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The Evaluation and Management of Shock

Shock. . Shock. Definition: Shock is a state of inadequate organ perfusion, which results in an imbalance of tissue oxygen delivery to meet the metabolic demands of tissue. Shock. Can there be shock without hypotension? - SBP does not decrease to less than 90mmHg until base deficit is worse than -20. - At this point mortality approaches 65% (Parks JK et al, Am J Surg 2006).

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The Evaluation and Management of Shock

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    1. The Evaluation and Management of Shock Alberto Nunez, MD Hahnemann University Hospital Department of Trauma

    2. Shock

    3. Shock Definition: Shock is a state of inadequate organ perfusion, which results in an imbalance of tissue oxygen delivery to meet the metabolic demands of tissue

    4. Shock Can there be shock without hypotension? - SBP does not decrease to less than 90mmHg until base deficit is worse than -20. - At this point mortality approaches 65% (Parks JK et al, Am J Surg 2006)

    5. Shock

    6. Shock Diagnosis: CLINICAL Look for signs of hypoperfusion: 1. Altered level of consciousness 2. Decreased urine output 3. Mottled skin 4. Hemodynamic instability

    7. Shock Management: Pathophysiology: 1. Hemodynamic component: initial resuscitation 2. Inflammatory component: leads to multiple system organ failure (MSOF)

    8. Shock Management Hemorrhagic Shock Phases of Hypovolemic shock: Phase I: hypovolemia vasoconstriction Impaired organ perfusion Increasing acidemia Phase II: ? intracellular and interstitial fluid Respiratory failure Abdominal compartment syndrome Phase III: diuresis

    9. Shock Management: GOAL To restore tissue perfusion in a timely fashion in order to prevent the systemic inflammatory response that would eventually lead to MSOF

    10. Shock Classification: 1. Hypovolemic 2. Vasodilatory 3. Cardiogenic

    11. Shock Pathophysiology: 1. Hypovolemic/Vasodilatory: Inadequate venous return to the heart: 1. Hemorrhage 2. Dehydration 3. Widespread vasoplegia: neurogenic 4. Loss of vascular tone: sepsis, anaphylaxis, ischemia-reperfusion syndrome

    12. Shock Pathophysiology: 2. Cardiogenic: Pump failure: 1. Loss of contractility: MI and its complications 2. Impaired diastolic filling: cardiac tamponade 3. Abnormal rate or rhythm 4. Obstruction to flow: valvular conditions, pulmonary embolus

    13. Shock Hypovolemic: 1. JVP is low 2. Poor capillary refill 3. Narrow pulse pressure 4. Evidence of bleeding or dehydration

    14. Shock Cardiogenic: 1. Narrow pulse pressure 2. Evidence of pulmonary edema 3. Gallop 4. Chest pain, EKG changes, abnormal cardiac enzymes, abnormal echocardiogram

    15. Shock Vasodilatory: 1. Hyperemic extremities 2. Bounding pulses, wide pulse pressure 3. Brisk capillary refill 4. Hyperdynamic heart sounds 5. Occurs in the setting of sepsis, anaphylaxis, burns, cyanide and CO poisoning, pancreatitis, ischemia-reperfusion injury

    16. Shock Assessment Primary Survey Airway and Breathing Decision to intubate and initiate ventilatory support should be made on clinical basis Recognize signs of early respiratory failure: Inability to speak Diaphoresis Labored breathing Cyanosis Tachypnea Mental obtundation Paradoxical breathing Accessory muscle use

    17. Shock Assessment Primary Survey Airway and Breathing Intubate EARLY Intubate before procedures or transporting patient Remember: multiple organ hypoperfusion (the definition of shock) is an indication for intubation and mechanical ventilation

    18. Shock Assessment Primary Survey Circulation Elaborate working diagnosis: hypovolemia vs. vasodilatation vs. pump failure Early empiric volume loading: Children: 20ml/kg Adults: 2000ml crystalloids Establish endpoints of resuscitation

