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SHOCK

SHOCK . NGA B. PHAM, MD, FAAP CRITICAL CARE MEDICINE CHILDREN’S HEALTHCARE OF ATLANTA EGLESTON 2006. Objectives. Review basic physiologic aspects of shock Define shock and its different categories Describe management of shock. What is Shock? Pathophysiology of shock. Oxygen

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SHOCK

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  1. SHOCK NGA B. PHAM, MD, FAAP CRITICAL CARE MEDICINE CHILDREN’S HEALTHCARE OF ATLANTA EGLESTON 2006

  2. Objectives • Review basic physiologic aspects of shock • Define shock and its different categories • Describe management of shock

  3. What is Shock?Pathophysiology of shock Oxygen Demand > Supply

  4. Definition of Shock • Inadequate tissue perfusion to meet tissue demands • Usually result of inadequate blood flow and/or oxygen delivery • Shock is not a blood pressure diagnosis

  5. Determinants of Oxygen Delivery • Oxygen Delivery = Content x Cardiac output

  6. Determinants of Oxygen Delivery • Oxygen content = 1.34 (Hgb x SaO2) + (PaO2 x 0.003) • SaO2: Oxygen saturation • Hgb: Hemoglobin concentration • PaO2: partial pressure Oxygen in plasma • To improve Oxygen content • Increase Hemoglobin concentration • Increase saturation

  7. Determinants of Oxygen Delivery • Cardiac output • C.O. = Heart rate x stroke volume • To improve Cardiac output • Increase Heart rate • Increase Stroke Volume • Preload – volume of blood in the ventricle • Afterload – resistance to contraction • Contractility – force applied

  8. Secondary Organ Dysfunction • Respiratory failure • Tachypnea • Decreased compliance • Pulm edema, pulm infiltrate, etc. • Increased resistance • Diaphragm fatigue • Central vs peripheral • Demand >> supply • Inadequate O2 delivery

  9. Secondary Organ Dysfunction • CNS – altered mental status • Renal insufficiency – pre-renal • Coagulation abnormalities – DIC • Hepatic/GI dysfunction – bowel ischemia • Endocrine – Calcium, hypo-adrenalism, vasopressin

  10. Classification of Shock • Hypovolemic Shock (#1 cause world wide) • Dehydration, hemorrhagic • Cardiogenic Shock • Pump failure, obstructive, L-R shunt • Distributive Shock • Neurogenic • Anaphylaxis • Septic Shock – All of the above

  11. Classification of Shock • Compensated • Organ perfusion is maintained • Uncompensated • Circulatory failure with end organ dysfunction • Irreverisble • Irreparable loss of essential organs

  12. Mechanical Requirements for Adequate Tissue Perfusion • Fluid • Pump • Vessels • Flow

  13. Hypovolemic Shock • #1 cause of death world wide • Gastroenteritis • Hemorrhagic – Trauma, GI bleed

  14. Diagnosis of Hypovolemic Shock • Early • Increase HR • Decrease perfusion • Normal BP, decrease pulse pressure • Late • Sign increase HR • Sign decrease perfusion • Decrease BP • End organ dysfunction

  15. Pathophysiology of Hypovolemic Shock • Decrease intravascular volume • Compensation – increase endogenous catecholamines • Increase HR – increase C.O., O2 delivery • Increase SVR – increase BP (esp diastolic) • Compensation for <15% dehydration

  16. Cardiogenic Shock Pump failure/malfunction (decreased contractility)

  17. Cardiogenic Shock • Electrical Failure • Arrhythmias • Mechanical failure • Cardiomyopathy • Metabolic – acidosis • Anatomic • Hypoxia/ischemia • Obstruction

  18. Cardiogenic ShockSymptoms • Tachycardia • Tachypnea • Respiratory distress • Mental status change • Cool extremities • Poor perfusion • Signs of dehydration

  19. Cardiogenic ShockObstruction of Flow • Causes • Pericardial tamponade • Pulmonary embolism • Pulmonary hypertension

  20. Cardiogenic ShockObstruction of Flow Cardiac tamponade • Causes • Pericarditis • Post-traumatic • Post-cardiac surgery • Complication of central line placement • Recognition • Tachycardia • Low C.O., narrow pulse pressure (inc. diastole) • Inc. CVP, JVD • PULSUS PARADOXUS (>10mmHg) • Muffled heart sounds (??rub) • NO RALES

  21. Distributive Shock • Abnormal vessel tone (decreased afterload)

  22. Distributive Shock Vasodilitation Venous Pooling Decreased Afterload Maldistribution of regional blood flow

  23. Distributive Shock • Neurogenic or Anaphylactic Shock • Diminished or absent sympathetic tone • Reduce peripheral vascular tone • Peripheral pooling of blood volume • Inadequate venous return • Decreased perfusion, acidosis, hypotension

  24. Septic Shock • Terminology in Sepsis • Infection = response to micro organism • Bacteremia = bug in blood • Systemic Inflammatory Response Syndrome (SIRS) • T>38, <36 • Increase HR • Increase RR, paCO2<32 • WBC>12,000, <4,000, >10% bands

