SHOCK I OBSTETRICS

1. PATHOPHYSIOLOGY
OF SHOCK

2. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
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

3. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
Cardiovascular Physiology: Tissue Perfusion
O2
O2
O2
O2O2

4. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
Shock = inability to maintain this homeostasis
Cellular Respiration
Tissue perfusion Local tissue hypoxia
Cell & mitochondrial death
Multi-organ failure
Death

5. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
•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

6. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
O2
O2
O2
O2O2
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)

9. TYPES OF SHOCK

10. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
Distributive Cardiogenic Hypovolemic Obstructive
Septic Non-Septic Cardio-
myopathic
Arrhythmo-
genic
Hemorrhagic Non-
Hemorrhagic
Pulmonary Mechanical
Bacterial
Fungal
Viral
Parasitic
Myco-
bacterium
Inflammatory
Neurogenic
Anaphylactic
TRALI
MI
Drugs
Myocarditis
PPCM
Severe
vavlular
disease
Tachy
Brady
Heart block
Trauma
Intra & post-
op
AVM
Ectopic
Abruption
PPH
GI losses
Burns
Heat stroke
Renal losses
Crush injury
3rd spacing
PE
PAH
Air embolus
Tension
pneumo
Tamponade
Pericarditis
Compartment
syndrome
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

13. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
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

15. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
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

20. MANAGEMENT
OF SHOCK IN THE
OBSTETRIC PATIENT

21. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
• 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

22. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
•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

24. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
500 mL boluses q 30 min
until CVP 8-12 mmHg
Vasopressors
Vasodilators

25. CRITICAL CARE OBSTETRIC WORKSHOP SERIES

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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

28. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
•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

30. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
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:

31. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
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

32. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
•Distributive
•Cardiogenic
•Hypovolemic
•Obstructive
Approach by Type of Shock (Pregnant Patient)

33. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
Hypoxia
↓ Cardiac Output
Hypotension
O2 Demand
O2 Delivery
Tissue Hypoxia
Optimize
Oxygenation
Reverse the
Etiology
Supportive
Care

34. CRITICAL CARE OBSTETRIC WORKSHOP SERIES
THANK YOU!!