    19. Shock Management Endpoints of Resuscitation “To provide the metabolic substrates, i.e., oxygen, to meet the consumptive demands of the tissues” The point at which these consumptive demands are met is called the Critical Oxygen Delivery (Critical DO2)

    20. Shock Management Endpoints of Resuscitation

    21. Shock Management Endpoints of Resuscitation Systemic Oxygen delivery (DO2): DO2 = CO x CaO2 CaO2 = Hb x O2 Sat x 1.39 + (0.003 PaO2) 1. Oxygen Saturation: ? FiO2, ? PEEP 2. Hemoglobin concentration: PRBC 3. Cardiac output: Starling curve

    22. Shock Management

    23. Shock Management Endpoints of Resuscitation Cardiac output: Blood pressure: = 90mmHg? Heart rate: 60 to 100bpm Urine output: = 0.5ml/kg/hr CVP: 8-15mmHg

    24. Shock Management Endpoints of Resuscitation Other: Lactate level, base deficit Pulmonary artery capillary wedge pressure (PCWP) SvO2 Right ventricular end diastolic volume index (RVEDVI) Left ventricular end diastolic area (LVEDA)

    25. Shock Management GOALS 1. DO2 of 500 to 600ml/min/m˛ 2. Re-establish perfusion early (within 6 h of injury) 3. Avoid the “bloody vicious cycle/lethal triad” 4. Avoid abdominal compartment syndrome 5. Avoid secondary brain insult in patients with TBI 6. Minimize the dysfunctional inflammatory response leading to MSOF

    26. Shock Management Goal-directed therapy. Why? Kern and Shoemaker: Goals: Increased CI and DO2 PACWP = 18mmHG Results: 23% absolute risk reduction in mortality Rivers et al: Goals: CVP 8-12mmHg MAP = 65mmHg SvO2 = 70% Results: Hospital mortality: 30.5% vs. 46.5% (p=0.009) 28 day mortality: 33.3% vs. 49.2% (p=0.01)

    27. Shock Management Goal-directed therapy…but Goals must be achieved EARLY! How early? Within the initial 6 hours Why? After onset of organ failure no amount of extra oxygen will restore irreversible oxygen debt or reverse cellular death

    28. Shock Management Hemorrhagic Shock Stop the Bleeding! Uncontrolled hemorrhage is responsible for over 40% of trauma deaths Injury to the central nervous system: 33% MSOF: 21%

    29. Shock Management Hemorrhagic Shock Stop the Bleeding! M Massive hemorrhage A Airway R Respiration C Circulation H Head injury/hypothermia

    30. Shock Management Classification of Hypovolemic Shock - Initial presentation: Class I, II, III and IV - Response to initial fluid resuscitation: Rapid response Transient response No response

    31. Shock Management Hemorrhagic Shock Delayed resuscitation/hypotensive resuscitation: Delay resuscitation until bleeding is controlled Resuscitate to the minimal BP required to achieve adequate organ perfusion Improved survival in patients with penetrating torso injury: Increased BP can cause disruption of early soft thrombus (“pop the clot”) Hemodilution of clotting factors can initiate coagulopathy

    32. Shock Management Delayed/hypotensive resuscitation: Bickel et al, 1994: survival advantage: 70% vs. 62%, p = 0.04 Animal study meta-analysis: reduced risk of death (RR=0.37) Committee on Tactical Combat Casualty Care: no fluids if palpable radial pulse and adequate mentation – First time since Crimean war that KIA rate has ? below 20% to around 10% to 14%

    33. Shock Management Hemorrhagic Shock Fluid resuscitation: 3:1 rule (8:1 in severe trauma)?? Colloid vs. crystalloid NS vs. LR vs. Hypertonic saline Blood and coagulation factors

    34. Shock Management Hemorrhagic Shock The bloody vicious cycle/lethal triad: Dilutional coagulopathy: - 33% to 55% of major trauma patients with pre-hospital resuscitation have an APTT > 55 secs and a PT > 18 secs Hypothermia: - Impaired platelet aggregation - At 35°C all factors have decreased function - In severe trauma patients (ISS>25) mortality is 100% when temp. is < 32°C vs. 7% when temp. is > 34°C Acidosis: - Coagulation factor activity is significantly reduced at pH < 7.4

