Algorithm of Algorithm of diagnostic and diagnostic and

emergency care emergency care for shock conditionsfor shock conditions

Prepared by:Prepared by:C.m.s.C.m.s., assistant professor , assistant professor

of outpatient therapy of outpatient therapy and emergency medical and emergency medical

emergency KSMUemergency KSMUA.R. AlpyssovaA.R. Alpyssova

The purpose or the lectureThe purpose or the lecture

• After completing the lecture, students After completing the lecture, students should focus on issues of diagnosis should focus on issues of diagnosis and emergency care in state of and emergency care in state of shock at the amount of the first shock at the amount of the first medical care (doctor's line crews), and medical care (doctor's line crews), and depending on the patient- in the amount depending on the patient- in the amount of specialized care (intensive of specialized care (intensive care team, intensive care team).care team, intensive care team).

The plan of the lectureThe plan of the lecture

• DeterminationDetermination, , classificationclassification• Factors predisposing to shockFactors predisposing to shock• The index value Algovera - Burri at different The index value Algovera - Burri at different

amounts of blood lossamounts of blood loss• Measurement of central venous pressure.Measurement of central venous pressure.• Hemorrhagic shockHemorrhagic shock• Traumatic shockTraumatic shock• Principles of anti-shockPrinciples of anti-shock

• Shock -Shock - Acute critical condition of the body with  Acute critical condition of the body with advanced life support system failure due advanced life support system failure due to acute circulatory failure, acute to acute circulatory failure, acute respiratory failure, microcirculation and tissue respiratory failure, microcirculation and tissue hypoxia is expressed in violation of hypoxia is expressed in violation of all physiological systems.all physiological systems.

• «Shock» in English - a blow, shock, shock. The «Shock» in English - a blow, shock, shock. The term was coined Army scientist and term was coined Army scientist and physician Louis XV Le Eran (XVIII).physician Louis XV Le Eran (XVIII).

• Every year the world gets seriously hurt 10 Every year the world gets seriously hurt 10 million, 250 thousand of them die from the million, 250 thousand of them die from the shock. In times of war - "traumatic epidemic" - shock. In times of war - "traumatic epidemic" - 60% -70% wounded on the battlefield die from 60% -70% wounded on the battlefield die from shock. World statistics: for every 1,000 seriously shock. World statistics: for every 1,000 seriously injured 100 people die from traumatic shock.injured 100 people die from traumatic shock.

• Shock -  poly etiological disease. Depending on Shock -  poly etiological disease. Depending on the cause of isolated the cause of isolated types of shock:types of shock:

• I.I.                                       Traumatic shock:Traumatic shock:• 1.     1.      As a result of mechanical trauma: As a result of mechanical trauma:•                WoundsWounds•               FracturesFractures•                Compression of the fabric (crush syndrome)Compression of the fabric (crush syndrome)• 2.     2.      Burn injury: Burn injury:•               ThermalThermal•                chemicalchemical• 3.   3.   Cold shock.Cold shock.• 4.     4.      Electric shock. Electric shock.• 5.     5.      Radiation. Radiation.• II. Hemorrhagic or hypovolemic, shock.II. Hemorrhagic or hypovolemic, shock.• 1.     1.      Acute hemorrhage - bleeding. Acute hemorrhage - bleeding.• 2.   2.   Acute impairment of water balance Acute impairment of water balance

- dehydration (sludge-syndrome).- dehydration (sludge-syndrome).

• III. Septic (bacterial-toxic) shock.III. Septic (bacterial-toxic) shock.• Common suppurative processes caused Common suppurative processes caused

by Gram "+" or Gram "-" microflora. by Gram "+" or Gram "-" microflora. Bacteremia, toxemia.Bacteremia, toxemia.

• IV. Anaphylactic shock.IV. Anaphylactic shock.• V. Cardiogenic shock.V. Cardiogenic shock.• 1. Myocardial infarction.1. Myocardial infarction.• 2. Acute heart failure.2. Acute heart failure.• VI. Transfusion shock.VI. Transfusion shock.• 1. Mismatch of blood groups in the 1. Mismatch of blood groups in the

system AB0, Rh factor.system AB0, Rh factor.• Depending on the speedDepending on the speed of shocks: of shocks:• Initial shock Initial shock - at the time of injury, - at the time of injury,

or immediately there after.or immediately there after.• The secondary shock The secondary shock - a few hours after injury.- a few hours after injury.

Factors predisposing to shock:Factors predisposing to shock:Precede or are developing at the time of the Precede or are developing at the time of the impact of genetic factors, Shoko, reduce the impact of genetic factors, Shoko, reduce the

overall resistance of the body, contribute to the overall resistance of the body, contribute to the development of shock and determine its development of shock and determine its

severity.severity.• 1.    1.     Chronic debilitating disease Chronic debilitating disease

- avitaminosis, tuberculosis, and anemia.- avitaminosis, tuberculosis, and anemia.• 2.    2.     Hypothermia. Hypothermia.• 3.    3.     Overheating. Overheating.• 4.    4.     Starvation. Starvation.• 5.    5.     Blood loss. Blood loss.• 6.    6.     Nervous shock. Nervous shock.• 7.     7.      Ionizing radiation. Ionizing radiation.• 8.     8.      Lack of transportation immobilization and Lack of transportation immobilization and

insufficient analgesia for immobilization and insufficient analgesia for immobilization and transportation.transportation.

