1. Algorithm of diagnostic and emergency care for shock conditions
Prepared by: C.m.s., assistant professor of outpatient therapy and emergency medical emergency KSMU A.R. Alpyssova

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

3. The plan of the lecture
Determination, classification
Factors predisposing to shock
The index value Algovera - Burri at different amounts of blood loss
Measurement of central venous pressure.
Hemorrhagic shock
Traumatic shock
Principles of anti-shock

4. Shock - Acute critical condition of the body with advanced life support system failure due to acute circulatory failure, acute respiratory failure, microcirculation and tissue hypoxia is expressed in violation of all physiological systems.
«Shock» in English - a blow, shock, shock. The term was coined Army scientist and physician Louis XV Le Eran (XVIII).
Every year the world gets seriously hurt 10 million, 250 thousand of them die from the shock. In times of war - "traumatic epidemic" - 60% -70% wounded on the battlefield die from shock. World statistics: for every 1,000 seriously injured 100 people die from traumatic shock.
Shock -  poly etiological disease. Depending on the cause of isolated types of shock:

5. I.                    Traumatic shock:
1.      As a result of mechanical trauma:
        Wounds
       Fractures
        Compression of the fabric (crush syndrome)
2.      Burn injury:
       Thermal
        chemical
3.   Cold shock.
4.      Electric shock.
5.      Radiation.
II. Hemorrhagic or hypovolemic, shock.
1.      Acute hemorrhage - bleeding.
2.   Acute impairment of water balance - dehydration (sludge-syndrome).

6. III. Septic (bacterial-toxic) shock.
Common suppurative processes caused by Gram "+" or Gram "-" microflora. Bacteremia, toxemia.
IV. Anaphylactic shock.
V. Cardiogenic shock.
1. Myocardial infarction.
2. Acute heart failure.
VI. Transfusion shock.
1. Mismatch of blood groups in the system AB0, Rh factor.
Depending on the speed of shocks:
Initial shock - at the time of injury, or immediately there after.
The secondary shock - a few hours after injury.

7. Factors predisposing to shock:
Precede or are developing at the time of the impact of genetic factors, Shoko, reduce the overall resistance of the body, contribute to the development of shock and determine its severity.
1.     Chronic debilitating disease - avitaminosis, tuberculosis, and anemia.
2.     Hypothermia.
3.     Overheating.
4.     Starvation.
5.     Blood loss.
6.     Nervous shock.
7.      Ionizing radiation.
8.      Lack of transportation immobilization and insufficient analgesia for immobilization and transportation.
9. Surgery for extensive injuries, especially gunshot wounds at.

8. Despite the different causes and pathogenesis of some features of the main shock is in the development of  vasodilation and thereby increasing the capacity of the vascular bed, hypovolemia - a decrease in volume of circulating blood  (VCB) as a result of various factors, blood loss, the redistribution of fluid between the bloodstream and tissues or non-normal volume of blood increasing capacity of the vascular bed as a result of vasodilation. VCB and the incompatibilities capacitance vascular bed leads to a decrease in minute volume of blood the heart and microcirculation disorders.
The main pathophysiological process caused by a violation of the microcirculation, develops at the cellular level. Disorders of the microcirculation system combining arterioles - capillaries - venules, leading to major changes in the body, as it is here that the main function of blood occurs - the exchange of substances between the cell and the blood.

9. Capillaries are the direct point of this exchange, and capillary blood flow in turn depends on the level of blood pressure, arteriolar tone and blood viscosity. Slowing of blood flow in the capillaries leads to the aggregation of formed elements, stagnation of blood in the capillaries, increasing the pressure and the transition insidecapillarial plasma from the capillaries into the interstitial fluid. Comes the blood clots that, along with the aggregation of red blood cells and platelets leads to an increase in its viscosity and coagulation with the formation of insidecappillar  micro thrombuses, and consequently the capillary blood flow ceases completely. Microcirculatory disorder threatens to dysfunction and cell death.
A feature of the pathogenesis of septic shock is that poor circulation under the action of bacterial toxins leads to the opening of arteriovenous shunts and blood bypasses the capillary bed, rushing out of the arterioles to venules. Nutrition cells disrupted by reducing capillary circulation and action of bacterial toxins directly to the cell, decreasing the supply of oxygen to the cells.

