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Value of ScvO2 Monitoring in PICU - The Canadian Association of ...

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<strong>The</strong> <strong>Value</strong> <strong>of</strong> Cont<strong>in</strong>uous<br />

ScvO 2 <strong>Monitor<strong>in</strong>g</strong> <strong>in</strong> <strong>PICU</strong><br />

Caulette Young, RN, BSN<br />

Pediatric Cl<strong>in</strong>ical Nurse Consultant<br />

Edwards Lifesciences, LLC


Disclaimers<br />

• Paid consultant for Edwards Lifesciences, LLC<br />

• Pediatric critical care products<br />

• Provide education, <strong>in</strong>-services, research &<br />

• Provide education, <strong>in</strong>-services, research &<br />

technical advice


Objective<br />

<strong>The</strong> goal <strong>in</strong> <strong>PICU</strong> is to ma<strong>in</strong>ta<strong>in</strong> a balance<br />

between oxygen delivery and consumption.<br />

Cont<strong>in</strong>uous ScvO 2 allows the cl<strong>in</strong>ician to<br />

2<br />

assess oxygen delivery and consumption <strong>in</strong><br />

real-time. Imbalances can rapidly be identified<br />

and treated earlier with improved outcomes.


What is our ma<strong>in</strong> goal for patients <strong>in</strong> ICU?<br />

• Adequate oxygenation & tissue<br />

perfusion<br />

How can we achieve this?<br />

• Ensure a balance between oxygen<br />

delivery & oxygen consumption<br />

How can we assess for this?<br />

• Cont<strong>in</strong>uous monitor<strong>in</strong>g ScvO 2


Reflection vs Transmission<br />

Spectrophotometry<br />

74<br />

LED photo detector<br />

Receiv<strong>in</strong>g fiber<br />

Transmission fiber<br />

SVC


Benefits <strong>of</strong> Cont<strong>in</strong>uous vs. Intermittent<br />

• Real-time, no wait<strong>in</strong>g for analysis results<br />

• Decrease risk for <strong>in</strong>fection<br />

• Decrease risk for transfusions<br />

• Early warn<strong>in</strong>g<br />

– Identification <strong>of</strong> DO 2/VO 2 imbalance<br />

– Traditional hemodynamic monitor<strong>in</strong>g unreliable<br />

• Cost sav<strong>in</strong>gs<br />

– F<strong>in</strong>ancial<br />

– Resources <strong>of</strong> staff<br />

– Prevention


Us<strong>in</strong>g cont<strong>in</strong>uous ScvO 2 monitor<strong>in</strong>g<br />

to evaluate tissue oxygenation at<br />

the bedside enables the cl<strong>in</strong>ician to<br />

detect early alterations <strong>in</strong> oxygen<br />

balance.<br />

(Goodrich 2006 Crit Care Nurs Cl<strong>in</strong> N Am)


“Oxygen delivery does not provide<br />

<strong>in</strong>formation about the adequacy <strong>of</strong><br />

tissue oxygenation.”<br />

Curley & Harmon<br />

Critical Care Nurs<strong>in</strong>g <strong>of</strong> Infants and Children 2 nd Ed


Uncorrected imbalances<br />

• Shift <strong>in</strong> dissociation curve: left or right<br />

• Hypoxia / hypoxemia<br />

• Acidosis<br />

• Redistribution or maldistribution <strong>of</strong> blood<br />

• MODS<br />

• Pulmonary hypertension<br />

• Cardiovascular collapse / cardiac arrest<br />

• Necrosis & irreversible cell death<br />

• Death


SVC-RA<br />

junction<br />

What is<br />

ScvO 2?<br />

Central venous oxygen saturation<br />

measured at the SVC-RA junction<br />

Indicative <strong>of</strong> balance between<br />

oxygen delivery & consumption<br />

Trends well with SvO 2<br />

Can be used as a surrogate for<br />

adequate cardiac <strong>in</strong>dex<br />

Early warn<strong>in</strong>g <strong>in</strong>dicator<br />

Used to guide therapy <strong>in</strong> sepsis &<br />

congenital cardiac surgery


ScvO 2<br />

Oxygen Delivery Oxygen Consumption<br />

Hemoglob<strong>in</strong> Cardiac<br />

output<br />

Heart<br />

rate<br />

Stroke<br />

volume<br />

Oxygenation<br />

/ventilation<br />

FiO 2<br />

Preload Afterload Contractility<br />

Metabolic demands


SvO 2 or ScvO 2: What’s the difference?<br />

• PA catheter or central l<strong>in</strong>e<br />

• Global or regional<br />

– SvO 2 represents mixed venous blood from:<br />

• SVC ≅ 70%<br />

• CS ≅ 37%<br />

• IVC ≅ 80%<br />

– <strong>ScvO2</strong> represents blood return<strong>in</strong>g from upper or<br />

