expense shock index. Its value depending on the BCC deficiency is presented in Table 3.
Table 3. Evaluation based on the shock index of Alforer
The test of the capillary fill, or the symptom of the "White Spot" allows you to evaluate the capillary perfusion. It is carried out by pressing the finger, the skin of the forehead or the uha lobe. Normally, the color is restored after 2 s, with a positive sample - after 3 or more. Central venous pressure (CVD) is an indicator of the filling pressure of the right ventricle, reflects its pumping function. Normally, the FED fluctuates from 6 to 12 cm water column. The decrease in the FSA testifies to hypovolemia. With a BCC deficiency in 1 liter, the CVD decreases by 7 cm of water. Art. The dependence of the value of FED from the BCC deficiency is presented in Table 4.
Table 4. Estimation of a circulating blood deficit based on the value of the central venous pressure
Hourly diuresis reflects the level of tissue perfusion or the degree of filling the vascular bed. Normally, 0.5-1 ml / kg of urine is released in the norm. The decrease in the diurere is less than 0.5 ml / kg / h testifies to insufficient blood supply to the kidneys due to the BCC deficiency.
Empirical methods for assessing the volume of blood loss are most often used in injuries and polytrams. They use medium-statistical values \u200b\u200bof blood luminosity set for a particular type of damage. In the same way, we can approximately assess the blood loss in various surgical interventions.
Medium blood loss (l)
1. Hemotorax - 1.5-2.0
2. Fracture of one edge - 0.2-0.3
3. Abdominal injury - up to 2.0
4. Fracture of the pelvic bones (retroperitone hematoma) - 2.0-4.0
5. Fracture of the hip - 1.0-1.5
6. Shoulder / Sun 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 size with palm - 0.5
Operating blood loss
1. Laparotomy - 0.5-1.0
2. Thoracotomy - 0.7-1.0
3. Shooting amputation - 0.7-1.0
4. Osteosynthesis of large bones - 0.5-1.0
5. Stomach resection - 0.4-0.8
6. Gastrectomy - 0.8-1,4
7. Colon resection - 0.8-1.5
8. Cesarean section - 0.5-0.6
Laboratory methods involve the determination of a hematocrit (HT), hemoglobin concentration (Hb), relative density (P) or blood viscosity.
They are divided into:
1. Estimated (the use of mathematical formulas);
2. Hardware (electrophysiological impedancetric methods);
3. Indicator (use of dyes, thermodilation, dextrans, radioisotopes).
Among the settlement methods, the Moore formula was most common:
PCP \u003d OCCD x HTTT-HTF / HTF
Where the CCP is blood loss (ml);
OCCD - due region of circulating blood (ml).
Normally, the Women's OCCD averages 60 ml / kg, in men - 70 ml / kg, in pregnant women - 75 ml / kg;
Report - due hematocrit (in women - 42%, in men - 45%);
FIF - the actual hematocrit patient. In this formula, instead of hematocrit, you can use the hemoglobin indicator, taking for its proper level 150 g / l.
You can also use the value of blood density, but this technique is applicable only with small blood loss.
One of the first hardware methods for the definition of the BCC was the basis of which the basis of the basic co-alignment of the body with the help of a reofitamograph (found an application in the "post-Soviet space").
Modern indicator methods provide for the establishment of the OCC to change the concentration of applicable substances and are conventionally divided into several groups:
1. Determination of plasma volume, and then all blood volume through HT;
2. Determination of the volume of erythrocytes and on it all blood volume through HT;
3. Simultaneous determination of the volume of erythrocytes and blood plasma.
As an indicator, Evans paint (T-1824), dextre (polyglyukine), human albumin, labeled with iodine (131i) or chromium chloride (51CrCl3), are used as an indicator. But, unfortunately, all methods for determining blood loss give a high error (sometimes to a liter), and therefore can only serve as a guideline during treatment. However, the definition of VO2 should be considered the simplest diagnostic criterion for the detection of shock.
The strategic principle of transfusion therapy of acute blood loss is the restoration of organ blood flow (perfusion) by achieving the necessary OCC. Maintaining the level of coagulation factors in quantities sufficient for hemostasis, on the one hand, and to confront excess disseminated coagulation - on the other. Replenishing the number of circulating erythrocytes (oxygen carriers) to the level providing minimal sufficient oxygen consumption in tissues. However, most of the specialists consider the most acute problem of blood loss of hypovolemia, and, accordingly, the first place in therapy schemes are filled with OCC, which is a critical factor for maintaining stable hemodynamics. The pathogenetic role of the reduction of the BCC in the development of severe homoseostasis disorders predetermines the importance of timely and adequate correction of volting disorders to the outcomes of treatment in patients with acute massive blood loss. The ultimate goal of all resuscitologist's efforts is to preserve adequate oxygen consumption by tissues to maintain metabolism.
General principles The treatment of acute blood loss is reduced to the following:
1. Stop bleeding, struggle with pain.
2. Ensuring adequate gas exchange.
3. Replenishment of the BCC deficiency.
4. Treatment of organ dysfunction and prevention of polyorgan insolvency:
Treatment of heart failure;
Prevention of renal failure;
Correction of metabolic acidosis;
Stabilization of metabolic processes in the cell;
Treatment and prevention of DVS syndrome.
5. Earlyprofilax for infection.
Stop bleeding and struggle with pain.
With any bleeding, it is important to eliminate its source as soon as possible. With outdoor bleeding - a vessel pressing, a gulling bandage, harness, ligature or clamp on a bleeding vessel. With internal bleeding - urgent surgery conducted in parallel with therapeutic measures to remove the patient from shock.
Table No. 5 presents data on the nature of the infusion therapy of acute blood loss.
| Min. | Average | So. | Hard. | Arrays | |
| Hell SIS. | 100–90 | 90–70 | 70–60 | \u003c60. | \u003c60. |
| Heart rate | 100–110 | 110–130 | 130–140 | \u003e 140. | \u003e 140. |
| Alghera index | 1–1,5 | 1,5–2,0 | 2,0–2,5 | \u003e 2.5 | \u003e 2.5 |
| Blood volume. | Up to 500. | 500–1000 | 1000–1500 | 1500–2500 | \u003e 2500 ml |
| V blood. (ml / kg) | 8–10 | 10–20 | 20–30 | 30–35 | \u003e 35. |
| % loss of OCC. | \u003c10 | 10–20 | 20–40 | \u003e 40. | \u003efifty |
| V infusion (in% of loss) | 100 | 130 | 150 | 200 | 250 |
| Hemotr. (% of V infusion) | - | 50–60 | 30–40 | 35–40 | 35–40 |
| Colloids (% v infus.) | 50 | 20–25 | 30–35 | 30 | 30 |
| Crystaloids (% v infusion) | 50 | 20–25 | 30–55 | 30 | 30 |
1. Infusion begins with crystalloids, then - colloids. Hemotransfusion - with a decrease in Hb less than 70 g / l, HT less than 25%.
2. Infusion rate with massive blood loss up to 500 ml / min !!! (Catheterization of the second central vein, infusion of pressure solutions).
3. Correction of voliable (stabilization of hemodynamic parameters).
4. Normalization of globular volume (HB, HT).
5. Correction of disorders of water-salt exchange
Fighting pain syndrome, protection against mental stress is carried out by intravenous (in / c) administration of analgesics: 1-2 ml of 1% morphine solution of hydrochloride, 1-2 ml of 1-2% of the propellant solution, as well as sodium oxybutirate (20-40 mg / kg body weight), sybazone (5-10 mg), it is possible to use subnarchical doses of CalipSola and sedation using propofo-la. Dose of narcotic analgesics should be reduced by 50% due to the possible oppression of respiration, nausea and vomiting arising from intravenous administration of these drugs. In addition, it should be remembered that the introduction of them is possible only after the exclusion of damage to the internal organs. The provision of adequate gas exchange is directed both to the utilization of oxygen by tissues and for removal carbon dioxide. The preventive introduction of oxygen through the nasal catheter at least 4 l / min was shown to all patients.
In the occurrence of respiratory failure, the main tasks of treatment are:
1. Ensuring Penthood respiratory tract;
2. Prevention of aspiration of the contents of the stomach;
3. Liberation of the respiratory tract of sputum;
4. Ventilation of the lungs;
5. Restoration of tissue oxygenation.
Developed hypoxemia can be due to:
1. hypoventilation (usually in combination with hypercaps);
2. The inconsistency between the ventilation of the lungs and their perfusion (disappears when breathing with pure oxygen);
3. Blood air shunt (protected with pure oxygen) caused by respiratory distress syndrome of adults (RAO2 \u003c60-70 mm Hg Fiio2\u003e 50%, double-sided pulmonary infiltrates, normal filling pressure of ventricles), edema of the lungs, heavy pneumonia ;
4. Violation of the diffusion of gases through the alveolo - capillary membrane (disappears with pure oxygen breathing).
The lung ventilation carried out after the trachea intubation is carried out in specially selected modes that create the conditions for optimal gas exchange and non-violating central hemodynamics.
Replenishment of the deficit of the BCC
First of all, with a sharp blood loss, the patient should create an improved position of Tretenherburg to increase the venous return. Infusion is carried out simultaneously in 2-3 peripheral or 1-2 central veins. The pace of blood loss is determined by the blood pressure. As a rule, at first infusion is carried out insert or quickly drip (up to 250-300 ml / min). After stabilization of hell at a safe level, infusion is carried out drip. Infusion therapy begins with the introduction of crystalloids. And in the last decade there is a refund to consider the possibility of using NACI hypertensive solutions.
Hypertonic solutions of sodium chloride (2.5-7.5%), due to a high osmotic gradient, provide quick mobilization of fluid from an interstice into the bloodstream. However, a small duration of their action (1-2 hours) and relatively small volumes of administration (no more than 4 ml / kg of body weight) determine the preferential use of them in the pre-hospital stage of treatment of acute blood loss. Colloidal anti-shock solutions are divided into natural (albumin, plasma) and artificial (dextrans, hydroxy-ethyl starchs). Albumin and plasma protein fraction effectively increase the volume of intravascular fluid, because Have high oncotic pressure. However, they easily penetrate through the walls of pulmonary capillaries and the basal membranes of the kidney glomers into the extracellular space, which can lead to an edema of the interrange tissue of the lungs (respiratory distress-syndrome of adults) or kidney (acute renal failure). The volume of dextre diffusion is limited, because They cause damage to the epithelium of the renal tubules ("dextran kidney") adversely affect the blood coagulation system and immunocomponent cells. Therefore, today "preparations of the first selection" are solutions of hydroxyethyl starch. Hydroxyethyl stroke is a natural polysaccharide obtained from amylopectin starch and consisting of high-molecular polarized glucose residues. The initial raw material for receiving the GEK serve starch from potatoes and tapioca tubers, grains of various varieties of corn, wheat, rice.
GEK of potatoes and corn, along with linear chains of amylase, contains a fraction of branched amylopectin. The starch hydroxylation prevents its rapid enzyme cleavage, increases the ability to keep water and increase colloid-osmotic pressure. In transfusion therapy, 3%, 6% and 10% GEC solutions are used. The introduction of GEC solutions causes iso-olomolemic (up to 100% during the maintenance of a 6% solution) or even initially hypervolemic (up to 145% of the injected 10% solution of the drug) volume, which is preserved at least 4 hours.
In addition, GEC solutions have the following properties that are absent in other colloidal plasma-changing pre-parats:
1. Prevent the development of the syndrome of increased permeability of capillaries, closing the pores in their walls;
2. Moderate the effect of circulating adhesive molecules or inflammation mediators, which, circulating in blood at critical states, increase the secondary damage to the tissues, binding to neutrophils or endotheliocytes;
3. Do not affect the expression of surface blood antigen, i.e. do not violate immune responses;
4. Do not cause activation of the complement system (consists of 9 serum proteins C1 - C9) associated with generalized inflammatory processes that violate the functions of many internal organs.
