SHOCK

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