    35. Shock Management Hemorrhagic Shock Prevent the bloody vicious cycle: Aim for normothermia Damage control surgery Consider use of blood products early: Consider PRBC when patient remains unstable after initial resuscitation (2000ml) Consider FFP early: If > 4U PRBC given within the first hour FFP:PRBC of 1:1.8 in severe trauma patients

    36. Shock Management Hemorrhagic Shock Massive transfusion: > 10 units PRBC in 24 hrs. 1 blood volume Blood loss = 5000 ml > 10 units: thrombocytopenia, ? fibrinogen, ? PT > 25 units/24hrs: mortality approx. 50% Cause: massive systemic inflammatory response TNFa, IL 1, IL 6, IL 8, other pro-inflammatory lipids

    37. Shock Management Cardiogenic Shock Mortality: 50% to 80% Initial approach should include fluid resuscitation unless patient is in pulmonary edema Vasoactive therapy is usually indicated Echocardiogram early to r/o tamponade or acute valvular dysfunction, evaluation of LVEDA IABP should be considered Thrombolytic therapy? Early revascularization is beneficial in patients < 75 years (survival 51.6% vs. 33.3%)

    38. Shock Management Septic Shock Initial management requires fluid resuscitation Vasoactive therapy is usually necessary Definitive management requires surgical debridement of necrotic tissue, drainage of purulent collections and antibiotic therapy Mortality rate has changed little over time Duration of antimicrobial therapy: 7-10 days Tight glucose control (80-110mg/dl) improves survival?

    39. Shock Management A word on vasoactive therapy Adequate Cardiac Output is more important than Blood Pressure ß agonists are used for cardiac contractility a agonists are used for maintenance of perfusion pressure No randomized controlled trials Titrate to SBP or MAP that achieves the goal of restoring autoregulation Confirm adequacy of CO/CI, SvO2, lactate

    40. Shock Management

    41. Shock Management Steroids Consider IV hydrocortisone for adult septic shock when hypotension responds poorly to adequate fluid resuscitation and vasopressors Hydrocortisone is preferred to dexamethasone ACTH stimulation test is no longer recommended to identify the subset of adults with septic shock who should receive steroids Hydrocortisone dose should be = 300 mg/day Steroid therapy may be weaned once vasopressors are no longer required Surviving Sepsis Campaign Guidelines, Crit Care Med 2008

    42. Shock Management Recombinant human activated protein C (Xigris®) Anti-thrombotic serine protease with anti-inflammatory properties Associated with a reduction in the relative (19.4%) and absolute (6.1%) risk of death in patients with organ failure due to acute infection Indicated in shock patients with end-organ dysfunction, acidosis, oliguria or hypoxemia Should be started within 24hrs. of initial organ failure Increased risk of bleeding

    43. Shock Management Use of Vasopressin (AVP) in hemorrhagic Shock AVP decreases crystalloid requirements to maintain target MAP (avoidance of secondary injury in TBI patients and ALI/ARDS in patients requiring massive resuscitation?) AVP is an alternative when response to a agonists ? due to down-regulation AVP is associated with worsening hemodynamic (? CI) and metabolic parameters (? lactate)

    44. Shock Management Sodium Bicarbonate for Lactic Acidosis Myocardial contractility ? with lactic acidosis? Coagulation factor activity decreases at pH < 7.4 Correction of acidosis with sodium bicarbonate does not improve hemodynamics or catecholamine responsiveness, even in the face of severe acidosis (pH < 7.2) Bicarbonate has been shown to raise PCO2 and lactic acid production. ? in CO2 can cause pH in intracellular spaces and CSF to drop Bicarbonate administration is not recommended for pH > 7.15

    45. Shock Management Summary Shock is an Emergency. Early resuscitation is key (first 6 hours) Continuous bedside evaluation, resuscitation and re-evaluation are required Initial management: intubation, ventilation and volume support Vasoactive therapy is started after the patient is well volume-resuscitated