It should be noted that in recent years, separate randomized studies have appeared. high level Estimates (A, b) indicating the ability of starch to cause impaired kidney function and preferred albumin and even gelatin preparations.
At the same time, since the end of the 70s of the 20th century, perfluorocarbon compounds (PFOS) began to be studied, laid out the basis of a new generation of plasma refinaries with O2 transfer function, one of which is a perfoor. The use of the latter during acute blood loss allows you to influence the reserves of three levels of O2 exchange levels, and the simultaneous use of hydroatherapy allows you to increase ventilation reserves.
Table 6. The proportion of perfluten use depending on the level of bloodstream
| Blood-replacement | The magnitude of blood loss | Total transfusion (% of blood loss) | Dose Perfluorina |
| 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 reflect the following signs:
1. Enhance arterial pressure;
2. Reducing cardiac frequency;
3. Warming and combustion of skin; expulsion of pulse pressure; -Diorez over 0.5 ml / kg / h.
Thus, by summing up the foregoing, we emphasize that the testimony for hemotransphus is: -cropotter more than 20% of the proper OCC, -Amiamia, in which hemoglobin content is less than 75 g / l, and a hematroric number is less than 0.25.
Treatment of organ dysfunction and polyorgan deficiency prevention
One of the most important tasks is the treatment of heart failure. If the victim before the accident was well healthy, then for the normalization of cardiac activity, the BCC deficiency is usually quite quickly and efficiently. If a history of the victim has chronic hearts or vessels, hypovolemia and hypoxia aggravate the current disease, therefore conduct special treatment. First of all, it is necessary to achieve an increase in preload, which is achieved by an increase in the BCC, and then increase the reduction of myocardium. Most often, vasoactive and inetropic drugs are not prescribed, but if hypotension acquires a persistent nature, non-infusion therapy, then these drugs can be applied. Moreover, the use of them is possible only after the complete reimbursement of the BCC. Of the vasoactive drugs with the preparation of the first row to maintain the activities of the heart and kidney is dopamine, 400 mg of which is divorced in 250 ml of isotonic solution.
The rate of infusion is chosen depending on the desired effect:
1. 2-5 μg / kg / min ("renal" dose) expands mesenterical and renal vessels without increasing the frequency of heart abbreviations and blood pressure;
2. 5-10 μg / kg / min gives a pronounced ionotropic effect, soft vasodilation due to the stimulation of β2 - adrenoreceptors or moderate tachycardia;
3. 10-20 μg / kg / min leads to a further strengthening of the ionotropic effect, pronounced tachycardia.
More than 20 μg / kg / min - sharp tachycardia with a threat of tachyarhythmias, narrowing veins and arteries due to stimulation A1_ adrenoreceptors and deterioration in tissue perfusion. Due to the arterial hypotension and shock, as a rule, acute renal failure is developing (OPON). In order to prevent the development of the oliguric form of the OPN, it is necessary to control the hourly diurea (normally in adults is 0.51 ml / kg / h, in children more than 1 ml / kg / h).
Measurement of sodium and creatine concentrations in urine and plasma (when the creatine of blood plasma exceeds 150 μmol / l, the speed of glomerular filtration is below 30 ml / min).
Dopamine infusion in the "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 on the background of the restoration of the BCC (CVD is more than 30-40cm water) and satisfactory heart emissions (furosemid, B / B in the initial dose of 40 mg with an increase, if necessary, 5-6 times).
Normalization of hemodynamics and reimbursement of circulating blood (BCC) should be carried out under the control of the DZLK (pressure of the enclosure of pulmonary capillaries), CR (cardiac output) and OPS. At shock, the first two indicators are progressively reduced and the latter rises. The methods for determining these criteria and their norms are well described quite well in the literature, but, unfortunately, they are routinely used in abroad clinics and rarely in our country.
Shock, as a rule, is accompanied by severe metabolic acidosis. Under its influence, the reduction of myocardial is reduced, cardiac output decreases, which contributes to a further decrease in blood pressure. The reactions of the heart and peripheral vessels on endo- and exogenous catecholamines are reduced. Inhalation O2, IVL, infusion therapy restore physiological compensatory mechanisms and in most cases eliminate acidosis. Sodium Bicarbonate is injected with severe metabolic acidosis (pH venous blood below 7.25), calculating it according to the generally accepted formula, after determining the indicators of the KSHC.
You can immediately enter 44-88 MEKV (50-100 ml of 7.5% NSO3), the rest of the next 4-36 hours. It should be remembered that the excessive administration of sodium bicarbonate creates prerequisites for the development of metabolic alkalosis, hypokalemia, arrhythmias. Perhaps a sharp increase in plasma osmolar and up to the development of the hyperosmolar coma. When a shock, accompanied by a critical deterioration of hemodynamics, is necessary to stabilize metabolic processes in the cell. Treatment and prevention of DVS-syndrome, as well as the early prevention of infections, are carried out, guided by generally accepted schemes.
Ronated, from our point of view, is a pathophysio-logical approach to solving the problem of indications for hemotransphus, based on the assessment of transport and consumption of oxygen. Oxygen transport is a cardiac output derivative and oxygen blood tank. Oxygen consumption depends on the delivery and ability of the tissue to pick up oxygen from the blood.
When filled with hypovolemia by colloid and crystalloid solutions, the number of erythrocytes is reduced and the oxygen capacity of the blood is reduced. Due to the activation of the sympathetic nervous system, the cardiac output is compensatory (sometimes exceeding normal values \u200b\u200bof 1.5-2 times), "revealed" microcirculation and reduces the affinity of hemoglobin to oxygen, tissue is taken from blood relative more oxygen (oxygen extraction coefficient increases). This makes it possible to maintain the normal consumption of oxygen at low oxygen blood tank.
In healthy people, normalolemic hemodilution with a hemoglobin level of 30 g / l and 17% hematocrit, although accompanied by a decrease in oxygen transport, but the oxygen consumption of tissues is not reduced, the blood lactate level does not increase, which confirms the sufficiency of the organism oxygen support and maintaining metabolic processes on sufficient level. With acute isoovolemic anemia to hemoglobin (50 g / l), in patients in peace, fabric hypoxia is observed before the operation. The oxygen consumption is not reduced, and even somewhat rises, the level of blood lactate does not increase. For normal oxygen, the oxygen consumption does not suffer at the level of delivery of 330 ml / min / m2, with a lower delivery there is a dependence of consumption from the delivery of oxygen, which corresponds to approximately the level of hemoglobin 45 g / l with a normal cardiac emission.
An increase in the oxygen tank of blood with a transfusion of con-served blood and its components has its own negative sides. First, the increase in hematocrit leads to an increase in blood viscosity and deterioration of microcirculation, creates an additional load on myocardium. Secondly, the low content of 2.3-DFG in red blood cells of donor blood is accompanied by an increase in oxygen affinity to hemoglobin, shifting the dissociation curve of oxymemoglobin left and, as a result, deterioration of tissue oxygenation. Thirdly, in the transfused blood, micropots are always present, which can "score" the capillaries of the lungs and sharply increase the pulmonary shunt, worsening blood oxygenation. In addition, overclocking red blood cells begin to fully participate in oxygen transport only 12-24 hours after hemotransfusion.
Our analysis of the literature showed that the choice of funds for the correction of blood loss and postgemorrhagic anemia is not a solved issue. This is mainly due to the lack of informative criteria for assessing the optimality of certain ways to compensate for transport and oxygen consumption. A modern tendency to reduce blood transfusions is due primarily, the possibility of complications associated with hemotransphus, limiting donation, the failure of patients from hemotransfusion for any reasons. At the same time, the number of critical states associated with blood loss of various genes increases. This fact dictates the need for further development of methods and means of substitution therapy.
An integral indicator that allows you to objectively assess the adequacy of tissue oxygenation, is the saturation of hemoglobin oxygen in mixed venous blood (SVO2). A decrease in this indicator less than 60% over a short period of time leads to the emergence of metabolic signs of tissue oxygen debt (lactoacidosis, etc.). Consequently, an increase in blood lactate can be biochemical marker The degree of activation of anaerobic metabolism and characterize the effectiveness of the therapy.
Acute blood loss causes deep rearrangement of blood circulation in the body and introduces the most complicated compensation mechanisms for impaired homeostasis. Clinical and pathological changes regardless of localization of the source of bleeding are characterized by general manifestations. A starting link in the development of these disorders is the growing reduction in the BCC (circulating blood volume). Acute blood loss is dangerous primarily by the development of circulatory and hemodynamic disorders representing a direct threat to life. In other words, with acute, especially massive, blood loss, the human body suffers not so much from a decrease in the number of erythrocytes and hemoglobin, as from the decrease in the BCC and Hypovolemia.
Each person responds to the loss of the same blood volume in different ways. If the blood loss in a healthy adult reaches 10% of the BCC, which is an average of 500 ml, it does not lead to pronounced changes in hemodynamics. In chronic inflammatory processes, disorders of water-electrolyte balance, intoxication, hypoproteinemia, the same blood loss should be filled with plasma proofs and blood.
The nature and dynamics of clinical manifestations of acute blood loss depend on various factors: the volume and speed of blood loss, the age, the initial state of the body, the presence of a chronic disease, the time of the year (in the hot season of the year, the blood loss is worse than) and others are heavier tolerable tolerate the sharp blood loss children and elderly , as well as pregnant women suffering from toxicosis. The body's response to acute blood loss is determined in each individual case by the degree of self-regulation of functional systems based on an academician L. K. Anochene "Golden Rules of Norma", according to which any deviation of any factor from a vital level is an impetus for the immediate mobilization of numerous apparatuses of the corresponding functional Systems repaired this important adaptive result (Wagner E. A. et al., 1986).
V. A. Klimansky and L. A. Rudaev (1984) distinguish three degrees of blood loss:
The sharp blood loss 25% of the BCC is compensated by a healthy organism as a result of the inclusion of self-regulation mechanisms: hemodilutions, blood redistribution and other factors.
The combination of various organs into functional systems with beneficial for the body always occurs on the principle of self-regulation. Self-regulation is the main principle of the duration of functional systems.
The sharp blood loss of 30% of the BCC leads to severe circulatory disorders, which, with timely assistance, consisting in a stopping of bleeding and intensive infusion-transfusion therapy, allow us to normalize the patient's condition.
Deep circulatory disorders are developing with acute blood loss of 40% of the volume of the BCC and more, are characterized by a clinical picture of hemorrhagic shock.
The condition of patients with acute blood loss can be different. Most patients with mechanical injury in the presence of combined damage come in serious condition and need urgent treatment.
Evaluating the overall condition of patients with acute blood loss, it is necessary to take into account the anatomical localization of damage. The degree and nature of clinical manifestations depend on which fabrics and organs are damaged. Heavy closed injuries of the limbs, a chest wall, back and lumbar region may be accompanied by extensive hemorrhages in subcutaneous tissue. Damage to the internal organs are conjugate with bleeding in serous cavities and the lumen of hollow organs.
The consequence of breast injuries may be hemotorax, often reaching a volume of 1-2 liters. With fractures of long tubular bones, with the bones of the back and fractures of the bones of the pelvis in the muscles, in the subcutaneous fatty cell, the hematomas are formed in the retroperitoneal space. Closed damage to the liver, spleen, as a rule, are accompanied by massive inner blood loss.
