2. shock

3. 一、Introduction ： 1. 1731. Le Dran : French He first used ‘shock’ to describe the severe condition of the patient of hurt.

4. 2. 1895 Warren describe the clinical manifestations of shock

5. the face is pale or cyanosis • cold and clammy skin • rapid and thready pulse • oliguria • apathy ★hypotension (Crile)

6. Mechanism: peripheral circulatory failure Vascular center — paralysis Treatment: pressor

7. 1960s: The theory of microcirculation: Sympathetic-adrenal medulla — hypersympathetic 70s : Cellular metabolic disturbance 80s: septic shock

8. 二、Concept: Causes disturbance blood flow of microcirculation functional and metabolic disorders of the vital organs Inadequate tissue perfusion

9. 三、Etiology and classification of shock ㈠ Etiology 1. Blood loss and body fluid loss SI=HR/SBP SI Blood Loss 0.5 10% compensation 1.0 20% ~ 30% shock 1.5 50% death

10. fluid loss vomit. diarrhea collapse 2.Burn/trauma: pain, plasma loss burn shock, infection shock(late)

12. 4. Infection: infectious shock 40% ※endotoxicshock：LPS, pseudosympathetic septic shock hypodynamic shock ： low-output,cold shock hyperdynamicshock：high-output,warm shock (pink,dry), NO,PGI,PGE

13. 5. Anaphy`laxis : anaphylaxic shock 6. Cardiogenic shock： 7. Neurogenic shock： ㈡ classification of shock 2. 1. According to the cause of shock

14. According to the start problem 1) Hypovolemic shock: CVP,CO,artery blood pressure PR 2) Vasogenic shock: 1/5 cap opening • Cardiogenic shock: CO CI<2.2L/min.m2 myoardiumgenic shock non myoardiumgenic shock

15. 四、Periods and pathogenesis ㈠ early phase of shock (ischemic phase, compensatory stage, Ⅰphase)

16. 1.changes of the microcirculation and its mechanism 1)Microcirculation

19. contraction: micro-artery Metarteriole precapillary sphincter Micro-vein

21. ⑵Axial flow particles flow ⑶ a. Capillaries were closed, b.thoroughfare channel and Arteriovenous shunts are open: β-receptor ⑷ perfusion flow perfusion < flow

22. 2) mechanism ： Sympathetic-adrenal-medullary system Renin-angiotensin system

23. (1)BP sympathetic contraction of the pain nerve artery and vein Endotoxin (2)sympathetic renal blood flow angiotesin nervous system catecholamine

24. (3) endothelin (ET) tissue impairment (4)TXA2 lecithoid （磷脂）

25. Opposite effect:TNF,NO,lactic acid 3) compensatory meaning: Bp ： self-transfusion self-blood transfusion CO HR redistribution of blood flow

26. 2. Manifestations: ☆ mental status : dysphoria, anxiety, consciousness ☆skin: cold and clammy, paleness of complexion ☆cardiovascular system: rapid and thready pulse, BP±, pulse pressure ☆urine: oliguria

27. ㈡ shock phase (stage of stagnant anoxia, Ⅱ phase)

28. 1. changes of microcirculation and its mechanism 1)Microcirculation Dilation: micro-artery. Metarteriole. precapillary sphincter perfusion flow perfusion > flow

30. Hemorheology ： RBC acetylneuraminate(唾液酸)COOH bring negative charge sulfate(endothelium) negative charge stack(叠化), “sludge”

32. 2) mechanism ： Hypoxia Histamine vasodilation congestion post-capillary resistance ＞ pre-capillary resistance Kinin(激肽)permeability blood Histamine of capillaries volume hypoxia of brain and heart

33. LPS,TNF,IL-1 P-selectin\E- selectin ICAM-1,VCAM（ endothelium ） WBC adhesion to endothelium cell

35. perfusion flow perfusion > flow 3)effects on body: a. Bp b. Peripherial resistance coronary artery

36. 2. manifestations ☆mental status: faintcoma ☆skin: cyanosis ,veined marble ☆BP heart sound slight pulse(septic shock: full pulse) ☆urine: oliguria or anuria

37. ㈢ Terminal shock (phase of DIC, Ⅲ stage, refractory shock stage,irreversible stage,) microcirculatory failure stage) VSMC in wall of vessel of micromirculation( paralysis)

39. 1．Formation of DIC 1)concentration fibrinogen of blood velocity of blood flow 2) acidosis damage of intrinsic blood endotoxin endothelium coagulation

40. 3)traumatic factor Ⅲ extrinsic blood shock (TF) coagulation Common pathway :Ⅹ

41. intrinsic blood coagulation extrinsic blood coagulation Cascade trigger Dominoespush over coagulation

42. 4)progressive decrease of vessel reaction : Vessel to CA H + , NO VSMC KATP open Kout Ca2+in PGI

43. 2.changes of microcirculation : “no perfusion , no flow” , no-reflow(, WBC sequestration 3.Effects on body a.venous return to heart b.Coagulation bleeding c. Thrombosis and embolism

44. 4. Manifestations Cogulation bleeding

45. 五、Cellular metabolism alteration (一) Dysfunction of Cellular metabolism : a. hypoxia glycolysislactic acidosis b. ATP Na+-K+ pump cellular edema c. metabolic acidosis

46. Cells damage mitochondria hypaoxia acidosis free radical lysosome

47. Experiment The function of WBC: leucocyte deficiency Copy shock model of Rat Test group40mmHg all alive Control 36% death Test group30mmHg all alive Control 100% death

48. H. Robert Horvitz Massachusetts Institute of Technology (MIT) Cambridge, MA, USA b. 1947 John E. Sulston The Wellcome Trust Sanger Institute Cambridge, United Kingdom b. 1942 Sydney Brenner The Molecular Sciences Institute Berkeley, CA, USA b. 1927(in Union of South Africa) （二）Injury and apoptosis of cells 2002 WHO: You ,he or she

49. apoptosis of cells: gene regulation procedure death Physiologic: pathologic:

50. .