    46. Shock Management Summary Vasoactive therapy consists of inotropic (ß) support for cardiogenic shock and pressor (a) therapy for vasodilatory shock Early shock has a hemodynamic component (reversible) Late shock has an inflammatory component (not easily reversed)

    47. Shock Management Summary Success in treatment of shock: 1. Early recognition 2. Rapid resuscitation Aim: 1. Resolution of hemodynamic component 2. Avoid “Second hit” (abdominal compartment syndrome, intracranial hypertension) 3. Prevention/modulation of inflammatory component

    48. Shock Management Room for Improvement Pre-ICU resuscitation monitoring: 1. Near-infrared spectroscopy 2. Central venous Hb oxygen saturation 3. CO monitoring: Trans-thoracic electrical bioimpedance

    49. Shock Management Room for Improvement Trauma as an immune disease: - Neutrophil-mediated cytotoxicity - Activation of adhesion molecules - Fluid resuscitation and apoptosis - Blood transfusions and immunosuppresion

    50. Shock Management Room for Improvement Fluid resuscitation: LR: pure L-isomer/ketone-pyruvate based 1. D-isomer up-regulates adhesion molecules (selectins, integrins) 2. Facilitates neutrophil-mediated cytotoxicity 3. Increases apoptosis (intestinal mucosa, smooth muscle, liver, lung)

    51. Shock Management Room for Improvement Hemorrhage control: recombinant activated Factor VII (rFVIIa) 1. Binds only to exposed subendothelial tissue factor 2. 63% reduction in need for massive transfusion 3. No systemic hypercoagulability 4. Effect on MSOF still unknown 5. Use in acidotic patient still controversial

    52. Shock Management Room for Improvement Tourniquets? Freeze-dried blood and FFP Non-antigenic blood

    53. Shock Management Room for Improvement

    54. Shock Management Room for improvement Trauma Induced Coagulopathy (TIC)

    55. Shock Management Room for improvement

    56. Shock Management Room for improvement Damage Control Resuscitation or Early Hemostatic Resuscitation (EHR): FFP:PRBC ratio of 1:1 Improves overall mortality in pts with TIC (28.3% vs. 51.2%) Pts given 1:3 and 1:4 ratio of FFP:PRBC were 3.76 and 4.17 times more likely to die in the OR (Duchesne et al, J Trauma, July 2009)

    57. Shock Management Room for Improvement Hypotensive Resuscitation: 1. Prevents disruption of early soft thrombus 2. Prevents coagulopathy 3. Prevents hemodilution

    58. Shock Management Room for Improvement In the absence of traumatic brain injury: “permissive hypotension” 1. SBP > 80mmHg 2. Consciousness 3. Palpable pulse 4. Control hemorrhage first

    59. Shock Management Room for Improvement Epigenetic Transcription Modulation Surviving blood loss without fluid resuscitation - Hemorrhage causes early transcriptional repression - ? transcription of immediate early response proteins - Acetylation of histones main mechanism - Hemorrhage associated with imbalance in HAT/HADC ratio

    60. Shock Management Room for Improvement Epigenetic Transcription Modulation - HDACI ( VPA or SAHA) in shock: up-regulates gene transcription attenuates organ injury improves survival - Survival after 60% blood loss in 60 min: 25% in control group 75% in SAHA group 83% in VPA group Shults et al, J Trauma 2008

    61. Shock Management Room for Improvement Fluid resuscitation: The best fluid for resuscitation? Fresh Whole Blood

    62. Shock Management Room for Improvement Fluid resuscitation: hypertonic saline dextran (HSD) 1. Small volume: avoid second hit 2. Increased perfusion of microcirculation 3. Decreases inflammatory response 4. Might increase bleeding

    63. Shock Management The Future What fluids? 1. 5% HTS or HSD, two 250mL boluses. 2. If further volume is needed: L-isomer LR 3. In the hypotensive, bleeding patient: Start blood early FFP:PRBC:Plts ratio 1:1:1 If fresh whole blood is available: use it!

    64. Shock

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