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  1. 1.
  2. 2. Shock“Transition between life and death”Failure to oxygenate & nourish the bodyadequatelyMortality > 20%
  3. 3. Shock in surgical practicesHypovolemic shock - due to decreased circulating bloodvolume in relation to the total vascular capacity andcharacterized by a reduction of diastolic filling pressuresCardiogenic shock - due to cardiac pump failure related toloss of myocardial contractility/functional myocardium orstructural/mechanical failure of the cardiac anatomy andcharacterized by elevations of diastolic filling pressures andvolumesExtra-cardiac obstructive shock - due to obstruction to flowin the cardiovascular circuit and characterized by eitherimpairment of diastolic filling or excessive afterloadDistributive shock - caused by loss of vasomotor controlresulting in arteriolar/venular dilatation and characterized(after fluid resuscitation) by increased cardiac output anddecreased SVR
  4. 4. Pathophysiology &Biochemistry
  5. 5. PathophysiologyShock affects mitochondria firstWithout oxygen mitochondria convert fuelsto lactate → lactic acidFailure of the krebs cycle Oxygen is the final electron accepter to form water
  6. 6. Mechanisms of Cellular Injury in Shock1) Cellular ischemia2) Free radical reperfusion injury3) Inflammatory mediators (local and circulating)
  7. 7. Physiologic Oxygen Supply DependencyOxygen Consumption Critical Delivery Threshold Oxygen Delivery Mizock BA. Crit Care Med. 1992;20:80-93.
  8. 8. Oxygen Consumption Pathologic Oxygen Supply Dependency Pathologic Physiologic Oxygen Delivery Mizock BA. Crit Care Med. 1992;20:80-93.
  9. 9. Lactic AcidEarly shock Skeletal muscle and splanchnic organs 1st affected Lactic acid productionResuscitation Pyruvate delivery from glycolysis can overwhelm krebs cycle
  10. 10. Systemic ResponseDecreased vascular wall tension increasessympathetic stimulation (blocked in sepsis) Increased epi, norepi, corticosteroids, renin, and glucagon Increased glycogenolysis and lipolysisIncreased glucose and FFA’s to TCA canoverwhelm it
  11. 11. Immune ResponseNeutrophil and macrophage activation dueto hypoxia Enzymatic organ damage Capillary plugs causing microischemia TNF and Interleukins released
  12. 12. Cardiac PhysiologyContraction created by Ca++, ATP/CP, andtroponin CCalcium inflow determines strength ofcontractionInotropics increase Ca++ release in thesarcoplasmic reticulum via β-receptors orcAMP
  13. 13. Cardiac PhysiologyATP/CP supply almost entirely fromoxidative phosphorylation by mitochondriaComplete turnover of ATP/CP every 5-10beats
  14. 14. Cardiac PhysiologyGregg Phenomenon Contractile strength decreases with decreased coronary perfusionDecreased coronary perfusion in shockDecreased workload due to lower SVRVery minimal cardiac ischemia even insevere shock
  15. 15. Cardiac PhysiologyInflammatory actions of TNFα,Interleukins, and NO decrease contractilityAcidosis can decrease contractility buteffect is minimal
  16. 16. Clinical Features & Management
  17. 17. ShockClassificationRapid, butdetailed H&Pto directtherapyFlow diagram  Figure 4-4 in Rosen’s
  18. 18. Clinical FeaturesFrequently no obvious etiologyRapid recognition H&P, ill appearance, diaphoresis HR and BP not reliable HR/SBP ratio better indicator Normal is less than 0.8 Urine output is great, but takes time Normal >1.0 ml/kg/hr Lactic acid or base deficit
  19. 19. Hypovolemic ShockDegree of volume loss response• 10% well tolerated (tachycardia)• 20 - 25% failure of compensatory mechanisms (hypotension, orthostasis, decreased CO)• > 40% loss associated with overt shock (marked hypotension, decreased CO, lactic acidemia)
  20. 20. Hypovolemic ShockRate of volume loss and pre-existingcardiac reserve response:• Acute 1L blood loss results in mild to moderate hypotension with decreased CVP and PWP• Same loss over longer period may be tolerated without hypotension due to increased fluid retention, increased RBC 2,3 DPG, tachycardia, and increased myocardial contractility• Same slow loss in patient with diminished cardiac reserve may cause hypotension or shock.
  21. 21. Clinical DataCXR – infection, contusionsEKG – ischemiaGlucoseCBC – anemia, leukocytosisElectrolytes – dehydration, GIbleed, acidosisABG – base deficit, acidosisUA – dehydration
  22. 22. Diagnosis and Evaluation Invasive MonitoringArterial pressure catheterCVP monitoringPulmonary artery catheter (+/- RVEF, oximetry)
  23. 23. Organ Blood Flow in ShockDependent on maintenance of bloodpressure within an acceptable rangeFor humans, good overall auto-regulationof blood flow between 60 - 100 mm HgHowever, experimental data in animalsshows brain and heart have wider rangeswhile skeletal muscle has a significantlynarrow auto-regulatory range.
