Shock in the Obstetric Patient - PowerPoint Presentation

1. Shock in the Obstetric PatientWilliam Schnettler, MD FACOG @Wschnettler #TrihealthCriticalCareOB

2. Next Events:- October 16, 2017 CCOB Team Meeting 5 pm GSH - February 24, 2018 CCOB #3 (GSH)

3. DISCLOSURESNone

4. Scope of the ProblemPathophysiology of ShockTypes of ShockManagement of Shock in PregnancyLearning Objectives:

5. MMR (Maternal Mortality Ratio) = # Maternal Deaths / 100,000 live births (per year)Worldwide – MMR dropped 2.3% annually from 1990-2015 (216/100,000 L.B’s.)U.S. – 1.7% annual increase (17.2/100,000 L.B’s.)TriHealth – equates to potentially 1-2 per yearAttributable FactorsIncreased: Maternal Age, BMI, Co-MorbiditiesRace (Non-Hispanic Black Women) Scope of the Problem

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7. Causes of Maternal DeathSay L, Chou D, Gemmill A. et al. Global causes of maternal death: a WHO systematic analysis. Lancet Glob Health. 2014;2(6):e323.

8. ICU AdmissionsPregnancy-related0.07-0.89% of all live births ~ 10-90 / year @ TriHealth> 50% due to hemorrhage & hypertensive disordersMortality rate = 8.4%

9. PathophysiologyOf Shock

10. Homeostasis in the ideal state Oxygen rich / nutrient rich blood reaches organ sites for metabolism via arterial system delivering substrate to the capillaries Increased metabolic demand increases perfusion to vital organs via increases in cardiac output, increased blood oxygenation, selective perfusion (arteriolar resistance alterations)70% total blood volume contained in venules (Capacitance Vessels) which can constrict causing auto-transfusion back into “active” circulationCardiovascular Physiology: Tissue Perfusion

11. Cardiovascular Physiology: Tissue Perfusion O2O2O2O2O2Tissue

12. Shock = inability to maintain this homeostasis Cellular Respiration Tissue perfusion Local tissue hypoxia Cell & mitochondrial death Multi-organ failure Death

13. Mitochondria evolutionarily linked to bacteriaDeath releases dAMPs (damage associated molecular patterns)Similar to pAMPs (pathogen associated molecular patterns)Innate immune system recognizes both the same = initiates INFLAMMATIONPathophysiology of Shock: Tissue Perfusion

14. O2O2O2O2O2TissuePathophysiology of Shock: Tissue Perfusion HomeostasisNo O2 for mitochondrial electron transport chainMitochondrial death – release of dAMPsSystemic response to InflammationIncrease cardiac output (HR & SV)Peripheral vasoconstriction ( SVR)Arteriolar vasoconstriction away from non-vital organs ( urine output, NRFHT)Mobilization of blood from venulesBuild-up of pyruvate (lactate) in Kreb’s cycle = Metabolic AcidosisCompensatory Mechanism FailureFailure of pre-capillary sphinctersCapillary endothelial damage / membrane pump failureis lost

15. Pathophysiology of Shock

16. Pre-Shock (compensated)Appropriate compensatory mechanisms are still homeostaticTachycardiaModest change in BPShock (compensatory mechanisms become overwhelmed)Signs & Symptoms of organ dysfunctionSymptomatic tachycardiaDyspneaRestlessnessHypotensionOliguriaCool clammy skinEnd-organ DysfunctionIrreversible organ damageMulti-organ failure (anuria, acute renal failure, acidemia, recalcitrant hypotension)Obtundation, coma, deathStages of Shock (Signs & Symptoms)

17. Types of Shock

18. DistributiveCardiogenicHypovolemicObstructiveSepticNon-SepticCardio-myopathicArrhythmo-genicHemorrhagicNon-HemorrhagicPulmonaryMechanicalBacterialFungalViralParasiticMyco-bacteriumInflammatoryNeurogenicAnaphylacticTRALIMIDrugsMyocarditisPPCMSevere vavlular diseaseTachyBradyHeart blockTraumaIntra & post-opAVMEctopicAbruptionPPHGI lossesBurnsHeat strokeRenal lossesCrush injury3rd spacingPEPAHAir embolusTension pneumoTamponadePericarditisCompartment syndromeTypes of Shock

19. SVR (Systemic Vascular Resistance)Key factor – vasodilation, 3rd spacingCardiac output (SV X HR)Compensatory increase initially (mainly HR)May fall later due to myocardial depressant factorsPreload Vasodilation, 3rd spacingDistributive Shock (ex. Sepsis)

