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7 shock


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for Undergraduate medical students (MBBS)

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7 shock

  1. 1. Hemodynamic derangementsHemodynamic derangements SHOCK Dr.CSBR.Prasad, M.D.
  2. 2. DEFINITION Shock: It’s a Clinical state of Inadequate perfusion resulting in O2 debt at cellular level
  3. 3. Common Pathophysiology Cellular dysfunction DO2 and energy substrate reduction anaerobic metabolism systemic acidosis (myocardial, smooth muscle depressant), organ failure Marked decrease VO2, may indicate irreversible shock
  4. 4. Hemodynamic Classification of Shock Type PAP CO SVR hemorrhagic decr decr incr cardiogenic incr decr incr distributive nl, nl, decr decr incr, decr obstructive incr decr incr
  5. 5. Etiologic Classification of Shock • Cardiogenic • Hemorrhagic / Hypovolemic • Distributive (SIRS, septic, high output failure, spinal cord injury, anaphylactic)
  6. 6. Etiologic Classification of Shock Cardiogenic - causes • Myocardial Infarction • Ventricular Arrhythmia • Cardiac tamponade • Pulmonary embolism Basic mechanism: Failure of myocardial pump owing to intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow
  7. 7. Pulmonary embolism – obstruction to out flow - failure
  8. 8. Myocardial infarction – pump failure
  9. 9. Myocardial infarction – pump failure
  10. 10. Myocardial infarction – pump failure
  11. 11. Myocardial infarction – Rupture of ventricle – External compression
  12. 12. Myocardial infarction – Rupture of ventricle – External compression Cardiac tamponade
  13. 13. Etiologic Classification of Shock Hypovolemic: • Hemorrhage • Fluid loss, e.g., vomiting, diarrhea, burns, or trauma Basic mechanism: Inadequate blood or plasma volume
  14. 14. Etiologic Classification of Shock Distributive: Increased vascular volume • SIRS - septic • high output failure • spinal cord injury • Anaphylactic • Superantigens Basic mechanism: Peripheral vasodilation and pooling of blood; endothelial activation / injury; leukocyte-induced damage; disseminated intravascular coagulation; activation of cytokine cascades
  15. 15. Septic shock Bacteremia Septicemia
  16. 16. Septic shock Septic shock results from spread and expansion of an initially localized infection (e.g., abscess, peritonitis, pneumonia) into the bloodstream
  17. 17. Septic shock • 25-50% mortality in ICUs • 70% are due to endotoxins
  18. 18. Septic shock • ~ 70%) are caused by endotoxin- producing GNB • Endotoxins are bacterial wall lipopolysaccharides (LPSs)
  19. 19. Lipopolysaccharide – LPS ENDOTOXIN
  20. 20. Septic shock
  21. 21. Septic shock
  22. 22. Effects of LPSs • At low doses - activate monocytes and macrophages, with effects intended to enhance their ability to eliminate invading bacteria. • with higher levels of LPS cytokine-induced secondary effectors (e.g., nitric oxide become significant. In addition, systemic effects of the cytokines such as TNF and IL-1 may begin to be seen; these include fever and increased synthesis of acute phase reactants. • LPS at higher doses also results in diminished endothelial cell production of thrombomodulin and TFPI, tipping the coagulation cascade toward thrombosis. • Finally, at still higher levels of LPS, the syndrome of septic shock supervenes • Systemic vasodilation (hypotension) • Diminished myocardial contractility • Widespread endothelial injury and activation - acute respiratory distress syndrome. • Activation of the coagulation system, culminating in DIC
  23. 23. Septic shock
  24. 24. Septic shock
  25. 25. Stages of Shock • Initial nonprogressive phase: during which reflex compensatory mechanisms are activated and perfusion of vital organs is maintained • A progressive stage: characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances, including acidosis • An irreversible stage: severe tissue damage -- even with the correction of hemodynamic defects survival is not possible
  26. 26. Morphology • Hypoxic injury • Failure of multiple organ systems brain heart lungs kidneys adrenals & GIT
  27. 27. Morphology – Multi Organ Failure • Brain: Ischemic encephalopathy • Heart: Subendocardial necrosis and contraction bands • Kidneys: Acute tubular necrosis • Lungs: Shock lung • Adrenals: Cortical cell lipid depletion • GIT: Hemorrhagic enteropathy • Liver: Centrilobular necrosis
  28. 28. Ischemic encephalopathy
  29. 29. Ischemic encephalopathy Hippocampal sclerosis
  30. 30. Ischemic encephalopathy
