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Hemodynamic Monitoring of the Critically Ill in the ED Kevin Ward, MD Michigan Center for Integrative Research in Critical Care www.micircc.org University of Michigan Department of Emergency Medicine

Definitions

• Shock: A a physiologic state produced with DO2 is not sufficient to meet the VO2 requirements of the body. – DO2 at this point is called critical DO2 (change from aerobic to anaerobic metabolism or ischemia) – Signaled by elevate lactate levels – Produced by anything that lowers DO2: • Hypoxia reducing SaO2 (lung injury, etc) • Decreases in hemoglobin (hemorrhage) • Decreases in cardiac output (hemorrhage, heart failure, sepsis) • Combination of things above

• Compensated Shock: A physiologic state where DO2 is decreased but oxygen extraction increases to continue to meet VO2 demands of the body.

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Basic Definitions • Hemoglobin: Protein in red blood cells that carries oxygen – Normal: 12-14 grams/deciliter of blood

• PaO2: Partial Pressure of oxygen dissolved in plasma: – Normal: 90-100 mmHg

• Arterial hemoglobin oxygen saturation: Percent of hemoglobin containing oxygen – SaO2 or SpO2: Normal 94-100%

• Arterial Oxygen Content: Total amount of oxygen contained in arterial blood – CaO2: (Hemoglobin x SaO2) Normal: 200 cc/liter of blood

• Cardiac output (CO): Amount of blood the heart pumps per minute. – Normal 4-6 liters per minute

• Oxygen Delivery: About of oxygen delivered by the heart to the body – DO2: CO X CaO2 Normal: 1000 cc/min

Definitions

• Central Venous Hemoglobin oxygen saturation: Percent of hemoglobin containing oxygen remaining in blood once it has passed through tissues. – SvO2: Normal 70-80%

• Oxygen Extraction Ratio: Percent of oxygen extracted from arterial hemoglobin from tissues – OER: : SaO2 –SvO2/ SaO2: Normal: 20-30%

• Oxygen Consumption: Amount of oxygen consumed by the body – VO2: Normal 200-300 cc/minute

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Oxygen Transport at a Central Level Venous Oxygen Delivery

200 mL/L (20% Vol)

750 mL/min

Hemoglobin x SaO2 SvO2 = 75%

5000 mL/min 25%

Arterial Oxygen Delivery

Oxygen Consumption

250 mL/min

1000 mL/min

Biphasic Oxygen Delivery/Consumption Relationship

Where is your patient on this curve? Sepsis, Heart Failure, Post-Arrest, Trauma, etc.

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DO2 and VO2 Relationship at the Tissue Level Based On: • Amount of hemoglobin • Amount of oxygen (hemoglobin oxygen saturation) • Amount of flow • Metabolic requirement of particular organ baseline Flow

O2 Extraction

O2 uptake/metabolism

SvO2

Hb amount Capillary filling/ density

Hemorrhage Mediated Change in DO2 and VO2 • Loosing blood (hemoglobin) • Arterial Hemoglobin oxygen saturation maintained. • Blood flow is slower through tissue • More time for cells to extract oxygen presented to it. baseline

O2 Extraction

Flow O2 uptake/metabolism

SvO2

Hb amount Capillary filling/ density

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A: Normal B: Moderate Hemorrhage C: Severe

A: PetCO2 38 mmHg B: PetCO2 30 mmHg C: PetCO2 25 mmHg

A: Mixed Venous PCO2: 45 mmHg PvO2: 43 mmHg SvO2: 70% Lactate: 2 meq/L

A (arterial) PaCO2: 40 mmHg PaO2: 97 mmHg SaO2: 99% Lactate: 2 meq/L

B: Mixed Venous PCO2: 55 mmHg PvO2: 35mmHg SvO2: 60% Lactate 2 meq/L

B (arterial) PaCO2: 33 mmHg PaO2: 88 mmHg SaO2: 96% Lactate < 3 meq/L

C: Mixed Venous PCO2: 65 mmHg PvO2: 25mmHg SvO2: 55% Lactate 2 meq/L A: Tissue venous PCO2: 50 mmHg Tissue venous PO2: 45 mmHg Tissue venous SO2: 65% Lactate: 2 meq/L

C (arterial) PaCO2: 30 mmHg PaO2: 88 mmHg SaO2: 96% Lactate > 4 meq/L

B: Tissue venous PCO2: 65 mmHg Tissue venous PO2: 30 mmHg Tissue venous SO2: 55% Lactate: 2-3 meq/L C: Tissue venous PCO2: 75 mmHg Tissue venous PO2: 15 mmHg Tissue venous SO2: 35% Lactate: > 5 me/L

Oxygen Debt • The magnitude and length of time spent below Critical DO2 • Mirrored by level of lactate and length of time it is elevated • Oxygen Debt it the biggest predictor of death and organ failure and is directly linked to the coagulopathy of trauma • Oxygen Debt must be repaid to a certain level over a certain period of time to reduce death and organ failure • Major emphasis in the field is to prevent further accumulation of oxygen debt (further rises in lactate). • Clearance of lactate is associated with repayment of oxygen debt but cannot guarantee adequate repayment

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Difference Between Deficit and Debt

Must Repay Debt. The Longer it takes to repay the more injury

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The CO2 Paradigm Delivery Dependent

Delivery Independent

VO2

VO2

VCO2 PetCO2 *CO2

+CO 2

VCO2 and PetCO2

#CO2 +CO

2

*CO2 #CO2

* Anaerobic Produced # CO2 produced by lactate and HCO3 + Combined * & + CO2

DO2crit

DO2

CO2 Caveats • Remember Cells Use O2 and Make CO2 • When blood flow decreases to tissues, aerobically made CO2 is washed out more slowing and accumulates in tissue • When critical oxygen delivery is tissue is reached, more CO2 is made when lactate combines with tissue bicarbonate elevating tissue CO2 even further. • End-tidal CO2 (PetCO2) decreases if ventilation is normal as tissue CO2 is not carried to the lungs well when Cardiac output is reduced. • Hypoventilation can increase tissue CO2 • Hyperventilation can decrease tissue CO2 • Need Arterial-Tissue gradient for best use

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Principles of Tissue Monitoring

• Distribution of blood volume within tissue – 80% venules – 10% capillaries – 10% arterioles

• Post-extraction compartment monitoring – Oxygen extraction – CO2 production

• Surrogate for OER at the tissue level – Reflection of DO2.

• Basis for StO2 and Tissue CO2 monitoring • What Target Tissue To Monitor?

Intravascular Volume Monitoring

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Basic Relationship Between Stroke Volume and Preload

Role of Venous Return (see next slide)

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CCM 2013:41:255-262

Pulmonary Mechanic Effect on Central Hemodynamics

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Basis for Stroke Volume and Pulse Pressure Variation

The Basis for Stroke Volume and Pulse Pressure Variation

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Stroke Volume Variation (SVV) or Pulse Pressure Variation (PVV) Determination

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Ventilation and Dynamic IVC Changes

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