• 9. 9. Surgery for Surgery for extensive injuries, especially gunshot wounds at.extensive injuries, especially gunshot wounds at.

• Despite the different causes and pathogenesis Despite the different causes and pathogenesis of some features of the main shock is in the of some features of the main shock is in the development of  vasodilation and thereby increasing development of  vasodilation and thereby increasing the capacity of the vascular bed, hypovolemia - a the capacity of the vascular bed, hypovolemia - a decrease in volume of circulating blood  (VCB) as a decrease in volume of circulating blood  (VCB) as a result of various factors, blood loss, the result of various factors, blood loss, the redistribution of fluid between the bloodstream and redistribution of fluid between the bloodstream and tissues or non-normal volume of tissues or non-normal volume of blood increasing capacity of the vascular bed as a blood increasing capacity of the vascular bed as a result of vasodilation. VCB and the incompatibilities result of vasodilation. VCB and the incompatibilities capacitance vascular bed leads to a decrease in capacitance vascular bed leads to a decrease in minute volume of blood the heart minute volume of blood the heart and microcirculation disorders.and microcirculation disorders.

• The main pathophysiological process caused by a The main pathophysiological process caused by a violation of the microcirculation, develops at the violation of the microcirculation, develops at the cellular level. Disorders of the cellular level. Disorders of the microcirculation system combining arterioles - microcirculation system combining arterioles - capillaries - venules, leading to major changes in capillaries - venules, leading to major changes in the body, as it is here that the main function the body, as it is here that the main function of blood occurs - the exchange of substances of blood occurs - the exchange of substances between the cell and the blood.between the cell and the blood.

• Capillaries are the direct point of this Capillaries are the direct point of this exchange, and capillary blood flow in turn depends on exchange, and capillary blood flow in turn depends on the level of blood pressure, arteriolar tone and blood the level of blood pressure, arteriolar tone and blood viscosity. Slowing of blood flow in the capillaries leads viscosity. Slowing of blood flow in the capillaries leads to the aggregation of formed elements, stagnation of to the aggregation of formed elements, stagnation of blood in the capillaries, increasing the pressure and the blood in the capillaries, increasing the pressure and the transition insidecapillarial plasma from the capillaries transition insidecapillarial plasma from the capillaries into the interstitial fluid. Comes the blood clots that, into the interstitial fluid. Comes the blood clots that, along with the aggregation of red blood cells and along with the aggregation of red blood cells and platelets leads to an increase in its platelets leads to an increase in its viscosity and coagulation with the formation of viscosity and coagulation with the formation of insidecappillar  insidecappillar  micro thrombuses, and consequently the capillary blood micro thrombuses, and consequently the capillary blood flow ceases completely. Microcirculatory flow ceases completely. Microcirculatory disorder threatens to dysfunction and cell death.disorder threatens to dysfunction and cell death.

• A feature of the pathogenesis of septic shock is A feature of the pathogenesis of septic shock is that poor circulation under the action of bacterial toxins that poor circulation under the action of bacterial toxins leads to the opening of arteriovenous shunts and blood leads to the opening of arteriovenous shunts and blood bypasses the capillary bed, rushing out of the bypasses the capillary bed, rushing out of the arterioles to venules. Nutrition cells disrupted by arterioles to venules. Nutrition cells disrupted by reducing capillary circulation and action of bacterial reducing capillary circulation and action of bacterial toxins directly to the cell, decreasing the supply toxins directly to the cell, decreasing the supply of oxygen to the cells.of oxygen to the cells.

• In anaphylactic shock under the influence of histamine In anaphylactic shock under the influence of histamine and other biologically active substances capillaries and and other biologically active substances capillaries and veins lose their tone, increasing peripheral vascular veins lose their tone, increasing peripheral vascular bed, increasing its capacity, which leads to a bed, increasing its capacity, which leads to a redistribution of blood redistribution of blood - congestion(stasis) in its capillaries and veins, - congestion(stasis) in its capillaries and veins, causing disruption of the heart. BCC does not match causing disruption of the heart. BCC does not match the available capacity of the vascular bed, the available capacity of the vascular bed, reduced cardiac output. Stagnation of blood in the reduced cardiac output. Stagnation of blood in the microvasculature causes a disorder of metabolism microvasculature causes a disorder of metabolism between the cell and the blood level of the capillary bed.between the cell and the blood level of the capillary bed.

• Microcirculation disorder regardless of the Microcirculation disorder regardless of the mechanism of its occurrence leads to mechanism of its occurrence leads to hypoxia, cells and disruption of redox processes in it. In hypoxia, cells and disruption of redox processes in it. In the tissues begin to predominate over aerobic anaerobic the tissues begin to predominate over aerobic anaerobic processes, developing metabolic acidosis. The processes, developing metabolic acidosis. The accumulation of acidic metabolic products, accumulation of acidic metabolic products, especially lactic acid, which increases acidosis.especially lactic acid, which increases acidosis.

• In the development of cardiogenic shock starting point is In the development of cardiogenic shock starting point is the reduction of pathogenic productive function of the the reduction of pathogenic productive function of the heart with subsequent breach of the microcirculation.heart with subsequent breach of the microcirculation.

