The Value of Continuous ScvO2 Monitoring in PICU

Caulette Young, RN, BSN

Pediatric Clinical Nurse Consultant

Edwards Lifesciences, LLC

Disclaimers

• Paid consultant for Edwards Lifesciences, LLC

• Pediatric critical care products

• Provide education, in-services, research & • Provide education, in-services, research & technical advice

Objective

The goal in PICU is to maintain a balance

between oxygen delivery and consumption.

Continuous ScvO2 allows the clinician to 2

assess oxygen delivery and consumption in

real-time. Imbalances can rapidly be identified

and treated earlier with improved outcomes.

What is our main goal for patients in ICU?

• Adequate oxygenation & tissue perfusion

Ensure a balance between oxygen

How can we achieve this?

• Ensure a balance between oxygen delivery & oxygen consumption

• Continuous monitoring ScvO2

How can we assess for this?

74

Reflection vs Transmission Spectrophotometry

Receiving fiber

SVC

LED photo detector

Transmission fiber

Receiving fiber

Benefits of Continuous vs. Intermittent

• Real-time, no waiting for analysis results

• Decrease risk for infection

• Decrease risk for transfusions

• Early warning• Early warning

– Identification of DO2/VO2 imbalance

– Traditional hemodynamic monitoring unreliable

• Cost savings

– Financial

– Resources of staff

– Prevention

Using continuous ScvO2 monitoring

to evaluate tissue oxygenation at

the bedside enables the clinician to

detect early alterations in oxygen detect early alterations in oxygen

balance.

(Goodrich 2006 Crit Care Nurs Clin N Am)

“Oxygen delivery does not provide information about the adequacy of

tissue oxygenation.”

Curley & Harmon Critical Care Nursing of Infants and Children 2nd Ed

Uncorrected imbalances

• Shift in dissociation curve: left or right

• Hypoxia / hypoxemia

• Acidosis

• Redistribution or maldistribution of blood

• MODS

• Pulmonary hypertension

• Cardiovascular collapse / cardiac arrest

• Necrosis & irreversible cell death

• Death

What is

ScvO2?

� Central venous oxygen saturation

measured at the SVC-RA junction

� Indicative of balance between

oxygen delivery & consumption

� Trends well with SvO2

SVC-RA

� Can be used as a surrogate for

adequate cardiac index

� Early warning indicator

� Used to guide therapy in sepsis &

congenital cardiac surgery

SVC-RAjunction

ScvO2

Oxygen Delivery Oxygen Consumption

Cardiac HemoglobinOxygenation/ventilation

Metabolic demandsCardiac output

Hemoglobin/ventilation

Stroke volume

Heart rate

FiO2

Preload Afterload Contractility

SvO2 or ScvO2: What’s the difference?

• PA catheter or central line

• Global or regional– SvO2 represents mixed venous blood from:

• SVC ≅ 70%• CS ≅ 37%• IVC ≅ 80%

– ScvO2 represents blood returning from upper or lower body (depending on site)lower body (depending on site)

• Normal values:– SvO2 (60-80%) – ScvO2 (70-75%)

• ScvO2 usually runs ~7% higher than SvO2

• Difference can widen in shock states when perfusion redistribution occurs

Regional oxygen saturation from upper body

Trends with SvO values, nearly interchangeable

ScvO2 ……SvO2

Trends with SvO2 values, nearly interchangeable

Reinhart et al Intensive Care Med. 2004

ScvO2 ……SvO2

Has been considered a surrogate for cardiac output / index in pediatrics

Tibby et al Arch Dis Child 2003

Usually consumption (VO2) independent of delivery (DO2)

DO2I= CO x SaO2 x Hgb x 1.34 x 10 = 650 + 50 ml/min/m2

VO2I= CO x (SaO2-SvO2) x Hgb x 1.34 x 10 = 120-200 ml/min/m2

�If VO2 increases or DO2 decreases, tissue oxygenation is maintained by increasing oxygen extraction

“Adequate” oxygenation can only be defined when tissue O2 supply matches tissue O2 demand

O2ER = VO2/DO2 x 100 = 25 + 2%

�If DO2 drops below a critical level, oxygen extraction becomes exhausted resulting in VO2 dependent on DO2 or oxygen debt

Tissue hypoxia occurs!