The initial state to a large extent can determine the resistance to blood loss. The assertion that the loss of blood does not exceed 10-15% of the BCC, is safe, valid only for persons with normal initial state. If at the time of blood loss, hypovolemia already occurred, even small bleeding can cause serious consequences.
Cachexia, purulent intoxication, long-term bedding preceding small bleeding - all this creates a dangerous background, in which new bleeding entails heavier consequences than usual. For elderly people, chronic hypovolemia is characterized in combination with a bad adaptive ability of the vascular channel, due to the morphological changes in the walls of the vessels. This increases the risk of even a small blood loss due to violations in the operation of the functional systems of self-regulation, in particular the so-called "internal self-regulation link".
Well known symptoms of the triad of acute massive blood loss - low blood pressure, a frequent threaded pulse and cold wet skin - are the main, but not the only signs of a critical state. Often there are confusion of consciousness, dry mouth and thirst, the expansion of pupils, the increase in breathing. However, it should be borne in mind that when assessing the severity of the patient's condition with massive blood loss, clinical signs can be manifested in varying degrees, and some even absent. The determination of the clinical picture during acute blood loss should be complex and include an assessment of the state of the central nervous system, skin and mucous membranes, the determination of blood pressure, the rate of the pulse, the volume of blood loss, the amount of hematocrit, the content of hemoglobin, the number of erythrocytes, platelets, fibrinogen, blood coagulation, clockwise (minute ) Diurea.
Changes in the central nervous system (CNS) depend on the initial state of the patient and the magnitude of blood loss. With moderate blood loss (no more than 25% of the BCC) in a practically healthy person who does not suffer from chronic somatic disease, consciousness can be clear. In some cases, patients are excited.
With a large blood loss (30-40% of the BCC), consciousness is preserved, a number of patients have drowsiness and indifference to the surrounding atmosphere. Most often, patients complain about thirst.
Massive blood loss (over 40% of the BCC) is accompanied by a significant depression of the CNS: Adamina, Apathimathy, possibly the development of a hypoxic coma. If patients with consciousness are preserved, they are sleepy and constantly asking to drink.
The color, humidity and temperature of the skin are simple, but important indicators of the state of the patient and, in particular, the nature of peripheral blood flow. Warm pink skin testifies to normal peripheral blood circulation, even if the blood pressure is low. Cold pale skin, pale nails allow us to talk about pronounced peripheral arterial and venous spasme. Such a violation or partial cessation of blood supply to the skin, subcutaneous fatty tissue in response to the reduction of the BCC is a consequence of blood circulation reduction in order to maintain blood flow in vital organs - "Centralization" of blood circulation. The skin on the touch is cold, it can be wet or dry. Peripheral veins on their hands and legs are narrowed. After pressing on the nail capillaries of the nail bed, they are slowly filled with blood, which indicates a disturbance of microcirculation.
With deep circulatory disorders - hemorrhagic shock and "decentralization" of blood circulation - the skin acquires a marble shade or a grayish-blue color. The temperature is reduced. After pressing on the nail capillaries of the nail bed filled very slowly.
The number of heart abbreviations. The decrease in the BCC and the decrease in the venous blood return to the heart lead to the excitation of a sympathetic-adrenal system and at the same time to the braking of the Vagus Center, which is accompanied by tachycardia.
Stimulation of the alpha-receptor of the sympathetic nervous system leads to arterial vasoconstriction of the vessels of the skin and kidneys. Thanks to vasoconstrictions, blood flow is ensured in vital organs ("Centralization" of blood circulation), such as the heart and brain, which do not tolerate inadequate blood flow over a few minutes. If the peripheral vasoconstriction is redundant or long, then the violation of the tissue perfusion leads to the release of lysosomal enzymes and vasoactive substances that themselves significantly exacerbate blood circulation disorders.
With a massive blood loss, the pulse frequency usually increases to 120-130 beats per minute, and sometimes to large values \u200b\u200bdue to stimulation of the sympathetic nervous system. This ensures the maintenance of cardiac output with a reduced blood volume. However, if the heart rate exceeds 150 per minute, the cardiac emission decreases, the duration of the diastole decreases, the coronary blood flow and filling of ventricles are reduced.
Tachycardia is a non-economic mode of the heart. The increase in cardiac abbreviations up to 120-130 per minute and more with acute blood loss is the basis for concerns and testifies to the noncompensated deficiency of the BCC, on the continuing vascular spasme and the insufficiency of infusion therapy. Given the arterial and central venous pressure, color and temperature of the skin, hourly diuresis, it is necessary to establish whether the tachycardia is not a consequence of hypovolemia and not sufficiently replenished by the BCC. If so, then you should look for a source of bleeding, eliminate it and intensify infusion-transfusion therapy.
Consequently, changing the heart rate with acute blood loss is an important clinical sign. The greatest value is manifested in dynamic observation, then this figure reflects the clinic and the result of treatment.
With acute blood loss, a compensatory decrease in the capacity of the vascular channel is provided by vasoconstriction of arterioles and a narrowing of large veins. Vasoconstriction venous vasoconstriction is one of the most important compensatory mechanisms that allows patients to carry the BCC deficiency up to 25% without the development of arterial hypotension.
In patients with acute blood loss or severe injury, if narcotic analgesics are injected to eliminate pain syndrome, especially morphine, blood pressure suddenly decreases. Most often, this is observed in patients with unstable hypovolemia, when blood pressure is maintained on relatively normal level Vasoconstriction, which decreases or removed by narcotic analgesics and vasodilators. They not only affect the vasoconstriction of the arteriole, but also contribute to venous dilatation and can increase the vascular capacity up to 1-2 liters or more, causing relative hypovolemia. Therefore, before entering narcotic analgesics, the patient with injury and blood loss is necessary to restore the OCC and normalize hemodynamics. Reducing blood pressure in response to the introduction of narcotic analgesics indicates persistent hypovolemia.
The functional state of self-regulation mechanisms can mutually influence the ability to compensate for hypovolemia.
The reaction to the sharp blood loss occurs very quickly - a few minutes after the start of bleeding, signs of sympathetic and adrenal activation are developing. The content of catecholamines, pituitary hormones and adrenal glands, and many clinical symptoms of hemorrhagic shock are signs of increased activation of the sympathetic-adrenal system in response to blood loss.
Arterial pressure is an integral indicator of systemic blood flow. Its level depends on the BCC, peripheral vascular resistance and heart work. When centralizing blood circulation, the spasm of peripheral vessels and an increase in cardiac output can compensate for the decrease in the BCC, the blood pressure may be normal or even increased, that is, the normal amount of blood pressure is maintained by cardiac emission and vascular resistance. When a heart rate decreases, due to a reduction in the vascular volume, blood pressure remains normal until the high peripheral vascular resistance is preserved, which compensates for the reduction of cardiac output. Moderate hypovolemia (15-20% BCC), especially in the position lying, may not be accompanied by a decrease in blood pressure.
Blood pressure may remain normal until the reduction in heart emissions or loss of blood volume will be so high that the adaptation mechanisms of homeostasis will not be able to compensate for the reduced volume. As the BCC deficiency increases, the progressive arterial hypotension is developing. It is more correct to consider the level of blood pressure during acute blood loss with an indicator of the compensatory capabilities of the body. Blood pressure reflects the condition of blood flow in large vessels, but not hemodynamics in general. In addition, low blood pressure does not necessarily indicate insufficiency of tissue blood flow.
| Recreation and treatment in sanatoriums - disease prevention |
|---|
| NEWS | ||||
|---|---|---|---|---|
Bleeding is determined as blood penetration outside the vascular bed, which takes place either when damaged the walls of blood vessels, or in disruption of their permeability. A number of states are accompanied by bleeding, which is physiological if blood loss does not exceed certain values. These are menstrual bleeding and blood loss in postpartum period. The causes of pathological bleeding are very diverse. The change in the permeability of the vessels is observed in case of diseases and pathological conditions, such as sepsis, ration, the last stages of chronic renal failure, hemorrhagic vasculitis. In addition to the mechanical reasons for the destruction of blood vessels due to injuries, the integrity of blood vessels may be disturbed due to hemodynamic factors and changes in the mechanical properties of the vascular wall itself: hypertensive disease Against the background of systemic atherosclerosis, the ripper of the aneurysm. The destruction of the vessel wall may occur as a result of a pathological destructive process: tissue necrosis, tumor decay, purulent melting, specific inflammatory processes (tuberculosis, etc.).
There are several bleeding classifications.
By type of bleeding vessel.
1. Arterial.
2. Venous.
3. Arteriovenous.
4. Capillary.
5. Parenchimatous.
On a clinical picture.
1. Outdoor (blood from the vessel falls into the external environment).
2. Internal (blood flowing from the vessel is located in the tissues (with hemorrhages, hematomas), hollow organs or body cavities).
3. Hidden (without a clear clinical picture).
For internal bleeding, there is an additional classification.
1. Blood expires in fabric:
1) blood hemorrhages in the tissue (blood expires in tissue in such a way that they can not be divided. The so-called impregnation occurs);
2) subcutaneous (bruise);
3) sublimated;
4) subarachnoidal;
5) subseroic.
2. Hematomas (massive bloodstream in tissue). They can be removed by puncture.
According to the morphological picture.
1. Frowning (blood spreads under the interstitial gaps).
2. Intranate (the expiration of blood occurs with the destruction of the tissue and the formation of the cavity).
On clinical manifestations.
1. Pulsating hematomas (in the case of a hematoma cavity with arterial barrel).
2. Hematomas non-executing.
Alsae intra-high bleeding.
1. Blood expirations in natural body cavities:
1) abdominal (hemoperitoneum);
2) the cavity of the cardiac bag (hemopericard);
3) pleural cavity (hemotorax);
4) The bias of the joints (hemartrosis).
2. The expiration of blood in the hollow organs: the gastrointestinal tract (gastrointestinal tract), urinary pathways, etc.
In the dark bleeding.
1. The acute (from large vessels, a large amount of blood is lost within minutes).
2. Acute (within an hour).
3. Subacious (within 24 hours).
4. Chronic (within weeks, months, years).
By time occurrence.
1. Primary.
2. Secondary.
Pathoanatomic classification.
1. Bleedings arising from the mechanical destruction of vessel walls, as well as with thermal lesions.
2. Arrosion bleeding arising due to the destruction of the vessel wall by the pathological process (the collapse of the tumor, breakdown, purulent melting, etc.).
3. Diapection bleeding (with impaired permeability of blood vessels).
2. Clinic of acute blood loss
Blood performs a number of important functions in the body, which are mainly reduced to maintaining homeostasis. Thanks to the transport function of blood in the body, a constant exchange of gases, plastic and energy materials becomes possible, hormonal regulation, etc. The buffer function of blood is maintained in maintaining acid-base equilibrium, electrolyte and osmotic balances. The immune function is also aimed at maintaining homeostasis. Finally, due to the thin balance between the coagulating and anticist blood systems, its liquid state is supported.
Bleeding clinicit consists of local (due to the expiration of blood into the external environment or inside the tissues and organs) and the general signs of blood loss.
Symptoms of acute blood loss- This is a unifying clinical sign for all types of bleeding. The severity of these symptoms and the reaction of the body on the loss of blood depend on many factors (see below). This volume of blood loss is considered fatal when a person loses half of all circulating blood. But this is a non-absolute statement. The second important factor determining the reaction of the body on blood loss is its pace, i.e. the speed with which a person loses blood. When bleeding from a large arterial trunk, death may occur with smaller volumes of blood loss. This is due to the fact that the compensatory reactions of the body do not have time to work at the proper level, for example, in chronic blood loss in volume. General clinical manifestations of acute blood loss of the same type with all bleeding. There are complaints about dizziness, weakness, thirst, flickering flies in front of the eyes, drowsiness. Skin of pale, at a high rate of bleeding, a cold sweat can be observed. Frequently, orthostatic collapse, development of trimming states. In an objective study, tachycardia is detected, decrease in blood pressure, low-filling pulse. When developing hemorrhagic shock, the diuresis is reduced. In red blood analyzes there is a decrease in hemoglobin, hematocrit and the number of erythrocytes. But the change in these indicators is observed only with the development of hemodilution and in the first hours after blood loss, a minimophosative. The severity of clinical manifestations of blood loss depends on the pace of bleeding.
