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Shock In The Obstetric Patient PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Shock in the Obstetric Patient".

This medical PowerPoint presentation talks about shock in an obstetric patient, a life-threatening condition that can occur during pregnancy, childbirth, or in the postpartum period. It is defined as a state of insufficient blood flow to meet the oxygen and nutrient demands of the bodys tissues. Obstetric shock can be caused by a variety of factors, including bleeding, infection, or fluid loss.

Tags : Shock in the Obstetric Patient, pregnancy, childbirth, postpartum period, critical care medicine, critical care medicine PowerPoint presentation

Published on : Mar 28, 2023 | Views : 2010 | Downloads : 3

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Shock in the Obstetric Patient William Schnettler, MD FACOG @Wschnettler #TrihealthCriticalCareOB
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Next Events:- October 16, 2017 CCOB Team Meeting 5 pm GSH - February 24, 2018 CCOB #3 (GSH)
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DISCLOSURES None
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Scope of the Problem Pathophysiology of Shock Types of Shock Management of Shock in Pregnancy Learning Objectives:
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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 year Attributable Factors Increased: Maternal Age, BMI, Co-Morbidities Race (Non-Hispanic Black Women) Scope of the Problem
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Causes of Maternal Death Say L, Chou D, Gemmill A. et al. Global causes of maternal death: a WHO systematic analysis. Lancet Glob Health. 2014;2(6):e323.
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ICU AdmissionsPregnancy-related 0.07-0.89% of all live births ~ 10-90 / year @ TriHealth > 50% due to hemorrhage & hypertensive disorders Mortality rate = 8.4%
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PathophysiologyOf Shock
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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” circulation Cardiovascular Physiology: Tissue Perfusion
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Cardiovascular Physiology: Tissue Perfusion O2 O2 O2 O2 O2 Tissue
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Shock = inability to maintain this homeostasis Cellular Respiration Tissue perfusion Local tissue hypoxia Cell & mitochondrial death Multi-organ failure Death
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Mitochondria evolutionarily linked to bacteria Death releases dAMPs (damage associated molecular patterns) Similar to pAMPs (pathogen associated molecular patterns) Innate immune system recognizes both the same = initiates INFLAMMATION Pathophysiology of Shock: Tissue Perfusion
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O2 O2 O2 O2 O2 Tissue Pathophysiology of Shock: Tissue Perfusion Homeostasis No O2 for mitochondrial electron transport chain Mitochondrial death – release of dAMPs Systemic response to Inflammation Increase cardiac output (HR & SV) Peripheral vasoconstriction ( SVR) Arteriolar vasoconstriction away from non-vital organs ( urine output, NRFHT) Mobilization of blood from venules Build-up of pyruvate (lactate) in Kreb’s cycle = Metabolic Acidosis Compensatory Mechanism Failure Failure of pre-capillary sphincters Capillary endothelial damage / membrane pump failure is lost
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Pathophysiology of Shock
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Pre-Shock (compensated) Appropriate compensatory mechanisms are still homeostatic Tachycardia Modest change in BP Shock (compensatory mechanisms become overwhelmed) Signs & Symptoms of organ dysfunction Symptomatic tachycardia Dyspnea Restlessness Hypotension Oliguria Cool clammy skin End-organ Dysfunction Irreversible organ damage Multi-organ failure (anuria, acute renal failure, acidemia, recalcitrant hypotension) Obtundation, coma, death Stages of Shock (Signs & Symptoms)
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Types of Shock
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Types of Shock
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SVR (Systemic Vascular Resistance) Key factor – vasodilation, 3rd spacing Cardiac output (SV X HR) Compensatory increase initially (mainly HR) May fall later due to myocardial depressant factors Preload Vasodilation, 3rd spacing Distributive Shock (ex. Sepsis)
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Pulse Pressure Too Slow < 40 MPH Too Fast > 80 MPH
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WIDE PULSE PRESSURE (>80 mmHg) Distributive Shock (ex. Sepsis)
