1. Shock Shock

2. History of shock Description Circulation failure Microcirculation obstruction Present

3. Shock is defined as a kind of acute, systemic or generalized reduction of tissue perfusion characterized by inadequate blood flow and oxygen delivery to the tissue of the body.

4. hemorrhagic shock burn shock hemorrhagic shock burn shock traumatic shock infectious shock traumatic shock infectious shock anaphylactic shock neurogenic shock anaphylactic shock neurogenic shock cardiogenic shock cardiogenic shock Etiology

5. Sufficient blood volume Normal vasomoter function Pumping ability of the heart Classification Hypovolemic shock Vasogenic shock Cardiogenic shock

6. Hypovolemic shock is characterized by diminished blood volume such that there is inadequate filling of the vascular compartment. Hypovolemic shock is characterized by diminished blood volume such that there is inadequate filling of the vascular compartment.

7. % of total blood removed Cardiac output and arterial pressure (% of normal) pressure (% of normal) Bp=CO×SVR

8. Cardiogenic shock is characterized by primary myocardial dysfunction resulting in the inability of the heart to maintain adequate cardiac output. These patients demonstrate clinical signs of low cardiac output, while evidence exists of adequate intravascular volume. Cardiogenic shock is characterized by primary myocardial dysfunction resulting in the inability of the heart to maintain adequate cardiac output. These patients demonstrate clinical signs of low cardiac output, while evidence exists of adequate intravascular volume.

9. Pathogenesis Ischemic Anoxia Phase Ischemic Anoxia Phase Stagnant Anoxia Phase Irreversible Stage

10. Micro-circulation

12. Ischemic Anoxia Phase Sympathetic-adrenal system activation

13. CAs CAs CAs CAs CAs Ang Ⅱ ET VP shock MDF TXA 2

14. （ 1 ） （ 1 ） （ Maintain arterial blood pressure ）

15. Ischemic Anoxia Phase Autotransfusion

16. Autotransfusion is the first-line defensive response which results from constriction of the capacitance vessel by disgorging stores red blood cells and plasma.

17. Autoperfusion is the second-line defensive response which results from the decreased capillary hydrostatic pressure by promoting tissue fluid circumfluence.

18. Ischemic Anoxia Phase Autoperfusion Hydrostatic pressure ↓ precapillary resistance > postcapillary resistance

19. NauseaWeaknessThirst Dizziness Dizziness Feeling cool or cold Feeling cool or cold Clinical Manifestation

20. Bp ↓↓ ？ Blood pressure is the force applied against the walls of the arteries as the heart pumps blood through the body. The pressure is determined by the force and amount of blood pumped and the size and flexibility of the arteries.

21. Clinical Manifestation Question 1: Bp ↓↓ ？  Autotransfusion  Autoperfusion  Renin-angiotension- aldosterone system  ADH

22. Clinical Manifestation Question 1: Bp ↓↓ ？ Question 2: Is Bp the most important index in diagnosis and management of shock ？ NO ！

23. This pressure is greatest in the arteries during ventricular contraction (systole) Pulse Pressure = Systolic Pressure - Diastolic Pressure During ventricular relaxation (diastole), blood pressure falls, reaching a minimum pressure just prior to the next systole.

24. Clinical Manifestation Sympathetic-adrenal system activation Hemorrhage, infection, trauma HR↑ Increase in small blood vessel resistance and redistribution of blood Activation of the sweat glands Urine output ↓ cool and moist skin

25. Sympathetic-adrenal system activation AutotransfusionAutoperfusion Blood redistribution

26. Clinical Manifestation Sympathetic-adrenal system activation AAAArterial pressure: normal or mildly reduced SSSSkin: cool and moist HHHHeart rate: increased WWWWeak and thready pulse OOOOliguria

27. Pathogenesis Ischemic Anoxia Phase Stagnant Anoxia Phase Stagnant Anoxia Phase Irreversible Stage

28. precapillary resistance postcapillary resistance Sympathetic adrenal system Ischemic anoxia Lactic acid Histamine Adenosine NO Venule contract Sympexis Leucocyte conglutination Platelet adhesion permeability Venous returnBpSympathetic adrenal system ？ Congestion Plasmexhidrosis

29. Hydrostatic pressure ↑ precapillary resistance < postcapillary resistance

30. Clinical Stasis in microcirculation Passive congestion of kidneys Returned blood volume CO Renal blood flow Oliguria anuria Bp Cerebral ischemia coma Congestion hemagglutination Cyanosis Piebaldism Manifestation