• ThusThus, the main initial pathogenetic , the main initial pathogenetic factorsfactors determining the development of  determining the development of shock shock are:are:

• decrease in blood decrease in blood volume - hemorrhagic, hypovolemic, shock;volume - hemorrhagic, hypovolemic, shock;

• vasodilatation, vasodilatation, increased vascular capacity, blood increased vascular capacity, blood redistribution - anaphylactic, septic, shock;redistribution - anaphylactic, septic, shock;

• violation of the productive function of the heart violation of the productive function of the heart - cardiogenic shock.- cardiogenic shock.

• Inadequate blood flow at the level of the Inadequate blood flow at the level of the capillaries in shock leads to changes in capillaries in shock leads to changes in metabolism in all organs and systems, as metabolism in all organs and systems, as manifested dysfunction of the heart, lungs, liver, manifested dysfunction of the heart, lungs, liver, kidneys and nervous system. The degree of lack kidneys and nervous system. The degree of lack of organ function depends on the severity of of organ function depends on the severity of shock, and this determines the outcome.shock, and this determines the outcome.

• Which developed circulatory problems in Phase Which developed circulatory problems in Phase I disorder of microcirculation leading to ischemia of the I disorder of microcirculation leading to ischemia of the liver and the violation of its functions, which contributes liver and the violation of its functions, which contributes to hypoxia in severe stages of to hypoxia in severe stages of shock. Disturbed detoxification, proteinformed shock. Disturbed detoxification, proteinformed glycogenformed and other educational functions of the glycogenformed and other educational functions of the liver. Disorder of trunk, regional blood flow, liver. Disorder of trunk, regional blood flow, impaired microcirculation in the kidneys causes impaired microcirculation in the kidneys causes a violation of both the filtration and concentration in renal a violation of both the filtration and concentration in renal function with the development of oliguria, anuria up function with the development of oliguria, anuria up to. This leads to the accumulation in the body of to. This leads to the accumulation in the body of nitrogenous wastes - urea, creatinine, and other toxic nitrogenous wastes - urea, creatinine, and other toxic products of metabolism.products of metabolism.

• Violation of the Violation of the microcirculation, hypoxia causes dysfunction of the microcirculation, hypoxia causes dysfunction of the adrenal cortexadrenal cortex and decrease the synthesis of cortico-and decrease the synthesis of cortico-s (glucocorticoids, mineralocorticoids,s (glucocorticoids, mineralocorticoids, andand rogenic rogenic hormones), which exacerbates the disorder of blood hormones), which exacerbates the disorder of blood circulation and metabolism.circulation and metabolism.

• Circulatory disorders in the lungs causes a violation of the Circulatory disorders in the lungs causes a violation of the external respiration, decreased alveolar exchange, external respiration, decreased alveolar exchange, shunting blood mikrotrombozy, resulting inshunting blood mikrotrombozy, resulting in respiratory respiratory failure develops, aggravates tissue hypoxia.failure develops, aggravates tissue hypoxia.

• 3. The index 3. The index value Algovera - Burri at different value Algovera - Burri at different

amounts of blood lossamounts of blood loss• After (often in the course of) to stop After (often in the course of) to stop

bleeding, to decide on appropriate ways to fill bleeding, to decide on appropriate ways to fill the volume of blood loss and need to set the the volume of blood loss and need to set the amount of blood loss. Absolute figuresamount of blood loss. Absolute figures may give the wrong information (blood may give the wrong information (blood loss 100 ml of a year-old child is comparable loss 100 ml of a year-old child is comparable to the loss of liters of blood an adult), so you to the loss of liters of blood an adult), so you need to know what percentage of bcc (blood need to know what percentage of bcc (blood volume), blood loss is a particular volume), blood loss is a particular patient. Tentatively it can be done using the patient. Tentatively it can be done using the index-Algovera Burri.index-Algovera Burri. The index is  The index is calculated calculated by dividing theby dividing the pulse rate on the pulse rate on the value of systolic blood pressure.value of systolic blood pressure.

• In cases of acute blood In cases of acute blood loss the initial loss the initial (proper) BCC is calculated by (proper) BCC is calculated by multiplying the multiplying the "ideal weight" of 85 ml / kg "ideal weight" of 85 ml / kg (if surveyed male) or 63 ml / (if surveyed male) or 63 ml / kg (if the woman is kg (if the woman is examined).examined).

INDEXINDEX The volume of blood loss(% of BCC)

0.8 and less

10 10

0,9-1,2 0,9-1,2 2020

1,3-1,4 1,3-1,4 3030

• "Ideal weight" - due weight to the "Ideal weight" - due weight to the person calculated on the person calculated on the Lorentz formula Xia M = Lorentz formula Xia M = P - (100 - (p-150) / 4), P - (100 - (p-150) / 4), where P - the growth where P - the growth of human M - an ideal weight. This calculation of human M - an ideal weight. This calculation makes it possible to avoid errors in the makes it possible to avoid errors in the obese people in terms of their weight bcc get too obese people in terms of their weight bcc get too high, because the subcutaneous adipose high, because the subcutaneous adipose tissue contains a small amount of blood. To tissue contains a small amount of blood. To determine the amount due VCB can use other, less determine the amount due VCB can use other, less accurate way.accurate way.

• First you define an "ideal weight", and then First you define an "ideal weight", and then computes the BCC, based on the fact that he is 8-12 computes the BCC, based on the fact that he is 8-12 percent of body weight (males more than females).percent of body weight (males more than females).