lower body (depend<strong>in</strong>g on site)<br />

• Normal values:<br />

– SvO 2 (60-80%)<br />

– ScvO 2 (70-75%)<br />

• ScvO 2 usually runs ~7% higher than SvO 2<br />

• Difference can widen <strong>in</strong> shock states when<br />

perfusion redistribution occurs


Regional oxygen saturation from upper body<br />

Trends with SvO SvO2 values, nearly <strong>in</strong>terchangeable<br />

Re<strong>in</strong>hart et al Intensive Care Med. 2004<br />

ScvO 2 ……<br />

SvO 2<br />

ScvO 2 ……<br />

SvO 2


Has been considered a surrogate for cardiac<br />

output / <strong>in</strong>dex <strong>in</strong> pediatrics<br />

Tibby et al Arch Dis Child 2003


“Adequate” oxygenation can only be def<strong>in</strong>ed when<br />

tissue O 2 supply matches tissue O 2 demand<br />

Usually consumption (VO 2) <strong>in</strong>dependent <strong>of</strong> delivery (DO 2)<br />

DO 2I= CO x SaO 2 x Hgb x 1.34 x 10 = 650 + 50 ml/m<strong>in</strong>/m 2<br />

VO 2I= CO x (SaO 2-SvO 2) x Hgb x 1.34 x 10 = 120-200 ml/m<strong>in</strong>/m 2<br />

If VO 2 <strong>in</strong>creases or DO 2 decreases, tissue oxygenation is<br />

ma<strong>in</strong>ta<strong>in</strong>ed by <strong>in</strong>creas<strong>in</strong>g oxygen extraction<br />

O 2ER = VO 2/DO 2 x 100 = 25 + 2%<br />

If DO 2 drops below a critical level, oxygen extraction<br />

becomes exhausted result<strong>in</strong>g <strong>in</strong> VO 2 dependent on DO 2 or<br />

oxygen debt<br />

Tissue hypoxia occurs!<br />

Note: O 2ER <strong>in</strong>creases well before lactate beg<strong>in</strong>s to accumulate


ScvO 2 / SvO 2<br />

70-75%<br />

< 70% and > 50%<br />

< 50% and > 30%<br />

Physiology<br />

Normal extraction<br />

(non-cyanotic cardiac)<br />

Compensatory extraction<br />

( demand or supply)<br />

Limits <strong>of</strong> extraction<br />

(beg<strong>in</strong>n<strong>in</strong>g <strong>of</strong> lactic<br />

acidosis)<br />

< 30% and > 25% Severe lactic acidosis<br />

< 25% Cellular death<br />

Bloos & Re<strong>in</strong>hart; Intensive Care Med (2005) 31:911–913


Factors to be considered <strong>in</strong> Oxygenation<br />

Alveolar-pulmonary capillary O 2 transport<br />

• Gas exchange <strong>in</strong> term<strong>in</strong>al portion <strong>of</strong> lungs<br />

O2 transport <strong>in</strong> the blood<br />

• Hemoglob<strong>in</strong> & oxyhemoglob<strong>in</strong><br />

− Arterial O2 content (CaO2) − Oxyhemoglob<strong>in</strong> dissociation curve<br />