Several emissions degrees of gravity of acute blood loss.
1. With a shortage of circulating blood (BCC) 5-10%. The general condition is relatively satisfactory, the increase in the pulse is noted, but it is sufficient filling. Blood pressure (blood pressure) is normal. When studying blood hemoglobin more than 80 g / l. On capillaroscopy The condition of microcirculation is satisfactory: on a pink background, fast blood flow, not less than 3-4 loops.
2. With a BCC deficiency up to 15%. The overall state of moderate. Tachycardia is noted to 110 in 1 min. Systolic blood pressure decreases to 80 mm Hg. Art. In red blood analyzes, the reduction of hemoglobin from 80 to 60 g / l. With capillaryroscopy, fast blood flow is revealed, but on a pale background.
3. With the BCC deficiency up to 30%. The general severe condition of the patient. Pulse threaded, with a frequency of 120 in 1 min. Arterial pressure is reduced to 60 mm Hg. Art. With capillaryroscopy Pale background, slowing down blood flow, 1-2 loops.
4. With a BCC shortage of more than 30%. The patient is in very hard, often agonal state. Pulse and blood pressure on peripheral arteries are absent.
3. Clinical picture of various types of bleeding
Clearly define, from which vessel bleed, it is possible only when outdoor bleeding. As a rule, with outdoor bleeding, the diagnosis is not difficult. In case of damage to the arteries, blood is poured into an external medium with a strong pulsating jet. Scarlet blood. This is a very dangerous state, since arterial bleeding quickly leads to a critical anemization of the patient.
Venous bleedingAs a rule, it is characterized by a constant expiration of dark blood. But sometimes (when the wounded of large venous stems) may be diagnostic errors, since the transfer ripple is possible. Venous bleeding is dangerous possible by the development of an air embolism (with low central venous pressure (CVD)). For capillary bleedingthere is a constant expiration of blood from the entire surface of damaged tissue (by the type of dew). Especially severe capillary bleeding, which occur in injury to parenchymal organs (kidneys, liver, spleen, lungs). This is due to the peculiarities of the structure of the capillary network in these bodies. Bleeding in this case is very difficult to stop, and during surgery on these organs it turns into a serious problem.
With different types internal bleedingthe clinic is different and not so applied as with outdoor.
Methods for determining the volume of blood loss
There is a method of indicative determination of the volume of blood loss in clinical features (see ch. "Clinic of acute blood loss").
The Libov method is used in operational interventions. The amount of blood lost by patients during the intervention is defined as 57% of the mass of all used gauze napkins and balls.
The method of determining blood loss on the specific weight of blood (van slice). The specific weight of the blood is determined by a dialing of tubes in which a solution of copper sulfate is located in various dilutions. The blood under study consistently dripped into solutions. The proportion of the dilution in which the drop is not sinking and is delayed for a while, and is considered equal to the specific weight of the blood. The volume of blood loss is determined by the formula:
VKR \u003d 37 x (1,065 - x),
where VKR is the volume of blood loss,
x is a certain specific weight of blood, as well as according to the Borovsky formula, taking into account the magnitude of the hematocrit and blood viscosity.
This formula is somewhat different for men and women.
DTSCM \u003d 1000 x V + 60 x HT - 6700;
Dzkzh \u003d 1000 x V + 60 x HT - 6060,
where DTSCM is a circulating blood deficiency for men,
Dzkzh - circulating blood deficiency for women,
V - blood viscosity,
HT - hematocrit.
The only disadvantage of this formula can be considered some inaccuracy determined with its help in the early period after the bloodsture, when there was no compensatory blood dilution (hemodilution). As a result, the volume of blood loss occurs.
4. The reaction of the body in response to bleeding
In the body of an adult, it contains approximately 70-80 ml / kg of blood, and not all it is in constant circulation. 20% of blood is in the depot (liver, spleen). The circulating volume is blood that is not in the vessels of the deposit organs, and its main part is contained in the veins. In the arterial system, 15% of the whole body of the body is constantly located, 7-9% is distributed in capillaries, the rest of the amount is deposited in the venous system.
Since blood performs in the body of homeostatic functions, all physiological mechanisms are aimed at preventing disorders of its operation.
The human body is sufficiently resistant to blood loss. There are both system and local mechanisms of spontaneous cessation of bleeding. Local mechanisms include the reactions of the damaged vessel, which are due both to its mechanical properties (due to the elastic properties of the vascular wall, it takes place to reduce and closing the enlightenment of the intima ointment) and vasomotor reactions (vessel reflex spasm in response to damage). General mechanisms include coagulative and vascular-thrombocyte mechanisms of hemostasis. In case of damage to the vessel, the processes of aggregation of platelets and the formation of fibrin bunches are launched. Due to these mechanisms, a thrombus is formed, which closes the clearance of the vessel and prevents further bleeding.
All mechanisms are aimed at maintaining central hemodynamics. To this end, the body is trying to maintain the volume of circulating blood by activating the following mechanisms: blood is ejected from the depot organs, the blood flow is slowed down, the blood pressure is reduced. In parallel, the bloodstream is maintained mainly on the main vessels (with the priority blood supply to vital organs - heart and brain). With the inclusion of the blood pressure centralization mechanism, microcirculation seriously suffers, and the blood flow of the microcirculatory channel begins long before the clinically detected signs of the macrocirculation disorders (it should be borne in mind that blood pressure may be normal with a loss of up to 20% of the BCC). Disruption of capillary blood flow leads to a violation of the blood supply to the biennies, the development of hypoxia and dystrophic processes in it. An adequate indicator of the state of microcirculation is the clinical indicator as a flow rate of urine.
The total reaction to bleeding in Glyaevo proceeds into four phases. This is a safety (until the bleeding stop), compensatory (centralization of blood flow), reparative (hemodilyuction due to the movement of the tissue liquid and lymph into the bloodstream) and the regenerative (restoration of the normal amount of hematocrit due to the regeneration of the shape elements) of the phase.
5. Stop bleeding
Temporary stop methods.
1. Finger pressed (mainly for arterial bleeding). Method for immediately stopping bleeding. Allows you to win time. Unfortunately, the cessation of bleeding this method is extremely short. Finger pressed arteries:
1) Sleepy artery. The inner edge of the mouse muscle at the level of the top edge of the thyroid cartilage. The artery is pressed against the sleepy tubercle on the transverse process of the Vi cervical vertebra;
2) Plug artery. Poor amenable finger pressedtherefore, it is possible to achieve blood flow restrictions on it, maximizing the hand back in the shoulder joint;
3) Mortgage artery. Pressed in the axillary depression to shoulder bone. Approximate place of pressed - on the front border of hair growth;
4) Shoulder artery. Pressed against the shoulder bone. Approximate place of pressed - the inner surface of the shoulder;
5) femoral artery. Pressed against the pubic bone. Approximate place of pressed - the border between the middle and the inner third-party ligament.
2. Maximum flexion of limb in the joint with roller (arterial) with:
1) the gulling bandage (with venous, capillary bleeding);
2) harness. It is superimposed proximal to the place of injury for arterial bleeding, distal - for venous. Using the harness in arterial bleeding, it can be added to a maximum of 1.5 hours. If, after this time, the need for its use is preserved, it is dissolved by 15-20 minutes and then superimposed again, but already at another place;
3) clamping on the vessel in the wound (with arterial or venous bleeding);
4) temporary endoprosthetics (with arterial bleeding in the absence of opportunity for an adequate final stop in the near future). Effective only with the obligatory heparinization of the patient;
5) exposure to cold (with capillary bleeding).
Methods of final stop.
1. Tinging the vessel in the wound.
2. Tinging the vessel for.
3. Vascular seam.
4. Vessel transplantation.
5. Embolization of the vessel.
6. Vessel prosthetics (previous methods are used in damage to large vessels that remained to stop bleeding mainly from small arterial stems).
7. Laser coagulation.
8. Determocoagulation.
In the presence of massive bleeding, occurring with serious violations in the hemostasis system (ICH syndrome, coagulopathy of consumption, etc.), listed methods of stopping bleeding can be a little, sometimes additional medical measures are required to correlate them.
Biochemical methodsimpact on the hemostasis system.
1. Methods affecting the body as a whole:
1) transfusion of blood components;
2) platelet mass, fibrinogen intravenously;
3) cryoprecipitate intravenously;
4) aminocaproic acid parenteral and enteral (as one of the hemostasis methods for gastric bleeding, especially erosive gastritis).
2. Methods of local exposure. Applied in operations flowing with damage to the tissue of parenchymal organs and accompanied by capillary employed bleeding:
1) Muscle wound tamponade or gland;
2) hemostatic sponge;
3) Fibrin film.
Much more difficult to diagnose internal bleedingnot accompanied by painful syndrome. If the blood loss during internal bleeding does not exceed 10-15% of the BCC, then the clinical manifestations in this case are pretty scarce and can manifest moderate tachycardia and shortness of breath, fainted states. With more massive blood loss in excess of 15% of the CCC, the centralization of blood circulation is developing with a typical picture of the hypovolemic shock.
Classification of bleeding by source
- Arterial bleeding is the most dangerous type of blood loss in which blood flows out of the damaged artery scarlet pulsating jet. If you do not take urgent action to stop bleeding, it is possible to quickly the death of the victim due to massive blood loss.
Classification of bleeding on clinical manifestations
- Outdoor bleeding - difficulties for diagnosis are not and observed in disruption of the integrity of the skin with various kinds of injuries.
Classification of bleeding in time of occurrence
- Primary bleeding - occur immediately after damage to the blood vessel.
- Early secondary bleeding - develop in the first hours or day after damage, the main reasons are the relief of the vascular spasm or the separation of the thrombolytic plaque due to the increase in blood pressure.
Classification of bleeding in the speed of development
- Lightning blood loss - arise after damage to the heart or aorta and quickly end in the death of the victim.
Acute blood loss
Acute blood loss - irrevocable loss of blood for a short time. Arises due to bleeding from damaged vessels. Affects the condition of all organs and systems. The loss of a significant amount of blood is accompanied by the development of hemorrhagic shock representing a threat to the life of the patient. The cause of acute blood loss can be injured and some diseases. It is manifested in pallor, tachycardia, decreased blood pressure, shortness of breath, euphoria or oppression of consciousness. Treatment is the elimination of the source of bleeding, blood infusion and blood substitutes.
Acute blood loss
Acute blood loss - a condition in which the body quickly and irrevocably loses a certain amount of blood as a result of bleeding. It is the most common damage to the human body throughout history. It occurs during injuries (both open and closed) and the destruction of the vessel wall in some diseases (for example, ulcerative processes in the gastrointestinal tract). Loss of large blood loss is a danger to life due to a sharp decrease in the BCC and the subsequent development of hypoxia, hypoxhemia, hypotension, insufficiency of the blood supply internal organs and metabolic acidosis. In severe cases, the development of DVS-syndrome is also possible.
The greater the volume of blood loss and the faster blood is poured, the hardest state of the patient and worse the forecast. In addition, factors such as age, the general condition of the body, intoxication, chronic diseases, and even the time of year are influenced by the body's response of the body (in the warm season, the blood loss is heavier). Loss 500 ml (10% BCC) in adult healthy man Does not lead to significant impairments of hemodynamics and does not need special correction. With a loss of a similar volume by a patient suffering from chronic disease, it is necessary to replenish the OCC using blood, blood and plasma reform. The elderly, children and pregnant women suffering from toxicosis are heavier than this condition.