31. Pathogenesis Ischemic Anoxia Phase Stagnant Anoxia Phase Irreversible Stage Irreversible Stage

32. Irreversible Stage of Shock  MSOF  DIC diffuse intravascular coagulation multiple system organ failure

33. Tissue anoxia Cell injury Collagen exposure Blood coagulation factors activation Cell injury Collagen exposure Blood coagulation factors activation Acidosis Blood rheology + + DIC Bleeding Phagocyte activation IL-1 TNF IL-6 etc Cell necrosis Apoptosis MODS

34. MODS MODS is the progressive dysfunction of two or more organ systems resulting from an uncontrolled inflammatory response to a severe illness or injury. MODS is the progressive dysfunction of two or more organ systems resulting from an uncontrolled inflammatory response to a severe illness or injury.

35. Tissue anoxia Cell injury Collagen exposure Blood coagulation factors activation Cell injury Collagen exposure Blood coagulation factors activation Acidosis Blood rheology + + DIC Bleeding Phagocyte activation IL-1 TNF IL-6 etc Cell necrosis Apoptosis MODS

37. infection anaphylaxis bleeding Myocardial infarction Wound Capacity of blood vessel Blood volume Returned blood volume CO Bp Sympathetico-adrenomedullary system Perfusion of microcirculation Tisssue anoxia Metabolic acidosis Stasis in microcirculation DIC MODS Plasmexhidrosis Bp

38. Functional and Metabolic Changes

39. Impaired cellular metabolism ↓Tissue perfusion Impaired oxygen use Anaerobic metabolism ↓Oxygen affinity for hemoglobin ↓ ATP ↑ Lactate ↓Na +,K + pump ↑Intracellular Na + and water ↓Circulatory volume Clotting cascade Impaired glucose use ↑Serum glucose Catecholamines, cortisol etc ↑Pyruvate ↑Lipolysis ↑Gluconeogenesis ↑Glucogenolysis Serum triglycerides, free fatty acids ↓Energy stores Metabolic acidosis Cellular edema Inflammatory response Release of lysosomal enzymes

40. Disturbances of cell metabolism

41. Organ Dysfunction

42. Renal failure  Oliguria  Azotemia  Hyperkalemia  Metabolic acidosis Functional renal failure Parenchymal renal failure

43. Shock lung  Rapid and labored respiration  P a O 2 Diffusion impairment Ventilation-perfusion imbalance

44. Heart failure  Discrepancy between myocardial oxygen availability and consumption  Decreased PO 2  Acidosis  Hyperkalemia  DIC  Endotoxin

45. gastrointestinal system dysfunction Hepatic insufficiency

46. Treatment Measures

47. Don’t ever wait for symptoms to develop before beginning the treatment for shock. For shock is easier to prevent than to cure. Don’t ever wait for symptoms to develop before beginning the treatment for shock. For shock is easier to prevent than to cure.

48. Treatment Measures  Blood and plasma transfusion Blood and plasma transfusion Blood and plasma transfusion  Vasoactive drugs Vasoactive drugs Vasoactive drugs  Oxygen therapy  Other therapy treatment on acidosis treatment on acidosis treatment by the head-down position treatment by the head-down position treatment with glucocorticoids treatment with glucocorticoids

49. Central Venous Pressure (CVP) ① Circulating blood volume ② Venous tone ③ Right ventricular function Volume Indicators Pulmonary artery wedge pressure Pulmonary artery wedge pressure (PAWP) is a reflection of left atrial pressure.

50. Vasoactive Drugs Vasoconstrictive substance Vasodilator substance neurogenic shock neurogenic shock anaphylactic shock

51. Anaphylactic shock results from a widespread hypersensitivity reaction known as anaphylaxis. The basic physiologic alteration is vasodilation, peripheral pooling, and relative hypovolemia, leading to decreased tissue perfusion and impaired cellular metabolism. Anaphylactic shock results from a widespread hypersensitivity reaction known as anaphylaxis. The basic physiologic alteration is vasodilation, peripheral pooling, and relative hypovolemia, leading to decreased tissue perfusion and impaired cellular metabolism.

52. Vasoactive Drugs Vasoconstrictive substance Vasodilator substance neurogenic shock anaphylactic shock Hemorrhagic shock

53. Treatment Measures  Blood and plasma transfusion  Vasoactive drugs  Oxygen therapy  Other therapy treatment on acidosis treatment by the head-down position treatment with glucocorticoids

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