  24. 24. ManagementIV, O2, monitorBP readings every 2-5 minutes Remember BP reading often underestimates the level of shock until severeUrine output >1 cc/kg/min
  25. 25. ManagementIV access Peripheral vs. Central Most patients OK with one large bore or two smaller bore peripheral IV’s CVP pressure may be required for patient with cardiac failure or renal failure Indwelling catheters should be used unless hospital policy states against it in the ED
  26. 26. Therapeutic StepsAdmit to intensive care unit (ICU)Venous access (1 or 2 wide-bore catheters)Central venous catheterArterial catheterEKG monitoringPulse oximetryHemodynamic support (MAP < 60 mmHg)• Fluid challenge• Vasopressors for severe shock unresponsive to fluids
  27. 27. Volume ReplacementWhen is the tank full? Goal CVP slightly elevated of 10-15 cm H2O Must correlate CVP with SBP, urine output, and lactate levels to adequately assess perfusion
  28. 28. VentilationRapid sequence intubation preferred Ketamine or etomidate are good choices due to minimal cardiovascular depression Intubation protects aspiration, decreases breathing workload, and initial treatment for acidemia High negative pressures in bronchospasm or ARDS can decrease LVEF and positive pressure removes this
  29. 29. AcidosisAcidosis is a negative inotropeNo evidence supports using bicarbonatefor treatmentTreat with improved ventilation and mildhyperventilationTHAM (tris[hydroxymethl]-aminomethane)may be used IV for acidosis reversal
  30. 30. Optimal HemoglobinHemoglobin carries oxygenHigh hematocrits increase viscosity andcardiac workloadOptimal balance is a hemoglobin of 10-12gm%
  31. 31. Goal-Directed TherapyGoal directed therapy is the practice ofresuscitating to a defined physiologic endpoint Wedge pressures – measures left ventricular filling pressures – controversial risk/benefit Lactate clearing index – decrease in arterial lactate by 50% in 1 hour and continued efforts until lactate < 2 mM GI tonography – permeable balloon in stomach or rectum measuring pH to estimate perfusion Questionable data supporting
  32. 32. Specific Causes & Treatment
  33. 33. A Clinical Approach to Shock Diagnosis and Management Immediate Goals in ShockHemodynamic support MAP > 60mmHg PAOP = 12 - 18 mmHg Cardiac Index > 2.2 L/min/m2Maintain oxygen delivery Hemoglobin > 9 g/dL Arterial saturation > 92% Supplemental oxygen andmechanical ventilationReversal of oxygen dysfunction Decreasing lactate (< 2.2mM/L) Maintain urine output` Reverse encephalopathy Improving renal, liver functiontests MAP = mean arterial pressure; PAOP = pulmonary artery occlusion pressure.
  34. 34. A Clinical Approach to Shock Diagnosis and Management Hypovolemic ShockRapid replacement of blood, colloid, orcrystalloidIdentify source of blood or fluid loss:• Endoscopy/colonoscopy• Angiography• CT/MRI scan• Other
  35. 35. Hemorrhagic ShockRapid reduction in blood volumeHeart rate and blood pressure responsescan be variableNo firm conclusion can be made by simplyHR and BP readings
  36. 36. Hemorrhagic Shock General Progression Increased heart rate Narrowed pulse pressureShunting from noncritical organs Decreased cardiac filling leading to decreased CO Decreased SBP
  37. 37. Hemorrhagic ShockDecreased perfusion to splanchnic organsprecedes lower BP Lactic acid production Base deficit Normal base deficit is greater than -2 mEq/LAfter 1/3 of blood volume lost hypotensionoccursAcidemia occurs about then as patientcannot create enough respiratorycompensation for the lactic acid
  38. 38. Hemorrhagic ShockOrgan injury in resuscitation Release of activated neutrophils & inflammatory cytokines Distorted balance of vasodilatation vs. vasoconstriction May lead to ARDS, acute tubular necrosis, & centrilobular ischemic liver damage
  39. 39. Consensus DefinitionHemorrhagic Shock – 3 classifications Simple hemorrhage Bleeding with normal vital signs and base deficit Hemorrhage with hypoperfusion Bleeding with base deficit < -5 mmol or persistent HR >100 Hemorrhagic shock Bleeding with 4 or more of below  Ill appearance or mental status  HR >100  RR >22 or PaCO2 <32  Base deficit < -5 or lactate > 4  Urine output < 0.5 cc/kg/hr  Hypotension > 20 minutes
  40. 40. Hemorrhagic Shock TreatmentSeveral liters of crystalloids in adultsThree 20 cc/kg boluses in childrenIf still in shock after bolus start PRBC’s at5-10 cc/kgBlood substitutes possibly in future but notcurrently advantageous
  41. 41. Hemorrhagic Shock TreatmentControlling hemorrhage is still always thecornerstone of treatmentImmediate surgery if hemorrhage cannotbe controlledIn very rare cases inotropics may bebeneficial
  42. 42. Septic ShockAny microbe may cause, but gramnegative most commonLipopolysaccharide is a key mediator1/3 of cases no organism is identifiedHigher causes recently of gram positivedue to Hospitalized patients Immunocompromised Indwelling catheters Increasing drug resistance
  43. 43. Septic Shock3 major effects Hypovolemia Relative due to increased venous capacitance Absolute due to GI loss, diaphoresis, tachypnea Cardiovascular depression Depression due to inflammatory mediators Systemic inflammation Capillary leak causing ARDS in up to 40%
  44. 44. Consensus DefinitionSIRS Two or more of the following Temperature > 38 C or <36 C Heart rate > 90 Respiratory rate > 20 resp/min or PaCO2 <32 WBC > 12,000, < 4,000, or >10% bandsSeptic Shock Severe sepsis with hypotension unresponsive to fluid resuscitation and perfusion abnormalities
  45. 45. Septic Shock TreatmentVentilatory support Decrease respiratory workload and correct hypoxiaFluids Increase ventricular filing 20-25 cc/kg crystalloids followed by 5-10 cc/kg colloidsBlood Used to keep Hct at 30-35% if needed
  46. 46. Septic Shock TreatmentAntibiotics If focus identified Use clinical experience If no focus identified Semisynthetic PCN with β-lactamase inhibitor with an aminoglycoside and vancomycin Imipenem-cilastatin good monotherapy choice Antifungal in immunocompromised
  47. 47. Septic Shock TreatmentVasopressors Dopamine Most common first line agent and a bad idea Remove from you armamentarium Norepinephrine Start 0.5-1 µg/min and titrate to response Excellent first choice; well studied Dobutamine Start 5 µg/kg/min Hypotension unresponsive to vasopressors and IVF.
