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shock

Objectives. Review basic physiologic aspects of shockDefine shock and its different categoriesDescribe management of shock. What is Shock? Pathophysiology of shock. OxygenDemand > Supply. Definition of Shock. Inadequate tissue perfusion to meet tissue demandsUsually result of inadequate blood flow and/or oxygen deliveryShock is not a blood pressure diagnosis.

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shock

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    1. SHOCK NGA B. PHAM, MD, FAAP CRITICAL CARE MEDICINE CHILDRENS 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 SeptSept

    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/PRBCs 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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