Note: O2ER increases well before lactate begins to accumulate

ScvO2 / SvO2 Physiology

70-75% Normal extraction

(non-cyanotic cardiac)

< 70% and > 50%Compensatory extraction (� demand or � supply)

< 50% and > 30%Limits of extraction(beginning of lactic

acidosis)

< 30% and > 25% Severe lactic acidosis

< 25% Cellular death

Bloos & Reinhart; Intensive Care Med (2005) 31:911–913

Factors to be considered in Oxygenation

� Alveolar-pulmonary capillary O2 transport• Gas exchange in terminal portion of lungs

� O2 transport in the blood• Hemoglobin & oxyhemoglobin

− Arterial O2 content (CaO2)

− Oxyhemoglobin dissociation curve

DO2

− Oxyhemoglobin dissociation curve

− O2 delivery (DO2)

� Cellular respiration• Oxygen consumption

• Oxygen extraction ratio (O2ER)

− Tissue oxygenation dependent on microcirculation

− Microcirculation adjusts to enhance O2

extraction

VO2

Once O2 extraction has been maximized,

VO2 becomes

dependent on DO2

Tissues extract what’s needed. If DO2 decreases or

VO2 increases, O2ER increases

to meet demands

Pathologic

Critical O2

VO2

DO2

Tissue hypoxia occurs when VO2

exceeds DO2

O ER

NormalO2ER may increase to

meet O2 demands, when DO2 is decreased or

VO2 is increased.

Normal O2ER 25-30%

O2 ER

DO2

Pathologic

VO

O2 debt: Why is it important?

It needs to be paid back with interest

Interest

VO2

Time

O2 debt

DO2 needs to meet current

O2 needs and satisfy the

needs that were previously

unmet

Oxygen Saturation Values

Site Acyanotic Cyanotic

Superior vena cava 70-75% 35-55%

Right atrium / ventricle 75% 67% / 80%

Pulmonary vein 95% 88%

Aorta 95% 80%

Left atrium / ventricle 95% 90%

Inferior vena cava 78%

� PVR � R � L shunt

Stimulant: Pain, agitation, hypoxia, hypothermia, suctioning, acidosis, hypercarbia

Pulmonary Hypertension in Post-op CardiacCritical Heart Disease in Infants & Children 2nd Ed

�Qp Qs

� ScvO2/SvO2

� Hypoxic vasoconstriction

� PaO2

� PaCO2

� DO2

Cardiac arrest

When is Change Significant?

• Change from baseline ≥ 5-10% sustained > 5 minutes

• Values may fluctuate ± 5%, with

activities or interventions (i.e. suctioning)suctioning)

• Slow recovery may indicate cardiopulmonary system’s inability to respond to increases in O2 demand

Causative Factors(Decreased O2delivery)

Left ventricular dysfunctionShock Hypovolemia

Hypoxemia

↓Cardiac Output (CO)

Clinical Conditions

ScvO2 < 70%

↓O2 Saturation (SaO2)HypoxemiaLung DiseaseRespiratory failure

AnemiaHemorrhageHemodilutionDyshemoglobinemias

↓ Hgb concentration

Causative Factors

Traumatic brain injury (138%)

Burns (100%)

Sepsis (50-100%)

Shivering (50-100%)

MODS (20-80%)

Increased O2 consumption

Clinical Conditions

ScvO2 < 70%

MODS (20-80%)

Increased WOB (40%)

Position change (31%)

Suctioning (27%)

Bath (23%)

Dressing change (10%)

Fever each °C (10%)

Causative Factors

� PaO2

� Hemoglobin � Cardiac output

Increased O2 delivery(DO2)

Clinical Conditions

ScvO2 > 70%

Decreased O2 consumption (VO2)

AnesthesiaHypothermiaDyshemoglobinemiasVenous hyperoxia

Understanding the clinical significance of

SvO2 (ScvO2) measurements….can help

guide clinical decision-making to assure

adequate oxygenation to meet tissue adequate oxygenation to meet tissue

needs.

(Sanders, 1997 Applied Pathophysiology)

• Congenital cardiac surgery

• Pediatric sepsis

• High risk surgery

• Respiratory failure

• Fluid administration &

boluses

• Vasoactive infusions

• Blood transfusions

“Useful in patient management”

“Useful in patient types”

• Respiratory failure

• Trauma

• Burns

• Jugular bulb

• Blood transfusions

• Ventilatory management

• Arrest resuscitation

• End-organ perfusion

Thank You!

“Hypoxia not only stops the machine, it wrecks

the machinery” the machinery”

John Scott Haldane, 1880

Caulette_young@edwards.comwww.Edwards.com/pediasat