  48. 48. Cardiogenic ShockPump failureResults when more than 40% ofmyocardium damagedSimilar circulatory and metabolic changesto hemorrhagic shockMay also be due to a PE
  49. 49. Consensus DefinitionsCardiogenic Cardiac failure Evidence of impaired cardiac outflow including dyspnea, tachycardia, rales, edema, or cyanosis Cardiogenic shock Cardiac failure plus four of below criteria  Ill appearance or mental status  HR >100  RR >22 or PaCO2 <32  Base deficit < -5 or lactate > 4  Urine output < 0.5 cc/kg/hr  Hypotension > 20 minutes
  50. 50. Cardiogenic Shock TreatmentVentilatory support Often needed in pulmonary edema or if respiratory failure imminent Avoid barbiturates, morphine, propofol and benzodiazepines Negative inotropic effects Fentanyl, ketamine and etomidate much better choices
  51. 51. Cardiogenic Shock TreatmentIonotropics/vasopressors Dobutamine and Milrinone are agents of choice Amrinone (Replaced by Milrinone) Milrinone Similar to amrinone Load at 50 µg/kg (Consider half loading dose) Infuse at 0.375 - 0.75 µg/kg/min Be prepared for hypotension
  52. 52. Cardiogenic Shock TreatmentIntraaortic balloon pump When all pharmacologic therapy is failing Requires appropriate facility and ICU/CCU Improves cardiac output by 30%
  53. 53. Cardiogenic Shock TreatmentMyocardial infarction causing cardiogenicshock Management not significantly different than another MI accept additional management Ventilatory support as needed Treat dysrhythmias Inotropic support Aspirin Heparin PTCA vs. thrombolytics
  54. 54. Cardiogenic Shock TreatmentPulmonary Embolism Ventilatory support IV fluids Norepinephrine Thrombolytics (systemic vs. intra-arterial) Possis catheter Surgical embolectomy at few centers
  55. 55. Anaphylactic ShockIgE mediated response to an allergenMast cells release histamineHistamine causes Smooth muscle relaxation Bronchial contraction Capillary leak
  56. 56. Anaphylactic Shock TreatmentEpinephrine 1 cc of 1:10,000 IV infused slowly and watch response 5 mg in 500 cc NS at 10 cc/hr thereafter May titrate to response Use even with coronary artery disease if hypotensive
  57. 57. Anaphylactic Shock TreatmentCorticosteroids Decrease immune response Methylprednisolone 125mg IV Hydrocortisone 5-10 mg/kg IVAntihistamines Diphenhydramine 0.5 mg/kg IV Cimetidine 2-5 mg/kg IV FamotidineIntubation if needed
  58. 58. Neurogenic ShockCNS cord lesions above T1 Heart gets unopposed vagal simulation Bradycardia and hypotensionAtropine First line therapy
  59. 59. Neurogenic Shock TreatmentVolume expansion Confirm by CVP and BPVasopressors Ephedrine 10 mg IV bolus good for 3-4 hours Phenylephrine 100-180 µg/min IV until stable
  60. 60. Fluid TherapyCrystalloids• Lactated Ringer’s solution• Normal salineColloids• Hetastarch• AlbuminPacked red blood cellsInfuse to physiologic endpoints
  61. 61. Fluid TherapyCorrect hypotension first (golden hour)Decrease heart rateCorrect hypoperfusion abnormalitiesMonitor for deterioration of oxygenation
  62. 62. SummaryEarly recognition of shock and earlytreatment is keyDo not rely solely on a HR and BP todetermine their statusAggressive and goal directed therapy haveproven to decrease mortality