Shock

1. Shock Zhao Mingyao BMC. ZZU

2. What is shock？ Is itfaint ？ Is itBP decrease ？ Is it ??？

3. Clinical Manifestation • Hypotension • Narrowed pulse pressure • Cold and clammy skin • Oliguria • Dulled sensorium

4. Clinical Manifestation • Hypotension • Hypoperfusion Epinephrine

5. Shock a acute, systemic pathological process in which ECBV decreased acutely leads to serious hypoperfuion in microcirculation and humoral factors change so that cell injury, metabolism disorder and organ dysfunction occur due to different seious disease and trauma

6. Shock Microcirculation disorder + Cellular injury + Humoral factors (inflammatory mediators)

7. Section 1 Etiology & Classification Who said I get shock now?

8. 1. Causes of shock ① Hemorrhagic（or lossfluid）~ ② Traumatic ~ ③Burn ~ ④ Infective ~ ⑤ Cardiogenic ~ ⑥ Anaphylactic ~ ⑦ Neurogenic ~

9. % Blood loss Clinical Signs < 15 Slightly increased heart rate, local swelling, bleeding 15-30 Increased heart rate, increased diastolic blood pressure, prolonged capillary refill 30-50 Above findings plus: hypotension, confusion, acidosis, decreased urine output > 50 Refractory hypotension, refractory acidosis, death Clinical Signs of Acute Hemorrhagic Shock

10. 2. Classification( By initial changes) Blood volume↓ Hypovolemic~ Acute heart pump↓ Cardiogenic ~ Vascular capacity↑ Vasogenic ~ Bp = CO × SVR

11. Classification（ By hemodynamic characteristics） Type CO TPR mBP Clinical (skin) Low CO + high R ↓ ↑↓ pale、cold 、 clamy High CO + Low R↑ ↓ ↓ flush、warm 、dry Low CO + Low R↓ ↓ ↓ cyanosis 、icelike-cold R: resistance

12. Section 2 Microcirculatory changes & stages of shock Microcirculatory constriction Microcirculatory Stagnancy Microcirculatory Failure

13. 后微动脉 Postcapillary resistance （ back sluice gate ） A-V shunt true capillary venule Precapillary sphincter arteriole • thoroughfare channel Precapillary resistance （ front sluice gate） postarteriole Microcirculation

14. 1. Microcirculatory constriction phase Sympathetic-adrenal system activation thoroughfare channel

15. (1) Characters of Microcirculation ①Precapillary R ↑↑> postcapillary R ↑ ②Many true capillary closing ③Arteriovenous shunts opening ④perfusion output↓ ↓ < flow output↓

16. Microcirculatory constriction Autotransfusion

17. (2) Significance of Compensation • Maintain Bp • Maintain blood supply to brain and heart

18. How to maintain Bp • Auto- blood-transfusion • Auto-fluid-transfusion • SVR ↑ • Cardiac contraction ↑ • ADH ↑ and ADS ↑etc

19. How to maintain blood supply to brain and heart *Maintain Bp in certain level *Redistribution of blood flow

20. catecholamine ↑ ↑ CNS + + ↑ vasoconstriction large sudoriferous gland+ + peripheral resistance↑↑ skin ischemia BP(–) pulse pressure ↓ rapid pulse oliguria pale face cold extremities dysphoria Cold sweat↑ (3)Clinicalmanifestation SAMS + + + HR ↑ myocardial contractility↑ renal ischemia

21. Shock index = HR / systolic pressure • 0.5，no shock • 1.0～1.5，with shock • >2，with serious shock rapid and thread pulse occurs before Bp ↓ SBp <90mmHg，pulse pressure<20mmHg

22. 2. Microcirculatory Stagnant Phase

23. (1)Microcirculatory changes Hydrostatic pressure↑ precapillary resistance < postcapillary resistance

24. (2)The Effects of Microcirculatory Stasis ① Return heart blood volume↓’ (Auto-blood-transfusion & auto-fluid-transfusion stop) ②The brain and heart blood flow↓ ③Heart function ↓ ④Arterial blood pressure ↓ Decompensation changes

25. Cardiac output↓ renal blood flow↓ Brain ischemia (3) Clinical Manifestation Lactic acid↑Histamine↑ Adenosine ↑ etc. Microcirculatory Stagnasis Return heartblood volume ↓ Peripheral R ↓ BP↓ Skin blood stasis renalblood stasis Oliguria or anuria Apathy cyanotic