  25. Septic Shock • Terminology in Sepsis • Sepsis = SIRS as response to a known infection • Severe sepsis = Sepsis + organ dysfunction • Septic Shock = Sepsis + inadequate oxygen delivery • Multiple Organ Dysfunction Syndrome (MODS) – organ dysfunction that requires intervention

  26. Septic Shock • Components of Septic shock • Decreased volume • Decreased pump function • Abnormal vessel tone

  27. Septic Shock • Therapy for Caridovascular Support Preload Volume Contractility Inotropes Afterload Vasodilators

  28. Septic Shock Etiologies • Inflammatory: too much, too little • Coagulation pathway: DIC-bleeding, pro-coagulant, microthombosis • Multiple organ system failure

  29. Recognition of Septic Shock • Early – warm shock – similar to neurogenic shock • Late – Cold shock – similar to cardiogenic shock

  30. Diagnosis of Septic Shock • Establish presence of infection • Inc. HR, normal or dec. BP & perfusion • Latic acidosis • Muti-organ dysfunction

  31. Early vs Late Septic Shock

  32. Early vs Late Septic Shock

  33. Treatment Strategies in Shock

  34. Principles of Resuscitation • Increase Oxygen Delivery\ • Increase Oxygen content • Increase Cardiac output • Increase blood pressure • Decrease Demand • Sedation/analgesia • Intubation

  35. Initial Treatment in Shock • Airway • Supplemental oxygen, intubation • Carefull with cardiovascular collapse post intubation due to positive thoracic pressure decrease venous return • Breathing • Circulation • Intravenous access – go early, go IO • Volume expansion (40cc/kg NS, repeat prn) • Carefull with cardiogenic shock (5cc/kg then reassess) • Optimize cardiac function, oxygenation

  36. Restoration of CirculationVolume Fluids, fluids, fluids Crystalloids vs Colloids

  37. Restoration of CirculationVolume • Crystalloids • NS is the fluid of choice, availability • Rapid redistribution out of intravascular space – capillary leak

  38. Restoration of CirculationVolume • Colloids: albumin, blood • Albumin • Worsening of edema due to cap leak in early sepsis • Blood • Great volume expanders • Side effects: with massive transfusion >1.5 blood volumes • Risk of infection • Dilutional thrombocytopenia and factors V & VIII • Calcium binding hemodynamic instability (citrate)

  39. Restoration of CirculationVolume – Fluid Choices • Based on: • Type of deficit • Urgency of repletion • Pathophysiology of shock

  40. Restoration of CirculationVolume – Fluid Choices • Crystalloids for initial resuscitation • Colloids/PRBC’s to replace blood loss

  41. Treatment of ShockCardiac Support Alpha Dopamine Beta Epinephrine Norepinephrine Dobutamine Neosynephrine

  42. Inotropes

  43. “New” Therapies in Septic Shock • Vasopressin • Steroids • Activated protein C (Xigris) in Septic Shock

  44. New” “ Therapies in Septic ShockVasopressin • Unclear mechanism of action • Bridging vascular instability in high exogenous catecholamines requirement septic shock, therefore decrease side effects of toxic dosage of catecholamines • Also shows greater blood flow diversion from non-vital to vital organs

  45. New” “ Therapies in Septic ShockVasopressin • Dosage 0.01 – 0.04U/min up to 0.08U/min

  46. New” “ Therapies in Septic ShockSteroids • Hypo-adrenalism: abnormal hypothalamus-pituitary-adrenal axis • At risk of adrenal insufficiency – in the presence of catecholamine requirement • Fluid refractory shock • Normal BP, cold shock • Low BP, cold shock • Dosage – stress dose • Hydrocortisone 150 mg/m2 ivp

  47. New” “ Therapies in Septic ShockSteroids Glucocorticoid function – immune response • Fall in circulating lymphocytes • Inhibits neutrophils migration to the inflammatory sites • Inhibits macrophages secretion • Promotes eosinophilic apoptosis • Modulates cytokines production

  48. New” “ Therapies in Septic ShockSteroids Glucocorticoid function – Cardiovascular • Modulate vascular reactivity to angiotensin II and to catecholamines -Not fully understood mechanism • Modulate vascular permeability and production of NO and other vasodilator factor INCREASE IN BLOOD PRESSURE

  49. New” “ Therapies in Septic ShockSteroids Glucocorticoid production in stress • Maintain homeostasis • Normalize vascular reactivity • Modulate inflammatory response

  50. New” “ Therapies in Septic ShockActivated Protein C (Xigris) • Recombinant Human Activated Protein C • Prevent DIC cascade with antithrombotic activity by inhibiting factors Va & VIIIa • May exerts anti-inflammatory effects by inhibiting TNF and by blocking leukocytes adhesions • Side effects • Bleeding • Pediatric trial terminated early (03/04) due to no benefit to known risk of bleeding

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