SHOCK

1. SHOCK • Shen Hong • Zhejiang University School of Medicine.

2. Historical Aspects • The concept of shock has evolved over the centuries from the earliest description in antiquity of traumatic wounds and hemorrhage. • Hippocratic facies (460~380 B.C.): tourniguet. Bloodletting • Galen (A.D. 130~200): erroneous knowledge of anatomy. Ligation of bleeding vessels • Vesalius. William Harvey (16 centuries): anatomy and circulation of the cardiovascular system • A French military surgeon: the use of simple bandages • Thomas Latta: in 1831. infusion of intravenous fluids into hypo-volemic patients inflicted with cholera caused clinical improvent.

3. Pathogenesis: • a. vasomotor exhaustion: neurogenic theory • b. traumatic toxemia: cannon. Bay(World War I) • c. hypovolemia: Keith, Blalock(experiments on dogs) • d. fat embolism; • e. acidosis • f. adrenal dysfunction

4. Pathogenesis: • resuscitation, individual argan dysfunction, cellular derangements(Korean, Vietnam conflict). • Shock lung. ARDS • molecular biology, inflammatory mediator, • metabolic support, oxygen delivery, organ ischemia, sepsis.

5. II. Definition of shock • A syndrome results from inadequate perfusion of tissues alterations in cellular metabolism, cellular dysfunction and cellular injury, MODS due to tissue hyperfusion, hypoxia. • Oxygen delivery; oxygen debt; oxygen demand exceeds the oxygen supply.

6. III. Cause, classification of shock

7. 1. hypovolemic shock • 1) hemorrhagic losses: trauma, gastrointestinal bleeding ruptured aneurysm. • 2) plasma volume losses: extravascular fluid sequestration, pancreatitis, burns, bowel obstruction.

8. 2. cardiogenic shock • dinminished cardiac output • intrinsic cause • extrinsic cause • myocardial infarction • cardiac rhythm disturbances. • Tension pneumothorax • pericardial tamponade

9. 3. neurogenic shock • failure of the sympathetic nervous system to maintain normal vascular tone. • Spinal cord injury, severe head injury. Spinal anesthesia

10. 4. vasogenic • endogenous or exogenous vaso-active mediators • systemic inflammatory response syndrome(SIRS) • sepsis (infectious) • noninfectious • Anaphylactic • Hypoadrenal • traumatic

11. IV. Pathophysiology of shock Impaired tissue perfusion Tissue hypoxia Inflammatory Mediators Circulatory redistribution Anaerobic metabolism Ischemia/ Reperfusion Acidosis Cellular dysfunction SIRS / Sepsis Multiple organ dysfunction syndrome

12. Pathophysiology: • Role of hypoxia • Anaerobic metabolism and acidosis • Hyperlactatemia • Circulatory redistribution • Impairment of gut perfusion

13. Anaerobic metabolism and acidosis Glycogen Glucose Anaerobic glycolysis lactate Pyruvate cytosol mitochondria Acetyl CoA Aerobic glycolysis Citric Acid cycle

14. Circulatory redistribution • Vaso-constrictive factors: • Catechol, angiotensin II, vasopressin, endothelin, thromboxan A2 • Vaso-dilatory: • Nitric oxide, prostaglandin E2, prostacyclin, interleukin-2, bradykinin.

15. Impairment of gut perfusion: • Subsequent bacterial or toxin translocation • Systemic inflammatory response, MODS

16. I. baroreceptors • Vasomotor center(medulla) • Sympathetic neural output • Increased systemic vascular resistance • Increased venous return to the heart • Arteriolar vasoconstriction(cutaneous tissue. Skeletal muscle. Renal and splanchnic vascular beds)

17. II. adrenal medullary output↑ • tachycardia, enhanced cardiac contractility

18. III. Antidiuretic hormone(posterior pituitary) • Vasoconstriction • Water reabsorption in the distal tubule of the kidney

19. IV. rennin(kidney) • Angiotensin I (liver) • Angiotensin II (lungs) • vasoconstrictor • aldosterone(adrenal cortex) →reabsorption of sodium

20. V. microcirculatory autoregulation

21. Mediator of shock and sepsis • Endotoxin • Complement fragments • Eicosanoids • Leukotrienes, Prostaglandins, Throbomxanes • Cytokines: • Interleukins(IL1, IL2, IL6); TNF-a; CSF, GCSF,GM-CSF; IFN-r • Neuroendocrine mediators: • catechols, cortisol, glucagons

22. V. diagosis and management of shock: General approach

23. Keep SaO2> 90% Optimize cardiac index Optimize Hb supply supplemental O2 mechanical ventilation, if necessary May need early hemodynamic monitoring 11-13g/dl Assess volume status(preload) PCWP<15 volume expansion PCWP>15 consider volume if PCWP<18 diureses if PCWP>18 Reassess to keep: PCWP 15-18 mmHg MAP 60-80 mmHg SvO2 >65-70% Delivery independent O2 consumption Goals not met Goals met Inotropic support (b agonism) Dobutamine Dopamine Epinephrine Treat inciting cause of shock control inflammatory response nutritional support