− O2 delivery (DO2) Cellular respiration<br />

• Oxygen consumption<br />

• Oxygen extraction ratio (O 2ER)<br />

− Tissue oxygenation dependent on<br />

microcirculation<br />

− Microcirculation adjusts to enhance O 2<br />

extraction<br />

DO 2<br />

VO 2


VO 2<br />

Once O 2 extraction<br />

has been maximized,<br />

VO 2 becomes<br />

dependent on DO 2<br />

Critical O 2<br />

DO 2<br />

Tissues extract<br />

what’s needed. If<br />

DO 2 decreases or<br />

VO 2 <strong>in</strong>creases,<br />

O 2ER <strong>in</strong>creases<br />

to meet demands<br />

Pathologic<br />

Tissue hypoxia<br />

occurs when VO 2<br />

exceeds DO 2


Normal<br />

O O2 ER<br />

DO 2<br />

O 2ER may <strong>in</strong>crease to<br />

meet O 2 demands, when<br />

DO 2 is decreased or<br />

VO 2 is <strong>in</strong>creased.<br />

Normal O 2ER 25-30%<br />

Pathologic


VO VO2 O 2 debt: Why is it important?<br />

It needs to be paid back with <strong>in</strong>terest<br />

O 2 debt<br />

Time<br />

Interest<br />

DO 2 needs to meet current<br />

O 2 needs and satisfy the<br />

needs that were previously<br />

unmet


Oxygen Saturation <strong>Value</strong>s<br />

Site Acyanotic Cyanotic<br />

Superior vena cava 70-75% 35-55%<br />

Right atrium / ventricle 75% 67% / 80%<br />

Pulmonary ve<strong>in</strong> 95% 88%<br />

Aorta 95% 80%<br />

Left atrium / ventricle 95% 90%<br />

Inferior vena cava 78%


Pulmonary Hypertension <strong>in</strong> Post-op Cardiac<br />

Critical Heart Disease <strong>in</strong> Infants & Children 2 nd Ed<br />

Stimulant: Pa<strong>in</strong>, agitation, hypoxia, hypothermia, suction<strong>in</strong>g,<br />

acidosis, hypercarbia<br />

PVR R L shunt<br />

Q p Q s<br />

ScvO 2 /SvO 2<br />

Hypoxic vasoconstriction<br />

PaO 2<br />

PaCO 2<br />

DO 2<br />

Cardiac arrest


When is Change Significant?<br />

• Change from basel<strong>in</strong>e ≥ 5-10%<br />

susta<strong>in</strong>ed > 5 m<strong>in</strong>utes<br />

• <strong>Value</strong>s may fluctuate ± 5%, with<br />

activities or <strong>in</strong>terventions (i.e.<br />

suction<strong>in</strong>g)<br />

• Slow recovery may <strong>in</strong>dicate<br />

cardiopulmonary system’s <strong>in</strong>ability to<br />

respond to <strong>in</strong>creases <strong>in</strong> O 2 demand


Causative Factors<br />

(Decreased O 2delivery)<br />

↓Cardiac Output (CO)<br />

ScvO 2 < 70%<br />

↓O 2 Saturation (SaO 2)<br />

↓ Hgb concentration<br />

Cl<strong>in</strong>ical Conditions<br />

Left ventricular dysfunction<br />

Shock<br />

Hypovolemia<br />

Hypoxemia<br />

Lung Disease<br />

Respiratory failure<br />

Anemia<br />

Hemorrhage<br />

Hemodilution<br />

Dyshemoglob<strong>in</strong>emias


Causative Factors<br />

Increased O 2 consumption<br />

ScvO 2 < 70%<br />

Cl<strong>in</strong>ical Conditions<br />

Traumatic bra<strong>in</strong> <strong>in</strong>jury (138%)<br />

Burns (100%)<br />

Sepsis (50-100%)<br />

Shiver<strong>in</strong>g (50-100%)<br />

MODS (20-80%)<br />

Increased WOB (40%)<br />

Position change (31%)<br />

Suction<strong>in</strong>g (27%)<br />

Bath (23%)<br />

Dress<strong>in</strong>g change (10%)<br />

Fever each °C (10%)


Causative Factors<br />

Increased O 2 delivery<br />

(DO 2)<br />

ScvO 2 > 70%<br />

Decreased O 2 consumption<br />

(VO 2)<br />

Cl<strong>in</strong>ical Conditions<br />

PaO 2<br />

Hemoglob<strong>in</strong><br />

Cardiac output<br />

Anesthesia<br />

Hypothermia<br />

Dyshemoglob<strong>in</strong>emias<br />

Venous hyperoxia


Understand<strong>in</strong>g the cl<strong>in</strong>ical significance <strong>of</strong><br />

SvO 2 (ScvO 2) measurements….can help<br />

guide cl<strong>in</strong>ical decision-mak<strong>in</strong>g to assure<br />

adequate oxygenation to meet tissue<br />

needs.<br />

(Sanders, 1997 Applied Pathophysiology)


“Useful <strong>in</strong><br />

patient types”<br />

• Congenital cardiac surgery<br />

• Pediatric sepsis<br />

• High risk surgery<br />

• Respiratory failure<br />

• Trauma<br />

• Burns<br />

• Jugular bulb<br />

“Useful <strong>in</strong> patient<br />

management”<br />

• Fluid adm<strong>in</strong>istration &<br />

boluses<br />

• Vasoactive <strong>in</strong>fusions<br />

• Blood transfusions<br />

• Ventilatory management<br />

• Arrest resuscitation<br />

• End-organ perfusion


Thank You!<br />

“Hypoxia not only stops the mach<strong>in</strong>e, it wrecks<br />

the mach<strong>in</strong>ery”<br />

John Scott Haldane, 1880<br />

Caulette_young@edwards.com<br />

www.Edwards.com/pediasat

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