20. Pulse PressureToo Slow< 40 MPHToo Fast> 80 MPH

21. WIDE PULSE PRESSURE (>80 mmHg)Distributive Shock (ex. Sepsis)

22. SVR (Systemic Vascular Resistance)Compensatory responseCardiac output (SV X HR)Key Factor: pump failurePreload Normal intravascular volumeCardiogenic Shock

23. NARROW PULSE PRESSURE (<40 mmHg)Cardiogenic Shock

24. SVR (Systemic Vascular Resistance)Compensatory responseCardiac output (SV X HR)Decreased stroke volumePreload Key FactorHypovolemic Shock

25. NARROW PULSE PRESSURE (<40 mmHg)Hypovolemic Shock

26. SVR (Systemic Vascular Resistance)Compensatory responseCardiac output (SV X HR)Key Factor: Obstruction of outflow (SV)Preload Normal intravascular volume in R heart failureCould be Key Factor in tension pneumothoraxObstructive Shock

27. NARROW PULSE PRESSURE (<40 mmHg)Obstructive Shock

28. Management of Shock in the Obstetric Patient

29. Identify Stage of ShockMulti-disciplinary ApproachAirway – ensure stable airwayIV accessMonitoring access / needs (arterial line, central line, PA catheter)Fetal monitoringIdentify Cause & Type of ShockLaboratory evaluation (CBC, CMP, Lactate, Coags, Cardiac enzymes & BNP, blood cultures, ABG) Imaging (CXR, POC US)IV Fluids (0.5-1L bolus Ringer’s lactate)Blood ProductsVasopressorsInitial Step-wise Approach Regardless of Type

30. DistributiveCardiogenicHypovolemicObstructiveApproach by Type of Shock (Pregnant Patient)

31. VasodilationMyocard DepresIV volume depl.Inc. MetabolismO2 DemandO2 DeliveryTissue HypoxiaIncrease PreloadManipulate AfterloadImprove Contractility

32. 500 mL boluses q 30 min until CVP 8-12 mmHgVasopressorsVasodilators

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34. DistributiveCardiogenicHypovolemicObstructiveApproach by Type of Shock (Pregnant Patient)

35. HypotensionMyocard DepresInc. MetabolismO2 DemandO2 DeliveryTissue HypoxiaOptimize PreloadVasopressors & InotropesReperfusion

36. DistributiveCardiogenic Hypovolemic Non-hemorrhagicObstructiveApproach by Type of Shock (Pregnant Patient)Hemorrhagic

37. PeT PiTT CaT 7 8, 9, 11, 12, plts Common Calcium 5 & dime Prothrombin  Thrombin Fibrinogen Fibrin Plasminogen  PlasminCoagulation Cascade

38. Medical ApproachAvoid large volumes of crystalloid – transfuse blood products earlyTransfusion should keep-up with blood lossEssential to follow Coagulation Panel, CBC, K+, Ca+ very closely to guide selection & timing for replacementINR > 1.5 : Start with FFPPlatelets < 100,000 : Start with PlateletsFibrinogen < 200 : Start with CyroprecipitateConsider drawing Red-Top Tube and watchingSurgical ApproachAtony First line (after uterotonics): bimanual compression, balloon tamponade, uterine packing, uterine compression sutures and devascularizationLast line: aortic compression & hysterectomyMorbidly Adherent PlacentaPlan for and move to hysterectomy without delayConsiderations:

39. Texas Children’s Pavilion for Women massive transfusion protocolDIRECTOR - OB/Anesthesia/Critical Care (MD)Activates MTPIdentifies RUNNER & REPORTERFollows & deactivates MTPRUNNER (PCA or nurse)Retrieves MTP pack from BBDelivers lab specimens & awaits more products (returns when done)REPORTER (charge or circulating RN)Notifies lab & blood bank of MTPInitiates rapid response teamReports lab results to directorINITIAL LAB DRAWCBC (purple top)OB Coag Panel (blue top)CMP (green top)Ionized Calcium (green top)Red topABG (heparin syringe)Prepare OR & Rapid InfuserInitial Blood Package:4 units PRBCs4 units FFPDeactivate MTPCriteria: normalization of lab values and / or no evidence of ongoing bleedingCall blood bankAnticipate Ongoing BleedingREPEAT LAB DRAWCBC (purple top)OB Coag Panel (blue top)CMP (green top)Ionized Calcium (green top)Red topABG (heparin syringe)Subsequent blood packages:4 units PRBCs4 units FFP1 apheresis platelet unit1 dose cryoprecipitate (30 min)NoYes

40. DistributiveCardiogenicHypovolemicObstructiveApproach by Type of Shock (Pregnant Patient)

41. Hypoxia↓ Cardiac OutputHypotensionO2 DemandO2 DeliveryTissue HypoxiaOptimize OxygenationReverse the EtiologySupportive Care

42. THANK YOU!!