Causes and classification of acute blood loss
Most often, injuries are becoming the cause: injuries of soft tissues and internal organs, multiple fractures or damage to large bones (for example, a heavy pelvis fracture). In addition, the sharp blood loss may occur as a result of a stupid injury with a breakdown of a particular organ. Especially dangerous wounds with damage to large vessels, as well as injuries and breaks of parenchymal organs. Among the diseases that can cause blood loss - stomach ulcers and duodenal gut, Mullder-Weis syndrome, liver cirrhrosis, accompanied by varicose veins of the esophagus, malignant tumors The gastrointestinal tract and organs of the chest, the gangrene of the lung, the infarction of light and other diseases, in which the destruction of the vessel wall is possible.
There are several classifications of acute blood loss. The most widely in clinical practice is the following classification:
In addition, supermassive or deadly blood loss is isolated, in which the patient loses over 50% of the BCC. With such an acute blood loss, even in the case of immediate replenishment of volume in the absolute majority of cases, irreversible changes in homeostasis are developing.
Pathogenesis of acute blood loss
In case of acute blood loss, the veins are annoyed, resulting in a persistent and total venous spasm. There are no significant hemodynamic disorders. Filling of the BCC in healthy people occurs within 2-3 days due to the activation of hematopois. With a loss of over 1 liters, not only venous receptors, but also alpha-receptors arteries are irritated. This causes the excitation of the sympathetic nervous system and stimulates the neurohumoral reaction - the ejection of the adrenal cortex of the large number of catecholamines. At the same time, the amount of adrenaline exceeds the norm of the enemy, the amount of norepinephrine is 5-10 times.
Under the influence of catecholamines, the capillaries are first spasched, and then larger vessels. The contractile function of myocardium is stimulated, tachycardia occurs. The liver and spleen are reduced by throwing blood from the depot to the vascular bed. Arteriovenous shunts are revealed in the lungs. All of the above allows for 2-3 hours to provide the necessary amount of blood vitally important organs, maintain hell and hemoglobin levels. Subsequently, nervous reflex mechanisms are depleted, vazodytation comes to replace angiospasm. The bloodstream in all vessels is reduced, erythrocyte stasis occurs. Exchange processes in tissues are even more violated, metabolic acidosis develops. All of the above forms the picture of hypovolemia and hemorrhagic shock.
The severity of hemorrhagic shock is determined taking into account the pulse, blood pressure, diuresis and laboratory indicators (hematocrit and hemoglobin content). Under the influence of aldosterone in the kidneys, arteriovenous shunts are opened, as a result, the blood is "reset", without passing through the YUCSTAGLOMERULAR unit, which leads to a sharp decrease in diuresis up to Anuria. Because of the hormonal changes in the plasma, it does not come out of the vessels in interstitial fabrics, which, along with the deterioration of microcirculation, further aggravates the disorders of the tissue exchange, takes the acidosis and provokes the development of polyorgan deficiency.
The listed violations are completely unable to stop even with immediate replenishment of blood loss. After the restoration of the BCC, the decrease in blood pressure is preserved for 3-6 hours, disorders of blood flow in the lungs - within 1-2 hours, circulating blood flow - for 3-9 hours. Microcirculation in tissues is restored only on 4-7 days, and complete elimination of the consequences takes a lot of weeks.
Symptoms and diagnostics of acute blood loss
The symptoms of acute blood loss include sudden weakness, pulse increase, decreased blood pressure, pallor, thirst, dizziness, pre-spanning states and fainting. In severe cases, shortness of breath is possible, periodic breathing, cold sweat, loss of consciousness and marble coloring of the skin. Along with clinical signs there are laboratory indicators, allowing to evaluate the volume of blood loss. The number of erythrocytes is reduced below 3x10¹² / l, hematocrit - below 0.35. However, the listed figures only indirectly indicate the degree of acute blood loss, since the results of the analyzes reflect the actual course of events with some "lag", that is, with a massive blood loss in the first hours of tests may remain normal. This is especially observed in children.
Given the above, as well as the nonspecification of signs of acute blood loss (especially easy or moderate), it is necessary to pay special attention to the external features. With external bleeding, the establishment of a blood loss fact is not difficult. In the inner bleeding, indirect signs are taken into account: hemochkali in pulmonary bleeding, vomiting of the "coffee grounding" and / or melanoe in the pathology of the esophagus, stomach and intestines, the voltage of the anterior abdominal wall and dulling at percussion in the detachments of the abdomen during the damage to parenchymal organs, etc. Data inspection and history complement the results of instrumental research. If necessary, they perform radiography, MRI, ultrasound, laparoscopy and other studies, prescribe consultations of a vascular surgeon, an abdominal surgeon, a thoracic surgeon and other specialists.
Treatment of acute blood loss
Tactics of treatment depends on the volume of acute blood loss and the state of the patient. With a loss of up to 500 ml, special events are not required, the restoration of the BCC occurs independently. With a loss of up to 1 liter, the volume of volume replenishment is solved differentially. With tachycardia, no more than 100 UD / min, the normal blood pressure and diocese of infusion are not shown, in the event of a violation of these indicators, plasma changes are transfused: saline, glucose and dextran. Reduced blood pressure below 90 mm Hg. Art is an indication for drip infusion of colloidal solutions. With a decrease in blood pressure below 70 mm Hg. Art. Produce jet transfuses.
At a moderate degree (up to 1.5 l), the transfusion of plasma substitutes in the amount, which is 2-3 times the value of the loss of the OCC is required. Along with this, blood transfusion is recommended. In case of severe, blood transfusion and plasma substitutes are necessary in volume, which is 3-4 times the value of the loss of the OCC. With a massive blood loss, 2-3 blood volumes and several plasma volumes are required.
The criteria of adequate restoration of the BCC: the pulse is not more than 90 UD / min, a stable pressure of 100/70 mm Hg. Art., hemoglobin 110 g / l, FLOLD 4-6 cm. Waters. Art. and diuresis more than 60 ml / h. At the same time, one of the most important indicators is diuresis. Restoration of the urination for 12 hours from the beginning of blood loss is one of the paramount tasks, since otherwise the kidney channels are necrotized, and irreversible renal failure develops. For normalization, diuresis use infusion therapy in combination with furosemide and euphilline stimulation.
Acute blood loss - treatment in Moscow
Manager of Diseases
ODS and injury disease
Latest news
- © 2018 "Beauty and Medicine"
it is intended only for familiarization
and does not replace qualified medical care.
Classification of bleeding
Bleeding (Haemorrhagia) is the expiration of blood from a blood vessel into an external environment or cavity and body fabric. As a bleeding vessel. Arterial. Venous 3. Arteriovenomous.4. Capillary.5. Parenchimatous. By clinical picture.1. Outdoor (blood vessel falls into the external environment) .2. Internal (blood flowing from the vessel is located in the tissues (with hemorrhages, hematomas), hollow organs or body cavities) .3. Hidden (without a clear clinical picture). For internal bleeding There is an additional classification. . Blood expires in fabric:1) hemorrhages in the tissue (blood expires in tissue in such a way that they are morphologically cannot be divided. The so-called impregnation occurs); 2) subcutaneous (bruise); 3) subtlety; 4) subarachnoidal; 5) subserosnial. Hematoma (massive bloodstream in tissue). They can be removed by puncture. According to the morphological picture. Metcasts (blood spreads under the interstitial gaps) .2. Intranate (the expiration of blood occurs with the destruction of the tissue and the formation of the cavity). By clinical manifestations. Hematoma pulsating (in the case of a hematoma cavity with arterial barrel) .2. The hematomas are non-executing. Also in intra-haired bleeding 1. Blood expirations in natural body cavities: 1) abdominal (hemoperitoneum); 2) cavity of the heart bag (hemopericard); 3) pleural cavity (hemotorax); 4) the cavity of the joints (hemarthrosis). 2. The expiration of blood in the hollow organs: the gastrointestinal tract (gastrointestinal tract), urinary pathways, etc.In the dark bleeding. The acute (from large vessels, a large amount of blood is lost within minutes) .2. Sharp (within an hour) .3. Subacute (within 24 hours) .4. Chronic (within weeks, months, years). At the time of occurrence. Primary 2. Secondary. Patientatomy classification. Bleedings arising from the mechanical destruction of the walls of the vessels, as well as with thermal lesions. Arrosion bleeding arising due to the destruction of the vessel wall by the pathological process (the collapse of the tumor, the breakdown, purulent melting, etc.). 3 Diapened bleeding (with impaired permeability of blood vessels).
26. Bleeding is internal and outdoor. Clinic, diagnostics, first aid. Right bleeding: The main sign of the presence of wounds is outdoor bleeding. The color of the blood is different: scarlet - with arterial, dark-cherry - with venous bleeding. Bleeding is not only of the aorta, but also from the femoral or axillary artery can lead to death a few minutes after the injury. Damage to large veins can also quickly cause a fatal outcome. In case of damage to the large veins of the neck and chest, such a dangerous complication as an air embolism is possible. This complication develops as a result of air from entering the wound in Vienna (in the right heads of the heart, and then into a moile artery) and blockage of large or small branches. Internal bleeding: with traumatic damage or development of the pathological process in the vessel area, internal bleeding occurs. Recognize such bleeding is more complicated than the outer. The clinical picture is made up of common symptoms caused by blood loss, and local signs depending on the localization of the source of bleeding. In case of acutely developed anemia (for example, a disturbed ectopic pregnancy or a break of a spleen capsule in the presence of a podcapsula hematoma) there are pallor of the skin and visible mucous membranes, the darkening in the eyes, dizziness, thirst, drowsiness, may be fainted. Pulse frequent per minute, hell lowered. With slow bleeding, signs of blood loss are developing gradually.
27. Acute blood loss. The degree of blood loss, diagnosis, danger and complications. Acute blood loss - This is a sudden blood flow from the vascular bed. The main clinical symptoms of the decrease in the BCC (hypovolemia) are the paleness of the skin and visible mucous membranes, tachycardia and arterial hypotension. The cause of acute blood loss There may be injury, spontaneous bleeding, operation. Of great importance are the speed and volume of blood loss. slow loss Even the large blood volumes of ml) have time to join compensatory mechanisms, hemodynamic disorders arise gradually and are not very serious. On the contrary intensive bleeding with a loss of a smaller blood volume leads to sharp hemodynamic violations and, as a result, hemmorrhagic shock. The following stages of gemmorrhagic shock are distinguished: Stage 1. (compensated shock) when blood loss is 15-25% of the BCC, the patient's consciousness is preserved, the skin's pale, cold, ad is moderately reduced, the pulse of weak filling, moderate tachycardia of dups / min. Stage 2. (decompensated shock) is characterized by an increase in cardiovascular disorders, a breakdown of compensatory mechanisms of the body occurs. The blood loss is 25-40% of the BCC, a violation of consciousness to sophore, acricyanosis, cold limbs, blood pressure is sharply reduced, tachycardiaud / min, the pulse is weak, threaded, shortness of breath, oliguria to 20 ml / hour. Stage 3. (irreversible shock) - this concept is relative and largely depends on the applied methods of resuscitation. The condition of the patient is extremely heavy. Consciousness sharply oppressed until the full loss, the skin of the pale, the "marble" of the skin, systolic pressure below 60 mm.rt.st., the pulse is determined only on the trunk vessels, sharp tachycardia douud / min.Ak express diagnostics Estimates of the severity of shock uses the concept of a shock index - shi - the ratio of the heart rate to the size of systolic pressure. With shock 1 degree shi \u003d 1 (100/100), shock 2 degrees - 1.5 (120/80), shock 3 degrees - 2 (140/70). Hemmorrhagic shock is characterized by the general serious condition of the body, insufficient blood circulation, hypoxy , impairment of metabolism and functions of organs. The basis of the pathogenesis of shock is hypotension, hypoperfusion (reduction of gas exchange) and hypoxia organs and tissues. The leading damaging factor is circulatory hypoxia. Relatively fast loss of 60% of the BCC is considered for a fatal person, blood loss 50% of the BCC leads to a disrupting of the compensation mechanism, the blood loss 25% of the BCC is almost completely compensated by the body. The size of the blood loss and its clinical manifestations: blood loss ), no hypovolemia, blood pressure is not reduced; The blood loss% of the BCC (ml), the lightweight degree of hypovolemia, the blood pressure is reduced by 10%, moderate tachycardia, the pallor of the skin, cooling limbs; blood loss% of the BCC ml), the average severity of hypovolemia, blood pressure is reduced to, tachycardia to 120 ° C / min, pallor skin covers, cold sweat, oliguria; Blood loss up to 50% of the BCC ml), the heavy degree of GGIPOVOLEMI, adhesion down - but to 60 mm. Hg, the pulse threaded, consciousness is absent or confused, sharp refreshment, cold sweat, anury; The blood loss of 60% of the BCC is deadly. Slowness is associated with the development of hemorrhagic shock.