24. Reassess Goals met Goals not met • Consider vasodilators • Nitroglycenin • Nitroprusside • Consider a agonist • Norepinephrine • Epinephrine • Neosynephrine • Plus • Dopamine Treat inciting cause of shock control inflammatory response nutritional support

25. SPECIFIC SHOCK SYNDROMES

26. Clinical signs and symptoms of hemorrhagic shock based on severity of blood loss 注：此图表太大，一个幻灯页面不能全部显示

27. Traumatic shock • Hypovolemic shock with • 1. larger volume losses • 2. greater fluid sequestration in the extravascular compartments • 3. more intense activation of inflammatory mediators development of SIRS • 4. microcirculatory derangements • 5. MODS frequently occur

28. Traumatic shock • treatment • 1. excessive fluid requirements • 2. mechanical ventilation • 3. pulmonary artery catheter monitoring • 4. cardiovascular support

29. Shock Associated with SIRS, Sepsis, and MODS • SIRS: two or more of following • 1. temperature greater than 38℃ or less than 36℃ • 2. heart rate greater than 90 beats per minute • 3. respiratory rate greater than 20 breaths per minute or PaCO2 less than 32mmHg • 4. white blood cell count greater than 12,000 per cu mm, less than 4000 per cu mm or greater than 10% band forms

30. VII. Diagnosis of hypovolemic shock • 1. clinical history; • 2. physical findings; • 3. blood tests. • 4. characteristic hemodynamics • 1. low right and left sided filling pressures(low central venous pressure, low PCWP) • 2. decreased cardiac output, decreased SvO2 • 3. increased systemic vascular resistance

31. VIII. Treatment • Patients airway; adequate ventilation, oxygenation • Fluid replacement isotonic electrolyte solutions • Crystalloid --- Ringer’s lactate solution • Blood transfusion --- type-specific type O packed red blood cells • Guide treatment • If absent • monitor the central venous pressure • Place a pulmonary artery catheter • Then: urinary output rate of 0.5 to 1.0 ml/kg/hour • The pneumatic anti-shock garment • Colloid solution; hyper-tonic saline(controversy)

32. SEPSIS • Sepsis: the presence of SIRS in association with culture-proven infection • Septic shock: sepsis with hypotension despite adequate fluid resuscitation, along with the presence of manifestations of hypoperfusion, including, but not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. • Mutiple organ dysfunction syndrome (MODS): the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention.

33. Mortality rate • 26% SIRS→SepsisMortality rate: 7%→16% • 4%Sepsis→Septic shock Mortality rate: 7%→46% • MODS mortality range from 20% to 100% depending on the number of failed organs severity of illness scoring systems

34. MODS • Primary MODS • Ischemic • Reperfussion • direct insult • Secondary MODS(two-hit model) • exaggerated uncontrolled systemic • inflammatory response

35. clinical features: • fever, tachycardia, hypotension, oliguria (obtundation, coma)altered mental status. Leukocytosis or leukopenia increased or decreased systemic vascular resistance. • Positive microbial cultures • gram-negative bacteria • escherichia coli, klebsiella • pseudomonas • staphylococcus streptococcus spices,fungal, viral , protozoal • pneumonia, gastrointestinal perforation biliary tract infection, urinary tract infection burn wounds

36. The Two-hit Theory of MODS Amplified Systemic Inflammation response Systemic Inflammatory response First Hit 2 ° MODS 1° MODS Second Hit Recovery Death Recovery Death

37. 1. Pulmonary failure ARDS • Mortality exceeds 50% • ventilation perfusion abnormalities • pulmonary edema • hypoxemia • decreased functional residual capacity • decreased infiltrates on chest X-rays

38. 2. Gastrointestinal dysfunction • Gastritis. Ulcerations. Pancreatitis; cholesystitis, mal-absorption, mucosal atrophy, translocation of bacteria or toxins.

39. 3. Renal dysfunction • Tissue hypoperfusion • Tissue damage by activated infalammatory cells and their mediators • Uremia electrolyte disturbances dialysis

40. 4. Cardiac dysfunction • 1 depreesed coronary blood flow • 2 direct endotoxin toxicity • 3 myocardia depressant factor(TNF)

41. 5. CNS manifestation of MODS • GCS scoring; mental status the patients’ best eye opening, verbal and motor responses

42. Treatment • To prevent the progression to MODS. To improve oxygen delivery and oxygen comsumption • Oxygen delivery: Volume expansion;Provision of red blood cell mass;Use of pharmacologic agents:Beta agonists & Vasodilators • For monitoring: e.g. pulmonary artery catheter • For hemodynamic and other physiologic evaluation • Antibiotics: to detect possible sources of infection(culture) • Surgical debridement • Drainage • Nutritional support

43. The End Thank you!