• To calculate the percentage loss of VCB and thus to To calculate the percentage loss of VCB and thus to determine the severity of bleeding, you need to set determine the severity of bleeding, you need to set the amount of blood loss. In some cases (bleeding the amount of blood loss. In some cases (bleeding into the body cavity) it can be done relatively into the body cavity) it can be done relatively simply. Cavity puncture or burst, blood was simply. Cavity puncture or burst, blood was evacuated electric pumps and measured.evacuated electric pumps and measured.

• If the patient has been If the patient has been a external bleeding, a external bleeding, history of bleeding judge exthistory of bleeding judge extremely difficult. In such remely difficult. In such cases adequately judge the cases adequately judge the degree of blood degree of blood loss rates allow the number loss rates allow the number of erythrocytes, the content of erythrocytes, the content of Hb, hematocritof Hb, hematocrit

• These indicators These indicators allow retrosp be allow retrosp be estimated blood loss, estimated blood loss, since meas-Ia in them are since meas-Ia in them are connected with the connected with the second phase gidremich cosecond phase gidremich compensation severe mpensation severe anemia andpres-anemia andpres-UT are from 2-3 hours from UT are from 2-3 hours from the time of bleeding. The the time of bleeding. The complete pictureappears in complete pictureappears in the display-Lyakh by the the display-Lyakh by the end of a 1.5-2.end of a 1.5-2.

TestsTests The degrees of blood lossThe degrees of blood loss

EasyEasy MiddleMiddle HeavyHeavy

DeficiDeficit of t of ACC ACC (Acute (Acute central central circulacirculation)tion)

untiluntil 20%20%

20-30%20-30% 30% 30% and and moremore

The The numbenumber of r of erythrerythrocytesocytes

4,4х4,4х

1010..1212//ll

3,5х3,5х

1010..1212//ll

2,5х2,5х

1010..1212//l l and lessand less

The The contencontent of t of hemoghemoglobin'slobin's

MoreMore

100 100 gg//ll

85-100 85-100 gg//ll

LowerLower

85 85 gg//ll

HemotHemotacritacrit

MoreMore 30%30%

25-30%25-30% LowerLower 25%25%

Measurement of central venous pressure (CVP)Measurement of central venous pressure (CVP)• CVP level perfusion assessed the ability of the heart CVP level perfusion assessed the ability of the heart

and the BCC, monitors theand the BCC, monitors the ongoing infusion therapy.ongoing infusion therapy.• Technique Technique

             Flebotonometr Waldman consists of a tripod with a Flebotonometr Waldman consists of a tripod with a linear scale, moved with the screw knob. In the center of linear scale, moved with the screw knob. In the center of the scale reinforced glass manometric tube, the lower the scale reinforced glass manometric tube, the lower end of which is put on the rubber tube connecting with end of which is put on the rubber tube connecting with a three-way stopcock. To the second output of a three-way stopcock. To the second output of the crane attached a rubber tube that goes to the the crane attached a rubber tube that goes to the glass tank with a capacity of 100 ml, fortified in a glass tank with a capacity of 100 ml, fortified in a special slot on a tripod. On the third output is put on a special slot on a tripod. On the third output is put on a rubber tube to connect to a vein patients. In the tank is rubber tube to connect to a vein patients. In the tank is filled isotonic sodium chloride solution or distilled filled isotonic sodium chloride solution or distilled water, which, by switching the three-way valve, filling the water, which, by switching the three-way valve, filling the entire system of pipes. The solution level in entire system of pipes. The solution level in the manometer tube is set on the zero line of the the manometer tube is set on the zero line of the scale. Tank, rubber tubing, a three-way valve, drip, scale. Tank, rubber tubing, a three-way valve, drip, gauge tube must be sterile.gauge tube must be sterile.

• CVP - pressure at the top or the inferior vena cava within the CVP - pressure at the top or the inferior vena cava within the thorax. To measure his catheter into the superior vena thorax. To measure his catheter into the superior vena cava (via the internal jugular, subclavian vein or brachial) or the cava (via the internal jugular, subclavian vein or brachial) or the inferior vena cava (via femoral or popliteal vein), connect it with inferior vena cava (via femoral or popliteal vein), connect it with the water manometer flebotonometrom Waldman, the water manometer flebotonometrom Waldman, connected by means of a three-way connected by means of a three-way valve and system for infusion. Apparatus placed close to the valve and system for infusion. Apparatus placed close to the patient. Zero pressure scale flebotonometra set at the level of the patient. Zero pressure scale flebotonometra set at the level of the right atrium by means of leveling screws and a tripod. To do right atrium by means of leveling screws and a tripod. To do this, one end of the leveling strengthen his lower foot restraint, this, one end of the leveling strengthen his lower foot restraint, and the other is supplied to the projection of the right atrium and the other is supplied to the projection of the right atrium to the patient - at the intersection of III or IV intercostal to the patient - at the intersection of III or IV intercostal space mid axillary ribs with a line or 5 cm below the angle formed space mid axillary ribs with a line or 5 cm below the angle formed by the connection between the handle and the body of the by the connection between the handle and the body of the sternum.sternum.

• After that the device attached to a catheter inserted into a vein. Turn off the faucet with a liquid reservoir, resulting in pressure in the vein of the system displaces the blood, which in turn displaces the solution. The latter rises in the glass tube to a value equal to venous pressure.

