Practical issues in ScvO2 monitoring

Practical issues
in ScvO2
monitoring
Prof. Jan Bakker MD PhD
Chair dept of Intensive Care
[email protected]
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Supply-Demand
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TO2 = Hb x SaO2 x CO x ζ
OXYGEN DEMAND
OXYGEN SUPPLY
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Oxygen Extraction Ratio
100 ml O2
consumption is
25 ml O2
50 ml O2
consumption is
25 ml O2
75 ml O2
O2ER = 25%
25 ml O2
O2ER = 50%
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Oxygen extraction
O2ER %
Decreased DO2
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ScvO2 - SvO2 monitoring
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Extraction and Mixed
venous oxygenation
O2ER =
CaO2 - CvO2
CaO2
O2ER =
[SaO2 x Hb + (0.0036xPaO2)] - [SvO2 x Hb + (0.0036 x PvO2)]
SaO2 x Hb + (0.0036xPaO2)
O2ER ≈ 1 - SvO2
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Oxygen extraction
Decreased DO2
Therapy Withdrawn in Brain Death Patient
Lactate (mmol/L)
6
5
4
3
2
1
0
0
10
20
30
40
SvO2 (%)
50
60
70
80
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Venous oximetry
‣ Understand basic physiology of oxygen demand and supply
‣ Understand compensatory mechanisms when either
changes
‣ What is the incidence of abnormal values
‣ What is the clinical impact of abnormal values
‣ When are abnormal values acceptable and unacceptable
‣ Can you treat abnormal values, by what measures and for
how long to benefit the patient
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Bracht et al. Crit Care 2007;11:R2
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Venous oximetry
‣ Understand basic physiology of oxygen demand and supply
‣ Understand compensatory mechanisms when either
changes
‣ What is the incidence of abnormal values
‣ What is the clinical impact of abnormal values
‣ When are abnormal values acceptable and unacceptable
‣ Can you treat abnormal values, by what measures and for
how long to benefit the patient
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Clinical relevance
60 patients abdominal surgery
Crit Care 2006;10:R158
48 elective surgery, 12 emergency surgery
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Adequacy of CO
Resuscitation using restoration to normal of
traditional hemodynamics does not restore
parameters associated with adequate global blood
flow and tissue oxygenation
Normal SO2 in the right atrium as a target of
therapy improves outcome
Am J Emerg Med 1996;14(2):218-225 § N Engl J Med 2001;345(19):1368-1377
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Venous oximetry
‣ Understand basic physiology of oxygen demand and supply
‣ Understand compensatory mechanisms when either
changes
‣ What is the incidence of abnormal values
‣ What is the clinical impact of abnormal values
‣ When are abnormal values acceptable and unacceptable
‣ Can you treat abnormal values, by what measures and for
how long to benefit the patient
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The New En g land Jo ur nal o f Medicine
EARLY GOAL-DIRECTED THERAPY IN THE TREATMENT OF SEVERE SEPSIS
AND SEPTIC SHOCK
EMANUEL RIVERS, M.D., M.P.H., BRYANT NGUYEN, M.D., SUZANNE HAVSTAD, M.A., JULIE RESSLER, B.S.,
ALEXANDRIA MUZZIN, B.S., BERNHARD KNOBLICH, M.D., EDWARD PETERSON, PH.D., AND MICHAEL TOMLANOVICH, M.D.,
FOR THE EARLY GOAL-DIRECTED THERAPY COLLABORATIVE GROUP*
ABSTRACT
Background Goal-directed therapy has been used
for severe sepsis and septic shock in the intensive care
unit. This approach involves adjustments of cardiac
preload, afterload, and contractility to balance oxygen
T
HE systemic inflammatory response syndrome can be self-limited or can progress to
severe sepsis and septic shock.1 Along this
continuum, circulatory abnormalities (intravascular volume depletion, peripheral vasodilatation,
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Venous oximetry
‣ Understand basic physiology of oxygen demand and supply
‣ Understand compensatory mechanisms when either
changes
‣ What is the incidence of abnormal values
‣ What is the clinical impact of abnormal values
‣ When are abnormal values acceptable and unacceptable
‣ Can you treat abnormal values, by what measures and for
how long to benefit the patient
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Treatment of low ScvO2
‣ Goal to treat abnormal ScvO2 is to restore the balance
between oxygen demand and oxygen delivery
‣ Decrease oxygen demand
‣ Mechanical ventilation, analgesia, sedation, antipyretics
‣ Increase oxygen delivery
‣ Increase arterial oxygen content (hemoglobin and oxygen
saturation)
‣ Increase cardiac output (fluids, inotropes, mechanical support)
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For how long should we
target Scv(v)O2
‣ Short duration following admission (4-8 hours)
‣ N Engl J Med 2001;345:1368
‣ BMJ 2004;329:258
‣ Crit Care 2005;9:R678
‣ Longer duration following admission (24 hours)
‣ JAMA 1993;270:2699
‣ Anesth Analg 2000;90:1052
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Low ScvO2
Increase in MAP
DO2 (ml/min.M2)**
VO2 (ml/min.M2)
SvO2 (%)
Lactate (mmol/l)
Urinary output (ml)
Cap.flow (ml/min.100g)
RBCvelocity (au)
Pa-rCO2 (mmHg)
MAP 65
620±59
119±12
76±3
3.1±0.9
49±18
6.0±1.6
0.42±0.06
13±3
MAP 75
670±59
138±20
76±2
2.9±0.8
56±21
5.8±1.2
0.44±0.06
17±3
MAP 85
703±74
153±20
70±2
3.0±0.9
43±13
5.3±0.9
0.42±0.06
16±3
LeDoux et al. Crit Care Med 2000;28:2729
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SvO2
Do
Nothing
≥ 70%
< 70%
SaO2
< 95%
FiO2
PEEP
95-100 %
Hb
< 4.3 mmol/l
Transfusion
>4.3 mmol/l
Fluid
respnsiveneess
VO2
comfort
yes
no
Pain - Agitation
Analgesia
Sedation
Fluids
Inotropes
Tim Jansen: Adapted from: Pinsky - Vincent Crit Care Med 2005;33:1119-1122
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Low ScvO2
Increase in CO
Effect of low dose dobutamine on ScvO2
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Hour following
admission
0
2
4
6
8
BP
100/50
109/58
105/44
95/43
100/39
HR
148
148
133
132
143
CVD
11
21
16
17
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Lactate
4.2
4.5
4.8
3.7
2.2
ScvO2
67%
52%
78%
71%
69%
Fluids (ml)
x
1670
2000
575
725
Dobu
x
3.2
6.3
11.0
11.0
Norepi
x
0.56
0.78
0.69
0.69
NTG
x
-
1 mg/h
2 mg/h
2 mg/h
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Conclusions
‣ ScvO2 reflects the balance between oxygen demand and oxygen supply
to the tissues
‣ Restoring the balance between demand and supply is the goal of
treatment in clinically relevant abnormal ScvO2
‣ Abnormal ScvO2 is frequently present on admission and following
initial resuscitation and cannot be predicted from global
hemodynamics
‣ Low ScvO2 is associated with increased morbidity and mortality
‣ Targeting normal ScvO2 is possible and benefits patients
‣ Monitoring ScvO2 should be standard practice in high risk patients
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