  31. 31. Clinical course The clinical manifestations depend on the precipitating insult. • In hypovolemic and cardiogenic shock, the patient presents with hypotension; a weak, rapid pulse; tachypnea; and cool, clammy, cyanotic skin. • In septic shock, however, the skin may initially be warm and flushed because of peripheral vasodilation. • The original threat to life stems from the underlying catastrophe that precipitated the shock state (e.g., myocardial infarct, severe hemorrhage, or uncontrolled bacterial infection). • Duration of shock: the cardiac, cerebral, and pulmonary changes secondary to the shock state may worsen the problem.
  32. 32. Hemorrhagic Shock Pathophysiology Volume deficit - decr. BP, CO Compensatory Mechanisms Catecholamine, sympathetic stimulation Interstitial fluid entry into intravascular compartment
  33. 33. Hemorrhagic Shock Clinical Presentation Early Phase Tachycardia, narrow pulse pressure, may exhibit orthostatic changes in HR/AP Healthy patient with 25-30% loss may exhibit only these signs
  34. 34. Hemorrhagic Shock Less healthy patients will exhibit rapid decompensation with this magnitude of volume loss Later Phase Cool moist skin, hypotensive, anxious, disoriented, oliguric KEY: EARLY RECOGNITION
  35. 35. Hemorrhagic Shock Management Therapeutic Goals Correct Hypotension, thereby normalizing cellular perfusion, reducing acidemia Increase SaO2, thereby increasing DO2
  36. 36. Hemorrhagic Shock Restoration of intravascular volume Fluid administered should replace fluid lost Initial Management: Crystalloids,N.S./ Ringer’s Colloids ( 5% alb., hetastarch) do not increase survival and are costly W.B. PRBC, when indicated
  37. 37. Parameters of Adequate Resuscitation Urine output (0.5 - 1.0 ml/kg/hr) acceptable renal perfusion Reversal of lactic acidosis (nl. pH) improved tissue perfusion Normal mental status adequate cerebral perfusion
  38. 38. Cardiogenic Shock Pathophysiology AMI- 10-15% cardiogenic shock Mortality > 80% Decreased CO, AP Neurohumoral compensatory mechanisms can be deleterious: > venoconstriction - >preload
  39. 39. Cardiogenic Shock Clinical Presentation Hypotension - < 80 syst., decr. of 90 mm Hg in patient with HTN Cool diaphoretic skin, dyspnea, disorientation, oliguria
  40. 40. Cardiogenic Shock > SVR > afterload > HR > VO2 < AP < coronary perfusion All contribute to extension of infarct and morbid progression of cardiogenic shock
  41. 41. Cardiogenic Shock Prognostic Parameters Group PAEDP CI Mortality I > 29 100% II < 29 ->15 < 2 92% III < 29 < 2 63% IV < 15 > 2 13% PAEDP=mm Hg, CI=L/M2/min.
  42. 42. Cardiogenic Shock Management Principles Primary Goal: Improve myocardial function Decrease O2 consumption (VO2) Intubation, sedation, analgesia Increase O2 delivery (DO2) Optimize CI, Hgb., Hgb. sat. (SaO2)
  43. 43. Cardiogenic Shock Management Methods Pharmacologic Manipulation Preload (RAP,PAP) - morphine, nitro, lasix, volume Cardiac contractility - inotropes, chronotropes, vasopressors Afterload (PVR,SVR) - nitro, beta-blockers
  44. 44. Cardiogenic Shock Interventional Therapy Intraaortic Balloon Pump (IABP) or Counterpulsation IABP + Early CABG (12-16 hr. post AMI) Left Ventricular Assist Device (LVAD)
  45. 45. Septic Shock Clinical Presentation Early Phase Vasodilatation CO normal or high fever Agitation / confusion hyperventilation Often, fever and hyperventilation are the earliest signs Hypotension may not be present
  46. 46. Septic Shock Late Phase CO decreased, hypotension, vasoconstriction, impaired perfusion, decreased level of consciousness, oliguria, DIC Atypical Presentation Elderly/debilitated – Fever, respiratory alkalosis, confusion, hypotension
  47. 47. Septic Shock Etiology Gram neg bacteria (gm. neg rods) Most common (E. coli, 31% all cases) Incidence - 12.8%/1000 hosp. adm. Mortality 25%; 30-50% if shock present 30% if Resp./GI/unkn. Source 15% if Biliary/GU/GYN source
  48. 48. Septic Shock Management Fluid resuscitation Pressor support After adequate volume restored Dopamine (5-10 ug/kg/min) Dobutamine (5-20ug/kg/min) Airway management
  49. 49. Septic Shock Management cont… Surgical drainage (abscess, infected organ (gangrenous gallbladder, bowel) Antibiotics Site established, consider organisms known to occur in such sites Unknown site in 30% of patients
  50. 50. Distributive Shock Pathophysiology Peripheral vascular dilatation disproportionate to existing intravascular volume Septic/Systemic inflammatory shock(SIRS), anaphylaxis, spinal shock
  51. 51. Summary - Shock • Shock is a clinical state of decreased BP with O2 debt at cellular level • If prolonged it may result in multiorgan failure • Septic shock has cytokine basis – TNF, IL1, DIC
  52. 52. E N D