•     The normal value of CVPThe normal value of CVP between 7-10 cm of  between 7-10 cm of water. Art. Slightly noticeablewater. Art. Slightly noticeable vibration in the vibration in the rhythm of breathing indicates its normal rhythm of breathing indicates its normal functioning. High levels of CVP on a large functioning. High levels of CVP on a large scale fluctuations indicates too deep catheter when scale fluctuations indicates too deep catheter when it reaches the right ventricular cavity - it it reaches the right ventricular cavity - it should pull up. Low central venous pressure (0-should pull up. Low central venous pressure (0-5 cm of water. Art.) Indicates hypovolemia 5 cm of water. Art.) Indicates hypovolemia and efficient work of the heart, it is necessary to and efficient work of the heart, it is necessary to fill the volume of blood. Critical value of CVP is the fill the volume of blood. Critical value of CVP is the level of 1.5-2 cm of water. Increased CVP beyond level of 1.5-2 cm of water. Increased CVP beyond 10 cm of water. Art. regarded as a sign of a 10 cm of water. Art. regarded as a sign of a probable heart failure.probable heart failure.

Possible complicationsPossible complications•    Obturation needle, catheter, a rubber tube blood Obturation needle, catheter, a rubber tube blood

clot. When this complication is necessary to clot. When this complication is necessary to replace thrombosed parts of the device.replace thrombosed parts of the device.

• Hemorrhagic shock Hemorrhagic shock in acute blood in acute blood loss develops over 10% of BCC.loss develops over 10% of BCC.

• In clinical practice, a "pure form", he observed:In clinical practice, a "pure form", he observed:• with suicide attempts (bloodletting)with suicide attempts (bloodletting)• ectopic pregnancy and stopped breaking pipes,ectopic pregnancy and stopped breaking pipes,• spontaneous rupture of the spleen,spontaneous rupture of the spleen,• ulcer bleeding, etc.ulcer bleeding, etc.In most cases, the pathogenesis of shock depends In most cases, the pathogenesis of shock depends

not only on the amount and rate of blood not only on the amount and rate of blood loss, but also on the mechanism of loss, but also on the mechanism of its appearance (size and nature ofits appearance (size and nature of injury).injury).

• Pathogenesis.Pathogenesis. Acute blood loss, reduction of BCC, venous  Acute blood loss, reduction of BCC, venous return and cardiac output, leading to activation of the return and cardiac output, leading to activation of the sympathetic-adrenal system, leading to a spasm of blood sympathetic-adrenal system, leading to a spasm of blood vessels, the arterioles and precapillary sphincters in the various vessels, the arterioles and precapillary sphincters in the various organs, including brain and heart. There is a redistribution organs, including brain and heart. There is a redistribution of blood vessel tion-m channel,of blood vessel tion-m channel, autogemodilyutsiya (transfer fluid autogemodilyutsiya (transfer fluid in the bloodstream), accompanied by in the bloodstream), accompanied by decreasinghydrostatic pressure. Continues to decrease cardiac decreasinghydrostatic pressure. Continues to decrease cardiac output, there is a persistentspasm of the arterioles, altered blood output, there is a persistentspasm of the arterioles, altered blood rheology (erythrocyte aggregation "sludge" - the phenomenon).rheology (erythrocyte aggregation "sludge" - the phenomenon).

• In the future peripheral vascular spasm a cause of abuse of μ-In the future peripheral vascular spasm a cause of abuse of μ-circulation and leads to irreversible shock, which is divided into circulation and leads to irreversible shock, which is divided into the following phases:the following phases:

• phase vasoconstriction with reduced blood flow in capillariesphase vasoconstriction with reduced blood flow in capillaries• phase of vasodilation with the expansion of the vascular space phase of vasodilation with the expansion of the vascular space

and reduced blood flow in capillaries;and reduced blood flow in capillaries;• phase of disseminated intravascular coagulation;phase of disseminated intravascular coagulation;

phase of irreversible shock.phase of irreversible shock.• In response to the internal combustion engine is In response to the internal combustion engine is

activated fibrinolytic system, and the lysed clots activated fibrinolytic system, and the lysed clots and broken blood flow.and broken blood flow.

• Clinic. Clinic. Determined by the mechanisms that Determined by the mechanisms that lead to a deficiency of the BCC, the change of lead to a deficiency of the BCC, the change of blood CBS and electrolyte balance disorders of blood CBS and electrolyte balance disorders of peripheral circulationperipheral circulation and the syndrome of DIC.and the syndrome of DIC.

• Clinical signs of symptoms include: Clinical signs of symptoms include: weakness, dizziness, thirst, nausea, dry mouth, weakness, dizziness, thirst, nausea, dry mouth, dark eyes, pale skin, cold clammy dark eyes, pale skin, cold clammy sweat, sharpen facial features, tachycardia and sweat, sharpen facial features, tachycardia and poor filling pulse of lowering blood poor filling pulse of lowering blood pressure, shortness of breath, cyanosis.pressure, shortness of breath, cyanosis.

• During hemorrhagic shock distinguish 3 stages.During hemorrhagic shock distinguish 3 stages.