28. Treatment of acute blood loss. Integrated treatment It may prevent the development of hemorrhagic shock, because it should be launched as quickly as possible. In the case of heavy bloodstures, they immediately begin to introduce blood fluids, the use of which is based on the fact that the loss of plasma and, therefore, the decrease in the BCC is carried out is much harder than the loss of red blood cells. Albumin, protein, dextran [cf. Like. Mass 000] are well held in the bloodstream. If necessary, you can use crystalloid solutions, but it should be remembered that they quickly leave the vascular channel. Low molecular weight dexts (dextran [cf. mol. Massive0 000]) replenish the volume of intravascular fluid, improve microcirculation and rheological properties of blood. The transfusion of blood preparations is necessary when the hemoglobin level is reduced below 80 g / l and the hematocrit rate is less than 30. With a heavy acute blood loss, treatment is starting with inkjet infusion into one, two or three veins and only after lifting the garden above 80 mm Hg. We go to drip infusion. The elimination of anemia is used by the erythrocyte infusion, it is advisable to enter it after infusion of blood substitutes, as it improves the capillary blood flow and reduces the deposit of blood formation elements.
29. Hemorrhagic shock. Causes, clinic, treatment. Gemorrhagic shock - the urgent state of the body, developing during the acute blood loss. In the first place among the causes of acute bleeding are injured. There are open and closed blood damage. The degree of blood loss. That is, the quantities that decreases the volume of circulating blood (BCC) for a sufficiently short time. It should be recalled that the blood loss of up to 0.5 liters (on average 25-30%) during several weeks will not lead to shock. The anemia clinic will be gradually developed. So, with a decrease in the total BCC to 10%, hemorrhagic shock does not develop. The patient can only disturb the weakness and reduction of tolerance to physical exertion. In other words, a person becomes harder to transfer the loads that were previously given to him easily. The fact is that such a volume of blood loss can be reserved by reserves from depositated (in other words - not participating in the general blood circulation) of blood. Gemorrhagic shock begins to develop when the volume of lost blood is 500 or more. This is 10-15% of the BCC. The loss of more than 3.5 liters of blood is considered fatal, which is 70% of the BCC. Therefore, in the clinic, for calculating the amount of medical care, it is customary to distinguish three severity. Primes of the first severity (it is observed with a loss of 10 to 25% of the BCC) there is a moderate decrease in blood pressure, breathing. Skin covers become pale. The patient complains of dryness in the mouth and the feeling of thirst. Weakness causes such patients to move as little as possible. Otherwise, dizziness is noted and, even, short-term loss of consciousness - syncopes. The average severity is observed in the blood loss from 25 to 45% of the BCC, or from one to two liters of blood. There is a more pronounced weakness. Consciousness becomes confused. Breathing is frequent and noisy. Cardiac frequency reaches 150 and arrhythmias can be marked. "Cracks" begin to appear on dry. This is the manifestation of its natural folds. The heavy degree of hemorrhagic shock develops with a loss of 40-65% of the BCC (2.5-3 liters). Consciousness is always oppressed, right up to coma. The pallor of the skin is expressed. Breathing superficial and not rhythmic. With a loss of 3 liters of blood, it acquires pathological nature - alternation of respiratory movements and pauses in breathing. Heart tones barely listened and always arrhythmic. The pulse is weak, even at the carotid arteries. The 70% (3.5-4 liters) is deadly. Almost instantly comes coma and death. Although, sometimes there is a short period of agony, which can be regarded as a short-term improvement. Intensiveness and intensive care drugs in patients with acute blood loss and in the state of hemmorrhagic shock at the prehospital stage are as follows: 1. Reducing or eliminating existing acute respiratory respiratory phenomena. Self (ODN), the cause of which may be aspiration of knocked teeth, blood, vomit, liquor, with a fracture of the skull base. Especially often, this complication is observed in patients with confused or absent consciousness and, as a rule, combined with the weave of the root of the language.
Treatment It comes down to the mechanical liberation of the mouth and oraloglot, aspiration of content using suction. Transportation can be carried out with an in-dale air duct or endotracheal tube and conducting IVL through them. 2. Holding anesthesia medical meansnot oppressing breathing and blood circulation. From central narcotic analgesics devoid side effects Opiates, you can use Lexir, Forers, tram. Nonarcotic analgesics (analgin, barallgyne) can be combined with antihistamine drugs. There are options for conducting oxygen analgesia, in / in the introduction of subnarchical doses of ketamine (Calipcola, Ketalar), but it is purely anesthetic benefits that require the presence of anesthesiologist and the necessary equipment. 3. Reducing or eliminating hemodynamic disorders, primarily hypovolemia. In the first minutes after severe injury, the main cause of hypovolemia and hemodynamic disorders is blood loss. Preventing the stop of the heart and all other serious violations - immediate and maximum possible elimination of hypovolemia. The main therapeutic event should be massive and fast infusion therapy. Of course, the stopping of outdoor bleeding should be preceded by infusion therapy.
Resuscitation in the case of clinical death due to acute blood loss is carried out according to the generally accepted rules. Transfusion therapy is only part of this complex and is aimed at replenishing the OCC. In carrying out intensive therapy with acute blood loss, it is necessary to ensure continuous transfusion therapy with a rational combination of existing funds. It is even less important to comply with a certain stratitude in the treatment, speed and adequacy of assistance in the most difficult setting.
Chapter 11. Bleeding and blood loss
11.1. Characteristics and classification of bleeding
Bleeding is the process of blood expiration from damaged blood vessels, which is the direct complication of combat wounds and the main cause of the death of the wounded on the battlefield and at the evacuation stages. In Velikhu, the Patriotic War, among the wounded, those killed on the battlefield, the died of bleeding were 50%, and in the military area they accounted for 30% of all fatal outcomes. In Afghanistan from bleeding and shock in medical institutions of the military district (Omnedb, garrison hospital), 46% of the wounded were dying.
Bleedings are classified depending on the time of their arbitration, the nature and caliber of the damaged blood vessels and the place of blood expiration.
Distinguish primary and secondary bleeding. Primary bleeding immediately after the injury or in the coming hours after it (weakening the gulling dressing, the outlet of the blood bundle from the vessel wound when shifting the wounded, bone fragment displacement, an increase in arterial pressure). Among the secondary bleeding distinguish early and late. Early secondary bleeding arise to the organization of thrombus. They appear on the 3-5th day after injury and are associated with the yield from the wound of the fusion of a loose blood thrombus (unsatisfactory immobilization, shocks during transportation, manipulation in the wound when dressing).
Late secondary bleeding occurs after the organization (granulation tissue) thrombus. They are associated with infectious process in the wound, the melting of blood cloth, the hematoma's suppuration, sequestration of the bruised vessel wall. Secondary bleeding is most often arising over the 2nd week after injury. They are preceded by the appearance of pain in the wound and an increase in body temperature without a disturbance of the outflow from the wound, a short-term breaking of blood bandages (the so-called signaling bleeding), the detection of vascular noise at auscultation of the wound circle. Secondary bleeding can also dwell; But threaten relapse.
Classification of bleeding
For the causal factor: injury, wound, pathological process. By the time limits: primary, secondary, one-time, re-, early, later.
In the form of a damaged vessel: arterial, venous, arteriovenous capillary (parenchymal).
At the place of blood outpouring: outer, internal, intramane, combined. As of hemostasis: continued, stopped. Depending on the place of blood expiration distinguishes bleeding outdoor, internal and intranate. Internal (hidden) bleeding can occur in anatomical body cavities and internal organs (Light, stomach, gut, bladder). Intranate bleeding even with closed fractures sometimes cause very large blood loss.
11.2. Definition and classification of blood loss
Clinical signs of bleeding depend on the volume of lost blood.
Bloodfromyerya - This state of the body arising after the bleeding and characterized by the development of a number of adaptive and pathological reactions.
With all the diversity of bleeding, their consequence - blood loss - has common features. It is necessary to know the signs of blood loss, allowing differential symptoms caused by the actual loss of blood, with other manifestations (consequences of injury, painful process, etc.). Features of each individual type of blood loss are considered in private sections of surgery.
The blood loss is classified both in terms of gravity of the occurrence of changes in the body. There are the magnitude of the blood loss and the severity of the postgalragic disorders, estimated primarily in the depth of developing hypovolemia, due to the value of the lost volume of circulating blood (BCC).
The amount of blood loss is considered from the position of a decrease in the amount of fluid filling the bloodstream; Erythrocyte losses that are carrier of oxygen; Plasma loss having a decisive value in tissue exchange.
Primary in the pathogenesis and tanatogenesis of blood loss remains a decrease in the volume of blood filling the vascular channel, which leads to a violation of hemodynamics. Another factor is important - a change in the organism oxygen regime. Hemodynamic and anemic factors lead to the inclusion of protective mechanisms of the body, due to which the bloodstream compensation may occur. Compensation becomes a consequence of the movement of extracellular fluid into the vascular channel (hemodulution); strengthening of lymphotoka; Regulation of the vascular tone, known as the "Circulatory Centralization"; increase the frequency of heart rate; Increase the extraction of acid in tissues. Compensation of blood loss is the easier, the less blood lost and the slower it expires. At the same time, with a violation of compensation and even more during decompensation, blood loss goes into a hemorrhoid shock, which was determined by the main causal factor.
The so-called death threshold is determined not by the magnitude of bleeding, but the number of erythrocytes remaining in circulation. This critical reserve is equal to 30% of the volume of erythrocytes and only 70% of the plasma volume. The body can survive with loss of 2/3 of the volume of erythrocytes, but does not transfer the loss of 1/3 of the plasma volume. Such a consideration of blood loss allows you to more fully take into account the compensator processes in the body.
Classification of blood loss
According to the form: traumatic (wound, operating), pathological (for the disease, pathological process), artificial (exfusion, therapeutic crochotus).
For the speed of development: acute, subacute, chronic.
By volume: Small - from 5 to 10% of the BCC (0.5 l); Average - from 10 to 20% of the BCC (0.5-1.0 l); large - from 21 to 40% of the BCC (1.0-2.0 l); Massive - from 41 to 70% BCC (2.0-3.5 liters); Mortal - more than 70% of the BCC (more than 3.5 liters).