26. 3. Microcirculatory Failure Phase

27. Change of MC • ①Microvessel paralysis dilation • ②Endothelia damage / Cell injury • ③DIC • ④Serious abnormal hemorheology: • (no perfusion&no flow) venule true capillary A-V shunt Precapillary sphincter arteriole postarteriole

28. (2) Effects of Microcirculatory Stasis • MODS/MOSF • DIC

29. (3) Clinical Manifestations 1 ) BP obviously ↓ 2 ) DIC (Bleeding ?) 3 ) Multiple Organs Dysfunction (MOD)

30. Section 3 Neural and humoral mechanism in shock • Amine: catecholamine, histomine, • Peptide: Ang II, 5-HT • inflammatory mediator: cytokines, enzyme, complement

31. Effects of humoral mechanism in shock 1. Vascular effect contraction dilation permeability increase 2. Heart effect enhance depress 3. Cellular damage

32. Section 4 Metabolic disorder and Cellular damage Causes Cell Perfusion↓ ? Bp↓ CNS ↓

33. 1. Cellular Metabolism Disorder Cell edema hyperkalemia Sodium Pump  ATP Ischemia hypoxia Lactic acid  acidosis

34. 2. Cell Damage ①Cellular membrane ~ ②Mitochondria ~ ③Lysosome~ ④Cellular necrosis and apoptosis

35. Section 5 Functional Changes of organs and system during shock

36. Part 1 Multiple Organ Dysfunction Syndrome SIRS, CARS, MARS ---→ MODS ---→ MOF

37. Case report Left leg open trauma Day 2: Shortness of breath, Oliguria Day 4: T 39.5 ℃↑WBC (18×109/L) ↑ R 35 /m, cyanosis, PaO2<60mmHg Urine <100ml/d Creatinine ↑↑ BUN ↑↑ Respiratory failure Renal failure Day 6: Death

38. 1. Definition MODSis dysfunction of two or more organs initially uninvolved developing within a short period of time. Cor pulmonale?

39. Shock Pancreatitis Multiple trauma Burn 2. Causes Intra-abdominal infection MODS Biliary tract infection Infective diseases Non-infective diseases

40. 3. Mechanism of MODS • Uncontrolled inflammatory response:SIRS, CARS, MARS • Microcirculatory hypo-perfusion • Ischemia/reperfusion injury • Bacterial translocation • Hypermetabolism

41. 4.Uncontrolled inflammatory response (1) SIRS • An uncontrolled inflammation process Pro-inflammatory signals exceed its normal domain or degree Result in end-organ damage and multi-system failure. TNF-α, IL-1, IL-6,IFN TXA2, PAF Cell activation

42. 【SIRS Clinical manifestations】 • BT> 38℃ or <36℃ • HR >90 /min • RR >20/min or PaCO2 <32 mmHg • WBC >12,000/mm3 or < 4000 /mm3, or >10% immature cells BT: Body temperature

43. (2) Compensatory anti-inflammatory response syndrome(CARS, 1996) Anti-inflammatory mediators released out of control ◆ Anti-inflammatory mediators inhibit production of inflammatory mediators from MФ and other cells ◆Excessive anti-inflammatory mediators inhibit immune, increase susceptility to infection

44. Anti-inflammatory reaction IL-10, IL-4,TGF-β IL-1ra, Lipoxin Cell eliminate Pro-inflammatory reaction TNF-a, IL-1, IL-6,IFN TXA2, PAF Cell activation Compensatory Anti-inflammatory Response Syndrome( CARS) • An uncontrolled anti-inflammation process • Anti-inflammatory signals exceed its normal domain or degree • Result in end-organ damage and multi-system failure Immune paralysis

45. (3) Mixed antagonists response Syndrome(MARS) The temporal relations between CARS and SIRS might lead to a syndrome termed MARS SIRS + CARS = MARS

46. Summary Infection/Injury Inadequate Adequate Host response Death Infection/injury controlled Excessive Uncontrolled inflammatory response SIRS CARS MARS MODS

47. Part 2 Functional Changes of organs and system in MODS

48. 1.Shock lung • Rapid and labored respiration • PaO2 ↓

49. ALI Highest incidence earliest occurring ？ inferior vena cava Mechanism superior vena cava 1. Filttrator of whole body’s blood 2. ECs of lung adhere activated NP 3. Rich in MФ, activated and produce pro-inflamatory mediated Respiratory circulation Systemic circulation

50. Mechanisms of shock lung • 1. Pulmonary vasoconstriction • 2. Decrease in alveolar surfactant • Formation of alveolar hyaline • membrane • 4. DIC in lungs • 5. ?