• Stage I Stage I - compensated, reversible shock occurs - compensated, reversible shock occurs when blood loss 15-25% of BCC (up to 1300 ml of when blood loss 15-25% of BCC (up to 1300 ml of blood). Blood pressure is lowered slightly, there blood). Blood pressure is lowered slightly, there is a moderate tachycardia.is a moderate tachycardia.

• Stage II Stage II - decompensated, reversible shock is - decompensated, reversible shock is accompanied by bleeding in 25-45% of the bcc accompanied by bleeding in 25-45% of the bcc (1300-1800 levels), there is a decrease in blood (1300-1800 levels), there is a decrease in blood pressure (systolic below 100 pressure (systolic below 100 mm. Hg. Art.) Tachycardia of 140 per minute.mm. Hg. Art.) Tachycardia of 140 per minute.

• Stage III Stage III - an irreversible shock, acute blood - an irreversible shock, acute blood loss occurs when more than 50% of VCB (2000-loss occurs when more than 50% of VCB (2000-2500 ml of blood), blood pressure below 60 2500 ml of blood), blood pressure below 60 mm. Hg. or not is determined, the mm. Hg. or not is determined, the pulse usually 150 beats per minute.pulse usually 150 beats per minute.

• In compensated shockIn compensated shock defined pale skin, cold  defined pale skin, cold sweat, small and frequent pulse, blood pressure within sweat, small and frequent pulse, blood pressure within normal range or slightly reduced, decreased urination.normal range or slightly reduced, decreased urination.

• In decompensated shock In decompensated shock reversible skin and mucous reversible skin and mucous membranes cyanotic, the patient is inhibited, the membranes cyanotic, the patient is inhibited, the pulse small, frequent, and reduced blood central pulse small, frequent, and reduced blood central venous pressure, oliguria develops, the venous pressure, oliguria develops, the index increased Algovera, the ECG indicated index increased Algovera, the ECG indicated myocardial malnutrition.myocardial malnutrition.

• Irreversible shockIrreversible shock is not consciousness, blood  is not consciousness, blood pressure is not determined by skin type of marble, pressure is not determined by skin type of marble, there is anuria - cessation of there is anuria - cessation of urination. Index Algovera high.urination. Index Algovera high.

• To assess the severity To assess the severity of hemorrhagic shock is of hemorrhagic shock is important to determine the VCB, the volume of blood important to determine the VCB, the volume of blood loss.loss.

• Treatment Treatment of hemorrhagic shock provides hemostasis, of hemorrhagic shock provides hemostasis, the use of fluid therapy forrestoration of the VCB, the the use of fluid therapy forrestoration of the VCB, the use of vasodilators.use of vasodilators.

Traumatic shockTraumatic shockErectile phaseErectile phase

Erectile stage is characterized by:Erectile stage is characterized by:• 1.      1.      Erectile stage is characterized by:Erectile stage is characterized by:• 2.     2.      Pale skin. Pale skin.• 3.     3.      Frequent and deep breathing. Frequent and deep breathing.• 4.     4.      Tachycardia. Tachycardia.• PathogenesisPathogenesis of erectile phases, in response to of erectile phases, in response to

strong stimulation (pain) is an activation of the strong stimulation (pain) is an activation of the hypothalamic-pituitary-adrenal, sympathoadrenal, renin-hypothalamic-pituitary-adrenal, sympathoadrenal, renin-angiotensin-aldosterone system.angiotensin-aldosterone system.

• In blood increasesIn blood increases конц-ция вазоконстрик-в: конц-ция вазоконстрик-в: adrenaline, angiotensin II,glucocorticoids, vasopressin.adrenaline, angiotensin II,glucocorticoids, vasopressin.

• In areas with In areas with α-α- adrenergicreception adrenergicreception  is vasospasm. Peripheral resistance arterioles  is vasospasm. Peripheral resistance arterioles (resistance vessels) increases. In areas with (resistance vessels) increases. In areas with β-β- adrenergicreceptionadrenergicreception vasoconstrictionvasoconstriction does not occur: the does not occur: the heart, lungs, brain.heart, lungs, brain.

• That is the centralization of blood circulation in blood That is the centralization of blood circulation in blood loss, maintenance of blood pressure within normal limits.loss, maintenance of blood pressure within normal limits.

Torpid phase.Torpid phase.• Accompanied by a general lethargy, low blood Accompanied by a general lethargy, low blood

pressure, filamentary Ps-mpressure, filamentary Ps-m• PathogenesisPathogenesis of torpid phases: a clear emphasis of torpid phases: a clear emphasis

on biologically active substanceson biologically active substances with vasodilator capacity, which accumulate in areas with vasodilator capacity, which accumulate in areas with α-adrenergicreception,with α-adrenergicreception, where there is ischemia, due where there is ischemia, due to insufficient blood getting to the O2.to insufficient blood getting to the O2.

• Due to lack of O2, the cells are transferred to an Due to lack of O2, the cells are transferred to an anaerobic mode. Accumulatesanaerobic mode. Accumulates lactic acid, carbonic acid, H lactic acid, carbonic acid, H + ions. Developing metabolic acidosis, which leads to the + ions. Developing metabolic acidosis, which leads to the activation of lipid peroxidation, enzymes, limited activation of lipid peroxidation, enzymes, limited proteolysis, liberated from lysosomes (BAS (proteolysis, liberated from lysosomes (BAS (БАВБАВ) - kallidin, ) - kallidin, bradykinin).bradykinin).