According to the severity and the possibility of developing a shock: light (BCC deficiency 10-20%, globular volume up to 30%), no shock; Average (CCC deficiency 21-30%, globular volume 30-45%), shock develops with long hypovolemia; Superior (BCC deficiency 31-40%, globular volume is 46-60%), shock is inevitable; Extremely heavy (BCC deficiency more than 40%, globular volume of more than 60%), shock, tercenual state
According to the degree of compensation: I period - compensation (BCC deficiency up to 10%);
II period - relative compensation (BCC deficiency up to 20%); Iii period - violation of compensation (CCC deficiency 30% -40%); IV period - decompensation (BCC deficiency more than 40%)
Internal bleeding recognize, tracing the course of the wound channel, with the help of auscultation and percussion of breasts and abdomen, by conducting punctures, toracotenate, laparing and x-ray research methods. General importance in diagnostics have generally crystal signs of blood loss:
weakness, drowsiness, dizziness, yawning, pale and cooling skin and mucous membranes, shortness of breath, frequent and weak pulse, decrease in blood pressure, violation of consciousness. However, the decisive role plays the calculation of the magnitude of blood loss.
The clinical picture does not always correspond to the number of lost blood, especially in young people who have the adaptive capabilities of the body. Sensitivity to blood loss increases with overheating or supercooling, overwork, injury, ionizing radiation.
11.4. Determination of blood loss
The determination of blood loss in field conditions is certain difficulties, as there is no enough informative and fast method for its accurate measurement and the doctor has to be guided by the Council of clinical signs and data of laboratory research.
In military field surgery, use 4 groups of methods for this purpose:
1. On localization of injury and indicator of damaged tissues.
2. In hemodynamic indicators ("shok index", systolic arterial pressure).
3. At concentration of blood indicators (hematocrit, hemoglobin content).
4. By changing the BCC.
When assisting the victim, it is recommended to approximately determine the magnitude of blood loss in localization of injury: with severe breast injury, it is 1.5-2.5 liters, the abdomen - up to 2 liters, with multiple fractures of the pelvic bones - 2.5-3.5 liters, open Fracture of hips - 1, more than 40%)
11.3. Diagnosis of bleeding and blood loss
Acute outdoor bleeding is quite clearly diagnosed and with timely assistance successfully stops. The danger is injured by large arteries and veins, as well as parenchymal organs. It is difficult to diagnose internal and secondary bleeding.
Internal bleeding recognize, tracing the course of the wound channel, with the help of auscultation and percussion of breasts and abdomen, by conducting punctures, thoracoteshetosis, laparocenesis and right into 4 groups:
1. Small wounds - the surface of damage less surface palm. Blood lodge is equal to 10% OCC.
2. Wounds of medium sizes - the surface of the damage does not exceed 2 palms. Blood loss up to 30% OCC.
3. Large wounds - the surface is more square 3 palms, but does not exceed the area 5 palms. The average blood loss is about 40% OCC.
4. Wounds of very large sizes - the surface is larger than the area 5 of it. Blood lodge about 50% OCC.
In all conditions, it is possible to determine the size of blood loss in hemodynational indicators - shock index. Despite the criticism of the use as a criterion for the severity of blood loss of blood pressure, it is invariably used with the frequency of heart abbreviations and will be used at the advanced steps of evacuation. Essentially, these are the first important objective indicators that allow us to approximately determine not only the severity of the state of the wounded, but also the amount of lost blood.
The shock index is the ratio of heart rate reduction to systolic arterial pressure. Normally, this indicator is 0.5. Each subsequent increase of 0.1 corresponds to the loss of 0.2 liters of crises, or 4% of the BCC. The increase in this indicator up to 1.0 corresponds to the loss of 1 liter of blood (20% of the BCC), to 1.5
1.5 liters (30% OCC), up to 2 - 2 l (40% of the BCC).
This method was informative in acute situations, but it admits the priority of the true size of blood loss by 15%. The method should not be used with slow bleeding. To simplify the calculations was developed by a nomogram based on the shock index (Table 11.1). In it, the main values \u200b\u200bof the index define the volume of blood loss in absolute figures in the wounded 3 weight categories, as well as the corresponding values \u200b\u200bin the percentage of proper OCC, which is 7% of the body weight for men and 6.5% for women. These data allow us to approximately calculate the magnitude of the bloodstream from any wounded. As purely approximately given indicators of systolic blood pressure, allowing to approximately judge the loss of blood. This bloodless method of determining acute blood loss can be used at the forefronts of medical evacuation, especially in emergency situations in the mass arrival of the wounded.
Among the 3rd group methods, the determination of blood loss is recommended on the basis of the specific gravity (relative density) of the blood using the G.A. nomogram Barashkova. However, the method gives a significant percentage of errors, increasing in the acute situation the magnitude of blood loss is almost visible. The magnitude of the error decreases as the autogriemodilation develops.
More appropriately used in the calculations, hematocrit or hemoglobin content. The highest propagation has a hematocrit MOORE method, presented by the following formula:
where kp is blood loss, l; OCCD - due BCC; GT D - proper hematocrit, constituting 45% in men and 42% in women; GTF is the actual hematocol, determined by the hemodynamic stabilization affected after stopping the bleeding and stabilization. In this formula, instead of hematocrit, the hemoglobin content can be used, considering the proper level 150 g / l.
To simplify calculations, you can use the nomogram (Fig. 11.1). The nomogram is calculated for the wounded 4 weight categories from 50 to 80 kg. After comparing the hematocrit and body weight and body weight we find the desired value. Straight radial lines connect the rounded values \u200b\u200bof the listed indicators, between which, if necessary, can be distinguished by intermediate values.
To continue download, you must collect a picture:
Classification of bleeding
All bleeding is distinguished by anatomical attribute, in relation to the occurrence, in relation to the external environment and clinical flow.
According to anatomical sign distinguish:
Arterial bleeding - It is characterized by emissions from wounds of scarlet, bright blood pulsing jet (in the form of a fountain). Very dangerous quickly coming blood loss.
Venous bleeding - The blood of the dark-cherry color flows slowly, smooth jet. Dangerous air embolism, i.e. The air intake into the lumen of the damaged vein (often occurs during damage to the neck of the neck). The threatening life is injured by the wounded of the major trunk veins of the chest and abdominal cavities (especially the hollow and portal veins).
Mixed bleeding - It occurs at deep wounds, when arteries and veins are damaged.
Capillary bleeding - Blood performs drops, in the form of dew, over the entire wound surface. Prosen for spontaneous stop, dangerous only for people with reduced blood intake.
Parenchimato bleeding - It is dangerous in that it is internal, from parenchymal organs (liver, spleen, kidneys, lungs). These bodies have their own characteristics, due to which parenchymal bleeding itself does not stop and requires compulsory operational intervention. These organs have a very branched network of arterial and venous vessels and capillaries. When damaged, they are gaping and do not fall. The fabric of parenchymal organs contains anticoagulants with which the flowing blood is mixed, therefore, thrombosis is disturbed.
By time occurrence distinguish primary bleedingthat occur immediately after the action of the damaging factor, and secondaryarising after a while after stopping primary bleeding at the same place.
Secondary early Bleeding is re-bleeding from the same vessel in a few hours or 1-3 days after stopping primary bleeding. It may result from slipping ligature with a bandaged vessel, breaking the thrombus closing the defect in the vessel wall, with rough dressing, improper transportation. The reason may be increased blood pressure and pushing the blood jet thrombub.
Secondary late bleeding It is usually happening with purulent complications in the wound. Purulent inflammatory process It can cause a thrombus melting, covering the clearance of the vessel, a teething of a ligature, or an embedded vascular seam, cause the destruction of any other vessel located in the wound. Secondary bleeding may occur due to the breakdown of the vessel wall of a solid foreign body, a bone fragment or metal, drainage. A long-term inflammatory process in the wound can lead to multiple renewal of bleeding.
In relation to the external environment There is a difference of external bleeding - if the blood is fused outside the body, and internal - if the blood accumulated in the cavities and tissues.
If the cavity has anatomical connection with the environment, then the bleeding is called internal open (nasal, pulmonary, uterine, gastric, intestinal or urinary tract).
If the cavity does not have anatomical connection with the external environment, then the bleeding is called internal closed (In the hollow of the joint, in the chest cavity, in the abdominal cavity, in the oily-carrying bag, in the cavity of the skull).
Urban bleeding Appears as a result of impregnating the blood of the fabrics surrounding the vessel. There are several types of urban bleeding: petechia (small hemorrhages in the skin), ekkimosis (point hemorrhages), hematoma (blood cluster in tissues and organs).
By clinical flow distinguish sharp and chronic bleeding.
Acute bleeding occurs suddenly and is characterized by the rapid clinical development of symptoms. The consequence of acute bleeding is hemorrhagic shock.
Chronic bleeding occurs with small, but often emerging bleeding (nasal, hemorrhoidal, etc.). Consequently chronic bleeding is chronic anemia.
The blood loss is more than 2000 ml with a decrease in OCC by more than 30% is considered massive.
Most often occurs such a complication as acute anemia which develops with a loss of 1-1.5 liters of blood. The clinical picture at the same time is manifested by a sharp impaired blood circulation. A sudden reduction in the BCC causes a sharp deterioration in the heart function, progressing the fall of blood pressure, which in the absence of medical care entails development hemorrhagic shock. In various organs, severe disorders of microcirculation arise: impaired blood flow rate in capillaries, the appearance of micropots (as a result of gluing erythrocytes into mint columns). In the lungs, this leads to a violation of gas exchange, blood is poorly saturated with oxygen, which in combination with sharply reduced BCC causes oxygen starvation of all organs and tissues. Hemorrhagic shock requires emergency resuscitation measures. The later the treatment of acute anemia began, the irreversible microcirculation and metabolic processes in the injury body are becoming irreversible.
No less terrible complication is compression of organs and fabrics of spearing blood - Tamponade Hearts, compression and destruction of the brain. These complications are so dangerous that they require emergency operation.
Chronic anemia Developed as a result of small, but frequent blood loss.
Acute respiratory failure It is evolving because due to blood loss, there are little blood carrier of oxygen tissues. OND is manifested by a violation of the rhythm, depth and frequency of breathing. In severe cases there may be a complete respiratory stop.
– Reducing the daily amount of urine to 50 ml, also occurs as a result of blood loss. Those substances that should be outlined with urine, while delaying in the body, causing its poisoning.
Aerial embolism - Frequent complication when wounded veins. The air from the external environment together with venous blood enters the right half of the heart and the vessels of the lungs. This can lead to a heart stop.
Clinical signs of acute blood loss.
Acute blood loss leads to blood bleeding due to the reduction of the BCC. This is primarily reflected on the activities of the heart and brain. Due to the acute blood loss, a patient appears dizziness, weakness, noise in the ears, drowsiness, thirst, darkening in the eyes, anxiety and feeling of fear, the features of the face are sharpened, faint and loss of consciousness can develop. Reducing the BCC is closely associated with a decrease in blood pressure. Therefore, following the fall, hell appear:
ü a sharp pallor of the skin and mucous membranes (due to the spasm of peripheral vessels);
ü tachycardia (compensatory heart reaction);
ü Dyspnea (respiratory system struggles with disadvantage of oxygen).
All these symptoms speak of blood loss, but in order to judge its magnitude, not enough hemodynamic parameters (pulse data and blood pressure), clinical data of blood (the number of erythrocytes, hemoglobin and hematocrit) are necessary.
BCC is the volume of uniform elements of blood and plasma. The number of erythrocytes during acute blood loss is compensated by the yield into the blood circuit not circulating to this erythrocytes in the depot.