10. In anaphylactic shock under the influence of histamine and other biologically active substances capillaries and veins lose their tone, increasing peripheral vascular bed, increasing its capacity, which leads to a redistribution of blood - congestion(stasis) in its capillaries and veins, causing disruption of the heart. BCC does not match the available capacity of the vascular bed, reduced cardiac output. Stagnation of blood in the microvasculature causes a disorder of metabolism between the cell and the blood level of the capillary bed.
Microcirculation disorder regardless of the mechanism of its occurrence leads to hypoxia, cells and disruption of redox processes in it. In the tissues begin to predominate over aerobic anaerobic processes, developing metabolic acidosis. The accumulation of acidic metabolic products, especially lactic acid, which increases acidosis.
In the development of cardiogenic shock starting point is the reduction of pathogenic productive function of the heart with subsequent breach of the microcirculation.

11. Thus, the main initial pathogenetic factors determining the development of shock are:
decrease in blood volume - hemorrhagic, hypovolemic, shock;
vasodilatation, increased vascular capacity, blood redistribution - anaphylactic, septic, shock;
violation of the productive function of the heart - cardiogenic shock.
Inadequate blood flow at the level of the capillaries in shock leads to changes in metabolism in all organs and systems, as manifested dysfunction of the heart, lungs, liver, kidneys and nervous system. The degree of lack of organ function depends on the severity of shock, and this determines the outcome.

12. Which developed circulatory problems in Phase I disorder of microcirculation leading to ischemia of the liver and the violation of its functions, which contributes to hypoxia in severe stages of shock. Disturbed detoxification, proteinformed glycogenformed and other educational functions of the liver. Disorder of trunk, regional blood flow, impaired microcirculation in the kidneys causes a violation of both the filtration and concentration in renal function with the development of oliguria, anuria up to. This leads to the accumulation in the body of nitrogenous wastes - urea, creatinine, and other toxic products of metabolism.
Violation of the microcirculation, hypoxia causes dysfunction of the adrenal cortex and decrease the synthesis of cortico-s (glucocorticoids, mineralocorticoids, and rogenic hormones), which exacerbates the disorder of blood circulation and metabolism.
Circulatory disorders in the lungs causes a violation of the external respiration, decreased alveolar exchange, shunting blood mikrotrombozy, resulting in respiratory failure develops, aggravates tissue hypoxia.

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

14. In cases of acute blood loss the initial (proper) BCC is calculated by multiplying the "ideal weight" of 85 ml / kg (if surveyed male) or 63 ml / kg (if the woman is examined).
INDEX
The volume of blood loss (% of BCC)
0.8 and less 10
0,9-1,2 20
1,3-1,4 30

15. "Ideal weight" - due weight to the person calculated on the Lorentz formula Xia M = P - (100 - (p-150) / 4), where P - the growth of human M - an ideal weight. This calculation makes it possible to avoid errors in the obese people in terms of their weight bcc get too high, because the subcutaneous adipose tissue contains a small amount of blood. To determine the amount due VCB can use other, less accurate way.
First you define an "ideal weight", and then computes the BCC, based on the fact that he is 8-12 percent of body weight (males more than females).
To calculate the percentage loss of VCB and thus to determine the severity of bleeding, you need to set the amount of blood loss. In some cases (bleeding into the body cavity) it can be done relatively simply. Cavity puncture or burst, blood was evacuated electric pumps and measured.

16. The degrees of blood loss
Tests
The degrees of blood loss
Easy
Middle
Heavy
Deficit of ACC (Acute central circulation)
until 20%
20-30%
30% and more
The number of erythrocytes
4,4х
10.12/l
3,5х
2,5х
10.12/l and less
The content of hemoglobin's
More
100 g/l
g/l
Lower
85 g/l
Hemotacrit
More 30%
25-30%
Lower 25%
If the patient has been a external bleeding, history of bleeding judge extremely difficult. In such cases adequately judge the degree of blood loss rates allow the number of erythrocytes, the content of Hb, hematocrit
These indicators allow retrosp be estimated blood loss, since meas-Ia in them are connected with the second phase gidremich compensation severe anemia andpres-UT are from 2-3 hours from the time of bleeding. The complete pictureappears in the display-Lyakh by ​​the end of a 1.5-2.