• ATP deficit, due to shift of pH in the acid side, ATP deficit, due to shift of pH in the acid side, because is denaturation of enzymesbecause is denaturation of enzymes of tissue of tissue respiration, further enhances the acidosis in a vicious respiration, further enhances the acidosis in a vicious circle.circle.

• Acidosis leads to degranulation of mast cells are Acidosis leads to degranulation of mast cells are distinguished: serotonin anddistinguished: serotonin and histamine. Vasodilators begin histamine. Vasodilators begin to dominate. As a result, decentralization of blood to dominate. As a result, decentralization of blood circulation, blood pressure drops, resistance vessels to circulation, blood pressure drops, resistance vessels to dilate.dilate.

• 11.    .       Slows down blood flow in the capillaries. Slows down blood flow in the capillaries.• 2.     2.      Increased capillary permeability. Increased capillary permeability.• 3.     3.      Exit the liquid part of blood and protein in the Exit the liquid part of blood and protein in the

tissue.tissue.• 4.     4.      Blood clots. Blood clots.   • 5.     5.      Aggregation of formed elements. Aggregation of formed elements.• 6.     6.      Thrombus (platelet-disturbed vascular homeostasis, Thrombus (platelet-disturbed vascular homeostasis,

as the damaged endothelium, giperkateholemium).as the damaged endothelium, giperkateholemium).On the severity of clinical manifestations On the severity of clinical manifestations

of torpid phase of shock are 4 levels:of torpid phase of shock are 4 levels:• I. Consciousness is preserved, the I. Consciousness is preserved, the

patient contact, slightly inhibited. BP to 90mm patient contact, slightly inhibited. BP to 90mm Hg, Algover - 0.8.Hg, Algover - 0.8.

• II .. Inhibited. Skin pale, cold clammy sweat. BP 90-II .. Inhibited. Skin pale, cold clammy sweat. BP 90-70 mm Hg. Algover - 0.9-1.1.70 mm Hg. Algover - 0.9-1.1.

• III. Adinamichen, withIII. Adinamichen, with drawn, does not react drawn, does not react to pain. Skin pale, cold, withto pain. Skin pale, cold, with sinyush.ottenkom. Urine stops. BP 70-sinyush.ottenkom. Urine stops. BP 70-50 mm. Hg. Algover - 1.5 and above.50 mm. Hg. Algover - 1.5 and above.

• IV. BP below 50 ml mmHg, pulse frequent, weak IV. BP below 50 ml mmHg, pulse frequent, weak filling, breathing rapid, shallow. Preagonic state.filling, breathing rapid, shallow. Preagonic state.

• End-stageEnd-stage• Advanced arterioles do not respond Advanced arterioles do not respond

to koteholaminy in conditions of hypovolemiato koteholaminy in conditions of hypovolemia catastrophic falls in blood pressure, leading catastrophic falls in blood pressure, leading to cerebral hypoxia and development of to cerebral hypoxia and development of the agonal state.the agonal state.

• Principles of anti-shockPrinciples of anti-shock• What matters most is an early victim anesthesia, What matters most is an early victim anesthesia,

transport immobilization.transport immobilization.• Injured in a state of traumatic shock is Injured in a state of traumatic shock is

treated using a number of complex funds.treated using a number of complex funds. Treatment aims to eliminate the frustration of Treatment aims to eliminate the frustration of vital body functions, caused by shock.vital body functions, caused by shock.

• Essential elements of a comprehensive Essential elements of a comprehensive method of treatment are as follows:method of treatment are as follows:

1.1. A moderate warming of the affected, while A moderate warming of the affected, while avoiding dangerous overheating. In the absence avoiding dangerous overheating. In the absence of a warm room, especially during the of a warm room, especially during the evacuation, warming achieved wraping evacuation, warming achieved wraping in blankets and putting the heaters. Soaked in blankets and putting the heaters. Soaked clothing, lingerie, shoesclothing, lingerie, shoes should be should be removed. Warming in antishock wards achieved removed. Warming in antishock wards achieved by relatively highby relatively high room temperature (24-room temperature (24-25 degrees). Contact heat in antishock Chamber25 degrees). Contact heat in antishock Chamber should not be used. Warming contributes to a  should not be used. Warming contributes to a strong hot tea, a small dose of alcohol, hot food.strong hot tea, a small dose of alcohol, hot food. However, abdominal injuries, as well as the However, abdominal injuries, as well as the presence of vomiting (regardless of thepresence of vomiting (regardless of the nature nature of the injury) victims should not be given neither of the injury) victims should not be given neither food nor drink. In shock,food nor drink. In shock, associated with combined associated with combined radiation lesions should not be radiation lesions should not be used simultaneously for more than used simultaneously for more than 50 g 40% alcohol, given intravenous infusions of 50 g 40% alcohol, given intravenous infusions of alcohol as acomponent alcohol as acomponent  antishock liquids.antishock liquids.

2.2. Giving Giving the affected provisions of Trendelenburg (raise the affected provisions of Trendelenburg (raise the foot of the litter, removethe foot of the litter, remove the the pillow from under his head.)pillow from under his head.)