But even faster blood dilution occurs due to an increase in the amount of plasma (hemodulution).
A simple formula for definition of the BCC: OCC \u003d body weight in kg, × per 50 ml.
It is more precisely to identify the BCC, taking into account the floor, body mass and the constitution of a person, since the muscles are one of the largest blood depot in the human body. The magnitude of the BCC affects an active lifestyle. If a healthy person is placed on 2 weeks to bed mode, its BCC decreases by 10%. Long-friendly people lose up to 40% of the BCC.
Hematokritis - This is the ratio of uniform elements of blood to its total volume. In the first day, after bloodstures, it is impossible to estimate its hematocrit, since the patient proportionally loses both plasma and red blood cells. After a day after hemodilution, the hematocrit is very informative.
Algover's shock index - This is the ratio of the pulse to systolic arterial pressure. Normally, it is equal to 0.5. At 1.0, the threatening state occurs.
Speaking of blood loss and loss of the SCC, you need to know that the body is not indifferent to what it loses blood: arterial or venous. 75% of blood in the body is in the veins; 20% - in the arteries; 5% - in capillaries. The blood loss in 300 ml from the artery significantly reduces the volume of arterial blood in line, changes and hemodynamics indicators are changed. 300 ml of venous blood loss changes of readings will not cause. The donor's body with a loss of 400 ml of venous blood compensates independently. Especially poorly carry the blood loss of old men and children, the body of women copes with blood loss easier.
Hemorrhagic shock is characterized by pulse and admin indicators depending on the degree of shock.
Characteristic of hemorrhagic shock
Gemarthrosis - This is a blood cluster in the custody of the joint, which is more often due to injury. The joint increases in the amount, the contours are smoothed, the movements are hampered and becoming painful. The diagnosis is confirmed by puncture.
Hemotorax - Blood accumulation in pleural cavity. Blood can come from a damaged lung or chest vessel. Blood accumulates in the lower departments of the pleural cavity. As a result, it is squeezed with a lung and shifts into a healthy side, which disrupts the work of the heart. The patient appears shortness of breath, cyanosis and clinical symptoms of blood loss. The diagnosis is confirmed by percussion, auscultation and radiography, which are conducted in the position of the patient sitting.
Hemoperikard - Blood accumulation in the window bag. The patient has pain in the heart of the heart, shortness of breath, the heart pusher disappears, the heart tones become deaf, the cervical veins swell, the pulse is expected.
Hemoperitoneum - Blood accumulation in the abdominal cavity, occurs during damage to parenchymal organs. Pains appear according to the anatomical location of the organs. We clinically there will be signs of acute blood loss, the bloating and pain in the palpation, the dullness of the percussion sound in the detached places of the abdomen.
Hypovolemic shock
Hypovolemic shock is caused by acute loss of blood, plasma or body fluids. Hypovolemia (reduction in blood volume - OCC) leads to a decrease in the venous return and a decrease in pressure filling pressure (DNS). This in turn leads to a decrease in the impact of the heart (WSA) and the fall of blood pressure (AD). Due to the stimulation of the sympathoadrenal system, the heart rate (heart rate) increases and vasoconstriction occurs (the growth of peripheral resistance - OPS), which allows maintaining central hemodynamics and causes centralization of blood circulation. In this case, essential in centralization of blood flow (the best supply of blood heart, brain and lungs) has the predominance of α-adrenoreceptors in vessels innervated N. Splanchnicus, as well as in the vessels of the kidneys, muscles and skin. Such a body reaction is fully justified, but if hypovolemia is not corrected, as a result of insufficient tissue perfusion, a shock pattern is developing.
For hypovolemic shock, it is characterized by a decrease in the BCC, a decrease in the pressure of the heart and heart emissions, a decrease in blood pressure and an increase in peripheral resistance.
Cardiogenic shock
Most frequent cause Cardiogenic shock is an acute myocardial infarction, less often myocarditis and toxic mistake of myocardium. If the pumping function of the heart, arrhythmias and other acute causes of the decline in heart rate decrease in the pump function of the heart, arrhythmias and other acute reasons. As a result, the decline of blood pressure arises, at the same time, the DNS increases due to the ineffectiveness of his work.
As a result, the sympatho-studary system is stimulated again, the heart rate and peripheral resistance increases.
Changes in principle are similar to those in hypovolemic shock and together with them belong to the hypodynamic forms of shock. The pathogenetic difference lies only in the meaning of the DNS: in the hypovolemic shock it is reduced, and with cardiogenic - elevated.
Anaphylactic shock
Anaphylactic reaction is an expression of a special high sensitivity of the body to foreign substances. The basis of the development of anaphylactic shock is a sharp decrease in the vascular tone under the influence of histamine and other mediator substances.
Due to the expansion of the capacitive part of the vascular channel (vein), the relative decrease in the BCC is developing: there is a discrepancy between the volume of the vascular channel and the BCC. Hypovolemia leads to a decrease in the inverse blood flow to the heart and a decrease in the DNS. This leads to a decrease in WOS and hell. A direct violation of myocardial contractivity contributes to a decrease in the performance of the heart. Characteristic of anaphylactic shock is the absence of a pronounced reaction of the sympathetic system, this largely explains the progressive clinical development Anaphylactic shock.
Septic shock
With septic shock, primary disorders concern the periphery of blood circulation. Under the influence of bacterial toxins, short arteriovenous shunts operate through which blood rushes, bypassing a capillary network, from the arterial bed to venous.
At the same time, the situation occurs when, with a decrease in blood flow into the capillary flow, blood flow on the periphery and the OPS is reduced. Accordingly, the blood pressure decreases, the WSA and heart rate increase compensatory. This is the so-called hypendynamic circulation reaction during septic shock. Reducing the blood pressure and OPS occurs at normal or increased WOS. With further development, the hypendynamic form goes into hypodynamic, which worsens the forecast.
Comparative characteristics of hemodynamic disorders
under various types of shock.
Despite the difference in the pathogenesis of the forms of shock, the final of their development is reducing capillary blood flow. As a consequence, the delivery of oxygen and energy substrates, as well as the removal of finite exchange products become insufficient. Hypoxia develops, the character of metabolism varies from the aerobic to the anaerobic. Less porvatite is included in the Krebs cycle and goes into lactate, which, along with hypoxia, leads to the development of tissue metabolic acidosis.
Under the influence of acidosis, two phenomena arise, leading to a further deterioration of microcirculation at shock:
1. shock specific vazomotia: Precapillary are expanding, while the postcases are still narrowed. Blood rushes into capillaries, and the outflow is broken. Intracapillary pressure increases, the plasma passes in interstics, which leads both to a further decrease in the BCC, and to the violation of the rheological properties of blood
2. violation of the rheological properties of blood: Cell aggregation occurs in capillaries. Erythrocytes glued into the coin columns, thrombocyte chuckles are formed. As a result of an increase in blood viscosity, almost insurmountable streams of blood flow are created, capillary microtromb is formed, develops disseminating intravascular blood coagulation.
So the center of gravity of changes in progressive shock is increasingly moving from macrocirculation to microcirculation.
Violation of the function of cells, their death due to a microcirculation disorder with shock may concern all organism cells, but certain organs are especially sensitive to circulatory shock. Such organs are called shock.
TO shock organs The person is primarily lungs and kidney, in the second place - the liver. At the same time, changes in these organs should be distinguished with a shock (lung with shock, kidney when shock, liver with shock), which are terminated when the patient output from the shock, and organ disorders associated with the destruction of the tissue structures, when there is deficiency or complete after exiting shock Function of the function of the organ (shock light, shock kidneys, shock liver).
Light with shock is characterized by a disorder of oxygen absorption and is recognized by arterial hypoxia. If a shock light (respiratory distress syndrome) is developing, then severe respiratory failure is rapidly progressing after eliminating shock, the partial pressure of oxygen in arterial blood decreases, the elasticity of the lung decreases, and it becomes increasingly discontinuous. It begins to increase the partial pressure of carbon dioxide for so much that everything becomes necessary for increasing volume of breathing. In this progressive shock phase, shock lung syndrome, apparently, is no longer subjected to reverse development: the patient dies from arterial hypoxia.
The kidneys under shock are characterized by a sharp limitation of blood circulation and a decrease in the amount of glomerular filtrate, a disorder of the concentration ability and a decrease in the amount of urine allocated. If these violations after elimination of the shock were not immediately exposed to reverse development, the diuresis is even more reduced and the number of slag substances increases - a shock kidney develops, the main manifestation of which is a clinical picture of acute renal failure.
The liver is a central metabolic authority and plays an important role during the shock. The development of a shock liver can be suspected when the level of hepatic enzymes increases and after stopping the shock.
Hypovolemic shocks
Facialitygipovolemia hemorrhagic shock it is a decrease in the oxygen capacity of the blood as the blood loss increases. In the launch of pathogenesis traumatic shock A significant role is played by pain factor, intoxication of tissue decay products. The severity of the traumatic shock does not always correlate with the volume of blood loss.
Clinic and diagnostics
Diagnostics is based on the assessment of clinical and laboratory signs. In the conditions of acute blood loss, it is extremely important to determine its magnitude. To do this, it is necessary to use one of the existing methods that are divided into 3 groups: clinical, empirical and laboratory.
Clinical methods Allow the volume of blood loss based on clinical symptoms and hemodynamic parameters.
The severity of blood loss is determined by her species, speed of development, the volume of lost blood, the degree of hypovolemia and the possibility of developing shock, which are most fully reflected in the classification of P. G. Brysov.
Classification of blood loss in Bryusov, 1998
| By sight | Traumatic pathological artificial | Wound, Operating Diseases, Pathological Processes Exfusion, Healing Blooding |
| For the speed of development | Acute treasure chronic | More than 7% of the OCC per hour 5-7% of the BCC per hour less than 5% of the BCC per hour |
| In volume | Small medium large massive deadly | 0.5-10% BCC (0.5 L) 10-20% BCC (0.5-1 L) 21-40% BCC (1-2 L) 41-70% BCC (2-3.5 liters) Over 70% OCC (more than 3.5 liters) |
| By the degree of hypovolemia and the possibility of developing shock | Light moderate heavy extremely heavy | CCC deficiency 10-20%, goal deficiency< 30%, шока нет Дефицит ОЦК 21-30%, дефицит ГО 30-45%, шок развивается при длительной гиповолемии Дефицит ОЦК 31-40%, дефицит ГО 46-60%, шок неизбежен Дефицит ОЦК > 40%, LE\u003e 60% deficiency, shock, terminal state |
The clinical picture is determined by the volume of blood loss and the stadium of the shock. Due to the fact that clinical signs of blood loss depend on the degree of inconsistency between delivery and consumption of 2 tissues of the body, then the factors contributing to the development of shock, or socularity criteria :
· Premorbide background, violating the main exchange;
· Hypotrophic syndrome;
· childhood;
· Elderly and senile age.
IN clinical conditions Severe 3 stages of shock:
1st stage - It is characterized by the paleness of mucous membranes and skin, psychomotor excitation, cold limbs, slightly elevated or normal blood pressure, rapid pulse and breathing, high FLVD, normal diuresis.
2nd stage - It is characterized by intake, pale gray leather, covered with cold sticky sweat, thirst, shortness of breath, decreased blood pressure and CVD, tachycardia, hypothermia, oliguria.
3rd stage - It is characterized by adamisia, moving to whom, pale, with an earthly tint and marble pattern of leather, progressive respiratory failure, hypotension, tachycardia, Anuria.
Evaluation of blood pressure levels and pulse frequency also makes it possible to estimate the value of the BCC deficiency (before the start of the pricillary therapy). The ratio of the pulse frequency to the systolic blood pressure level allows you to calculate the Alg expense shock index.