17. Measurement of central venous pressure (CVP)
CVP level perfusion assessed the ability of the heart and the BCC, monitors the ongoing infusion therapy.
Technique        Flebotonometr Waldman consists of a tripod with a linear scale, moved with the screw knob. In the center of the scale reinforced glass manometric tube, the lower end of which is put on the rubber tube connecting with a three-way stopcock. To the second output of the crane attached a rubber tube that goes to the glass tank with a capacity of 100 ml, fortified in 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 filled isotonic sodium chloride solution or distilled water, which, by switching the three-way valve, filling the entire system of pipes. The solution level in the manometer tube is set on the zero line of the scale. Tank, rubber tubing, a three-way valve, drip, gauge tube must be sterile.

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

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

20. Hemorrhagic shock in acute blood loss develops over 10% of BCC.
In clinical practice, a "pure form", he observed:
with suicide attempts (bloodletting)
ectopic pregnancy and stopped breaking pipes,
spontaneous rupture of the spleen,
ulcer bleeding, etc.
In most cases, the pathogenesis of shock depends not only on the amount and rate of blood loss, but also on the mechanism of its appearance (size and nature of injury).

21. Pathogenesis. Acute blood loss, reduction of BCC, venous return and cardiac output, leading to activation of the sympathetic-adrenal system, leading to a spasm of blood vessels, the arterioles and precapillary sphincters in the various organs, including brain and heart. There is a redistribution of blood vessel tion-m channel, autogemodilyutsiya (transfer fluid in the bloodstream), accompanied by decreasinghydrostatic pressure. Continues to decrease cardiac output, there is a persistentspasm of the arterioles, altered blood rheology (erythrocyte aggregation "sludge" - the phenomenon).
In the future peripheral vascular spasm a cause of abuse of μ-circulation and leads to irreversible shock, which is divided into the following phases:
phase vasoconstriction with reduced blood flow in capillaries
phase of vasodilation with the expansion of the vascular space and reduced blood flow in capillaries;
phase of disseminated intravascular coagulation; phase of irreversible shock.
In response to the internal combustion engine is activated fibrinolytic system, and the lysed clots and broken blood flow.

22. Clinic. Determined by the mechanisms that lead to a deficiency of the BCC, the change of blood CBS and electrolyte balance disorders of peripheral circulation and the syndrome of DIC.
Clinical signs of symptoms include: weakness, dizziness, thirst, nausea, dry mouth, dark eyes, pale skin, cold clammy sweat, sharpen facial features, tachycardia and poor filling pulse of lowering blood pressure, shortness of breath, cyanosis.
During hemorrhagic shock distinguish 3 stages.

23. Stage I - compensated, reversible shock occurs when blood loss 15-25% of BCC (up to 1300 ml of blood). Blood pressure is lowered slightly, there is a moderate tachycardia.
Stage II - decompensated, reversible shock is accompanied by bleeding in 25-45% of the bcc (  levels), there is a decrease in blood pressure (systolic below 100 mm. Hg. Art.) Tachycardia of 140 per minute.
Stage III - an irreversible shock, acute blood loss occurs when more than 50% of VCB (  ml of blood), blood pressure below 60 mm. Hg. or not is determined, the pulse usually 150 beats per minute.

24. In compensated shock defined pale skin, cold sweat, small and frequent pulse, blood pressure within normal range or slightly reduced, decreased urination.
In decompensated shock reversible skin and mucous membranes cyanotic, the patient is inhibited, the pulse small, frequent, and reduced blood central venous pressure, oliguria develops, the index increased Algovera, the ECG indicated myocardial malnutrition.
Irreversible shock is not consciousness, blood pressure is not determined by skin type of marble, there is anuria - cessation of urination. Index Algovera high.
To assess the severity of hemorrhagic shock is important to determine the VCB, the volume of blood loss.
Treatment of hemorrhagic shock provides hemostasis, the use of fluid therapy forrestoration of the VCB, the use of vasodilators.

25. Erectile stage is characterized by:
Traumatic shock
Erectile phase
Erectile stage is characterized by:
1.      Erectile stage is characterized by:
2.      Pale skin.
3.      Frequent and deep breathing.
4.      Tachycardia.
Pathogenesis of erectile phases, in response to strong stimulation (pain) is an activation of the hypothalamic-pituitary-adrenal, sympathoadrenal, renin-angiotensin-aldosterone system.
In blood increases конц-ция вазоконстрик-в: adrenaline, angiotensin II,glucocorticoids, vasopressin.
In areas with α- adrenergicreception  is vasospasm. Peripheral resistance arterioles (resistance vessels) increases. In areas with β- adrenergicreception vasoconstriction does not occur: the heart, lungs, brain.
That is the centralization of blood circulation in blood loss, maintenance of blood pressure within normal limits.