3. 3. Introduction analgesic (promedol, omnopon, etc.) Introduction analgesic (promedol, omnopon, etc.) under the skin or intravenouslyunder the skin or intravenously better. The use better. The use of analgesics is contraindicated in disorders of of analgesics is contraindicated in disorders of external respirationor blood pressure external respirationor blood pressure reduction to a critical level and below, as well reduction to a critical level and below, as well as traumatic brainas traumatic brain injury.injury.

4. 4. Production Production of novocaine blockade of Wisniewski. The of novocaine blockade of Wisniewski. The blockade takes strong stimuli, but she acts like blockade takes strong stimuli, but she acts like a weak stimulus to the mobilization of a weak stimulus to the mobilization of compensatory mechanisms in shock. When compensatory mechanisms in shock. When damaged, the breast is used one-or two-sided damaged, the breast is used one-or two-sided wagosympathetic blockade in injuries of stomach wagosympathetic blockade in injuries of stomach - a bilateral perirenal blockade, damaged limbs - a bilateral perirenal blockade, damaged limbs - case blockade.- case blockade.

• intravein and intra arterial blood transfusion, intravein and intra arterial blood transfusion, transfusion of blood plasma, albumin infusion fluid transfusion of blood plasma, albumin infusion fluid antishock liquids. Depending on the degree of blood antishock liquids. Depending on the degree of blood loss, shock, depth and availability of canned. Blood loss, shock, depth and availability of canned. Blood poured from 500 to 1000 ml or more blood. In shock poured from 500 to 1000 ml or more blood. In shock grade 4 initially injected into the artery blood (250-500 grade 4 initially injected into the artery blood (250-500 ml), and then move on intra vein drip transfusion. In ml), and then move on intra vein drip transfusion. In shock grade 3 blood transfusions or polyglukin initially shock grade 3 blood transfusions or polyglukin initially blasted, and after raising the blood pressure drop. If blasted, and after raising the blood pressure drop. If the blood pressure in shock grade 3 is very low, it is the blood pressure in shock grade 3 is very low, it is advisable to begin at once intra arterial injection of advisable to begin at once intra arterial injection of blood. Apart from blood transfusion in shock are blood. Apart from blood transfusion in shock are important infusion of polyglyukin. The latter is important infusion of polyglyukin. The latter is administered in doses of 400-1500 ml, depending on administered in doses of 400-1500 ml, depending on the severity of the affected. In shock 3-4 degree, if the severity of the affected. In shock 3-4 degree, if there is no blood, part of the polyglyukin type intra there is no blood, part of the polyglyukin type intra arterial in the same doses, and blood. In shock, not arterial in the same doses, and blood. In shock, not accompanied by large blood loss, especially in burn accompanied by large blood loss, especially in burn shock, often limited to the introduction of poliglyukin shock, often limited to the introduction of poliglyukin in combination with albumin or plasma. Along with in combination with albumin or plasma. Along with this, and pour reopoligljukin. The introduction of this, and pour reopoligljukin. The introduction of crystalloid intra shock solution yields good results only crystalloid intra shock solution yields good results only when the shock of 1 degree.when the shock of 1 degree.

6. 6. The introduction of cardiovascular The introduction of cardiovascular drugs (strophanthin,  korglyukon, in 5% glucose drugs (strophanthin,  korglyukon, in 5% glucose solution). In more severe cases are solution). In more severe cases are shown adrenermimetic drugs (ephedrine, shown adrenermimetic drugs (ephedrine, noradrenaline, mezaton) and glucocorticoids noradrenaline, mezaton) and glucocorticoids (hydrocortisone and prednisone in particular). It (hydrocortisone and prednisone in particular). It must be emphasized that these drugs should be must be emphasized that these drugs should be used in conjunction with blood used in conjunction with blood transfusion or infusion of colloid substitutes.transfusion or infusion of colloid substitutes.

7. 7. To combat the lack To combat the lack of oxygen inhalation administered wet oxygen of oxygen inhalation administered wet oxygen injection tsititona or lobeline. Disturbancies breainjection tsititona or lobeline. Disturbancies breathing resort to tracheal intubation thing resort to tracheal intubation or tracheostomy and use impose a ventilator. or tracheostomy and use impose a ventilator. 

8. 8. In order to combat violations of the In order to combat violations of the exchange shows the introduction of vitamins, exchange shows the introduction of vitamins, particularly ascorbic acid and particularly ascorbic acid and vitamin B1, calcium chloride (10 ml 10% vitamin B1, calcium chloride (10 ml 10% solution into the vein).solution into the vein).

• 9. 9. Along with Along with the antishock therapy affected by the testimony the antishock therapy affected by the testimony of injected tetanus toxoid serum and antibiotics.of injected tetanus toxoid serum and antibiotics.         Each additional injury the severity of          Each additional injury the severity of shock. On this basis, should refrain from shock. On this basis, should refrain from surgery until removal of victims from a state of surgery until removal of victims from a state of shock. For health reasons for surgery include:shock. For health reasons for surgery include:

• stop the ongoing internal bleedingstop the ongoing internal bleeding• asphyxiaasphyxia• anaerobic infectionanaerobic infection• blowing woundblowing wound• Surgeries performed in the presence of shock at Surgeries performed in the presence of shock at

the same time continuing with antishock therapy.the same time continuing with antishock therapy.• In affected with severe forms of shock may In affected with severe forms of shock may

develop a state of agony and death develop a state of agony and death experiences, which are considered as a form experiences, which are considered as a form of terminal states.of terminal states.

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