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SVR (Systemic Vascular Resistance) Compensatory response Cardiac output (SV X HR) Key Factor: pump failure Preload Normal intravascular volume Cardiogenic Shock
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NARROW PULSE PRESSURE (<40 mmHg) Cardiogenic Shock
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SVR (Systemic Vascular Resistance) Compensatory response Cardiac output (SV X HR) Decreased stroke volume Preload Key Factor Hypovolemic Shock
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NARROW PULSE PRESSURE (<40 mmHg) Hypovolemic Shock
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SVR (Systemic Vascular Resistance) Compensatory response Cardiac output (SV X HR) Key Factor: Obstruction of outflow (SV) Preload Normal intravascular volume in R heart failure Could be Key Factor in tension pneumothorax Obstructive Shock
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NARROW PULSE PRESSURE (<40 mmHg) Obstructive Shock
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Management of Shock in the Obstetric Patient
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Identify Stage of Shock Multi-disciplinary Approach Airway – ensure stable airway IV access Monitoring access / needs (arterial line, central line, PA catheter) Fetal monitoring Identify Cause & Type of Shock Laboratory 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 Products Vasopressors Initial Step-wise Approach Regardless of Type
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Distributive Cardiogenic Hypovolemic Obstructive Approach by Type of Shock (Pregnant Patient)
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Vasodilation Myocard Depres IV volume depl. Inc. Metabolism O2 Demand O2 Delivery Tissue Hypoxia Increase Preload Manipulate Afterload Improve Contractility
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500 mL boluses q 30 min until CVP 8-12 mmHg Vasopressors Vasodilators
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Distributive Cardiogenic Hypovolemic Obstructive Approach by Type of Shock (Pregnant Patient)
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Hypotension Myocard Depres Inc. Metabolism O2 Demand O2 Delivery Tissue Hypoxia Optimize Preload Vasopressors & Inotropes Reperfusion
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Distributive Cardiogenic Hypovolemic Non-hemorrhagic Obstructive Approach by Type of Shock (Pregnant Patient) Hemorrhagic
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PeT PiTT CaT 7 8, 9, 11, 12, plts Common Calcium 5 & dime Prothrombin  Thrombin Fibrinogen Fibrin Plasminogen  Plasmin Coagulation Cascade
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Medical Approach Avoid large volumes of crystalloid – transfuse blood products early Transfusion should keep-up with blood loss Essential to follow Coagulation Panel, CBC, K+, Ca+ very closely to guide selection & timing for replacement INR > 1.5 : Start with FFP Platelets < 100,000 : Start with Platelets Fibrinogen < 200 : Start with Cyroprecipitate Consider drawing Red-Top Tube and watching Surgical Approach Atony First line (after uterotonics): bimanual compression, balloon tamponade, uterine packing, uterine compression sutures and devascularization Last line: aortic compression & hysterectomy Morbidly Adherent Placenta Plan for and move to hysterectomy without delay Considerations:
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Texas Children’s Pavilion for Women massive transfusion protocol DIRECTOR - OB/Anesthesia/Critical Care (MD) Activates MTP Identifies RUNNER & REPORTER Follows & deactivates MTP RUNNER (PCA or nurse) Retrieves MTP pack from BB Delivers lab specimens & awaits more products (returns when done) REPORTER (charge or circulating RN) Notifies lab & blood bank of MTP Initiates rapid response team Reports lab results to director INITIAL LAB DRAW CBC (purple top) OB Coag Panel (blue top) CMP (green top) Ionized Calcium (green top) Red top ABG (heparin syringe) Prepare OR & Rapid Infuser Initial Blood Package: 4 units PRBCs 4 units FFP Deactivate MTP Criteria: normalization of lab values and / or no evidence of ongoing bleeding Call blood bank Anticipate Ongoing Bleeding REPEAT LAB DRAW CBC (purple top) OB Coag Panel (blue top) CMP (green top) Ionized Calcium (green top) Red top ABG (heparin syringe) Subsequent blood packages: 4 units PRBCs 4 units FFP 1 apheresis platelet unit 1 dose cryoprecipitate (30 min) No Yes
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Distributive Cardiogenic Hypovolemic Obstructive Approach by Type of Shock (Pregnant Patient)
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Hypoxia ↓ Cardiac Output Hypotension O2 Demand O2 Delivery Tissue Hypoxia Optimize Oxygenation Reverse the Etiology Supportive Care
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THANK YOU!!