26. Torpid phase.
Accompanied by a general lethargy, low blood pressure, filamentary Ps-m
Pathogenesis of torpid phases: a clear emphasis on biologically active substances with vasodilator capacity, which accumulate in areas with α-adrenergicreception, where there is ischemia, due to insufficient blood getting to the O2.
Due to lack of O2, the cells are transferred to an anaerobic mode. Accumulates lactic acid, carbonic acid, H + ions. Developing metabolic acidosis, which leads to the activation of lipid peroxidation, enzymes, limited proteolysis, liberated from lysosomes (BAS (БАВ) - kallidin, bradykinin).
ATP deficit, due to shift of pH in the acid side, because is denaturation of enzymes of tissue respiration, further enhances the acidosis in a vicious circle.
Acidosis leads to degranulation of mast cells are distinguished: serotonin and histamine. Vasodilators begin to dominate. As a result, decentralization of blood circulation, blood pressure drops, resistance vessels to dilate.

27. 1.      Slows down blood flow in the capillaries.
2.      Increased capillary permeability.
3.      Exit the liquid part of blood and protein in the tissue.
4.      Blood clots.  
5.      Aggregation of formed elements.
6.      Thrombus (platelet-disturbed vascular homeostasis, as the damaged endothelium, giperkateholemium).
On the severity of clinical manifestations of torpid phase of shock are 4 levels:
I. Consciousness is preserved, the patient contact, slightly inhibited. BP to 90mm ​​Hg, Algover - 0.8.
II .. Inhibited. Skin pale, cold clammy sweat. BP 90-70 mm Hg. Algover - 
III. Adinamichen, with drawn, does not react to pain. Skin pale, cold, with sinyush.ottenkom. Urine stops. BP 70-50 mm. Hg. Algover - 1.5 and above.
IV. BP below 50 ml mmHg, pulse frequent, weak filling, breathing rapid, shallow. Preagonic state.

28. Principles of anti-shock
End-stage
Advanced arterioles do not respond to koteholaminy in conditions of hypovolemia catastrophic falls in blood pressure, leading to cerebral hypoxia and development of the agonal state.
Principles of anti-shock
What matters most is an early victim anesthesia, transport immobilization.
Injured in a state of traumatic shock is treated using a number of complex funds. Treatment aims to eliminate the frustration of vital body functions, caused by shock.

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

30. Giving the affected provisions of Trendelenburg (raise the foot of the litter, remove the pillow from under his head.)
Introduction analgesic (promedol, omnopon, etc.) under the skin or intravenously better. The use of analgesics is contraindicated in disorders of external respirationor blood pressure reduction to a critical level and below, as well as traumatic brain injury.
Production of novocaine blockade of Wisniewski. The blockade takes strong stimuli, but she acts like a weak stimulus to the mobilization of compensatory mechanisms in shock. When damaged, the breast is used one-or two-sided wagosympathetic blockade in injuries of stomach - a bilateral perirenal blockade, damaged limbs - case blockade.

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

32. The introduction of cardiovascular drugs (strophanthin,  korglyukon, in 5% glucose solution). In more severe cases are shown adrenermimetic drugs (ephedrine, noradrenaline, mezaton) and glucocorticoids (hydrocortisone and prednisone in particular). It must be emphasized that these drugs should be used in conjunction with blood transfusion or infusion of colloid substitutes.
To combat the lack of oxygen inhalation administered wet oxygen injection tsititona or lobeline. Disturbancies breathing resort to tracheal intubation or tracheostomy and use impose a ventilator. 
In order to combat violations of the exchange shows the introduction of vitamins, particularly ascorbic acid and vitamin B1, calcium chloride (10 ml 10% solution into the vein).

33. 9. Along with the antishock therapy affected by the testimony of injected tetanus toxoid serum and antibiotics.          Each additional injury the severity of shock. On this basis, should refrain from surgery until removal of victims from a state of shock. For health reasons for surgery include:
stop the ongoing internal bleeding
asphyxia
anaerobic infection
blowing wound
Surgeries performed in the presence of shock at the same time continuing with antishock therapy.
In affected with severe forms of shock may develop a state of agony and death experiences, which are considered as a form of terminal states.

34. THANK YOU FOR ATTENTION!!!