ATS / ESICM / ERS /
SCCM / SRLF
7th International Consensus
Conference
Paris, 2006
What is the relevance of central or mixed venous
oxygen saturation ?
K. Reinhart MD
Dept. of Anaesthesiology and Intensive Care Medicine
Friedrich-Schiller-University Jena, Germany
Shock is defined as
inadequate tissue
oxygenation
Which are the most
appropriate cardiorespiratory variables
to detect and to
monitor the course of
tissue hypoxia in the
clinical setting ?
What can we learn
from physiology ?
Conventional cardiorespiratory parameters are
of limited value for the
assessment of the adequacy
of tissue oxygenation !
The cardio-respiratory system
fullfills its physiological task by
guaranteeing cellular oxygen
supply and to remove the waste
products of metabolism
Pflüger 1872
It was fatal for the development of our
understanding of circulation, that blood
flow is relatively difficult to measure,
whereas blood pressure is easily
measured:
This is the reason why the blood
pressure meter has gained such a
fascinating influence, although most
organs do not need pressure, but blood
flow.
A. Jarisch, “Kreislauffragen“ 1928
The two main
determinants of
oxygen supply to the
tissues are arterial
oxygen content and
cardiac output
Correlation Between Arterial
Pressure And Oxygen Delivery
180
MAP mmHg
150
120
90
60
n= 1232
30
100
300
500
700
900
DO2 ml*m-2*min-1
1100
Correlation Between Heart Rate
And Oxygen Delivery
180
HR b/min
150
120
90
60
n= 1236
30
100
300
500
700
900
DO2 ml*m-2*min-1
1100
12
Control Oxygen 10
Consumption
8
6
ml/ min/ kg
4
260
220
Control Cardiac 180
Output ml/ min/ kg
140
100
60
0
2
4
6
8
Control A-VO2 vol.%
Shepard AP et al. 1973 Am.J.Physiol. 225: 747
10
12
Individual points of limb O2 uptake vs. O2
delivery over range of progressive ischemia
O2 Uptake (ml*kg-1*min-1 )
8
6
4
2
0
0
5
10
15
O2 Delivery (ml*kg-1*min-1 )
Reinhart K et al. (1989) Am J Physiol 257: H238
20
25
Oxygen Debt: To Pay or Not to Pay?
3.5
Lactate (mMol/l)
3.0
**
2.5
2.0
1.5
n=9
n=29
n=77
n=150
n=110
n=148
n=27
1.0
50
**p < 0.01
60
70
80
SvO2 (%)
90
10
1100
8
900
6
700
500
4
300
2
4
6
8
10
A-V Oxygen Content Difference Vols. %
Donald K.W. et al. (1954) J.Clin.Invest. 33: 1146
12
O2 Uptake ml/min/m2
Cardic Index l/min/m2
12
6
4
500
400
2
300
200
100
0
2
4
6
8
10
12
14
A-V Oxygen Content Difference Vols. %
Kenneth WD et al. (1954) J.Clin.Invest. 33: 1146
16
O2 Uptake ml/min/m2
Cardic Index l/min/m2
8
The arterio-venous
oxygen content difference
informs on the extent to
which the compensatory
mechanisms of the cardiorespiratory system are
exhausted
Correlation of Arterio- Venous Oxygen Content
Difference with Mixed Venous Oxygen
Saturation
9.3
8.2
avDO2 ml/dl
7.1
6.0
4.9
3.8
2.7
r= -0.864
y= 12.7 -0.12x
n= 1191
1.6
0.5
25
40
55
70
SO2 %
85
100
ScvO2 vs. avDO2
8.0
7.0
6.0
avDO2 ml/dl
5.0
4.0
3.0
2.0
r= -0.707
1.0
0
n= 447
avDO2= 11.4 -0.1*ScvO2
30
Rudolph, T., et al., 1989
40
50
60
70
ScvO2 %
80
90
100
Correlation of Oxygen - Supply to - Demand
Ratio with Mixed Venous Oxygen Saturation
10.0
DO2/ VO2
8.2
6.4
4.6
2.8
r= 0.906
y= -9.58 + 0.19*x
n= 1149
1.0
25
40
55
70
SO2 %
85
100
Factors that influence mixed and central venous
SO2
75%
_
VO2
DO2
Stress
Pain
Hyperthermia
Shivering
 PaO2
 Hb
 Cardiac output
+
 DO2
 PaO2
 Hb
 Cardiac output
VO2
Hypothermia
Anesthesia
What can we learn
from clinical studies ?
November 8, 2001
Mortality
Control Treatment
RR (95% C.I.)
P-value
In-hospital
46.5
30.5
0.58 (0.38-0.87)
0.009
28-day
Mortality
49.2
33.3
0.58 (0.39 – 0.87)
0.01
60-day
Mortality
56.9
44.3
0.67 (0.46-0.96)
0.03
Resuscitation Endpoints
80
* *
8
*
*
*
*
ScvO2
Lactate
70
60
40
0
24
36
48
60
*
72
0 3 6
12
7.45
*
*
*
7.40
*
*
6
*
*
*
2
pH
Base Deficit
10
*
Treatment
Control
*
*
24
36
48
60
72
36
48
60
72
4
2
12
*
6
50
0 3 6
*
7.35
*
*
*
7.30
-2
7.25
0 3 6
12
24
36
48
60
72
0 3 6
12
24
Hours
Global Tissue Hypoxia (Cryptic Shock)
Despite Normalization of Vital Signs
• 39.8% of control vs. 5.1% of treatment
group had global tissue hypoxia ( ScvO2
and  lactate) at 6 hours.
SVO2 Monitoring in Cardiac Surgery
• Polonen et al have studied a cohort 403 of
cardiac surgical patients
– The control group received standard care whilst in the
protocol group, SvO2 was maintained above 70% and
lactate below 2mmol/l with fluid and inotropes
– The study was undertaken in the immediate 8 hour
post-operative period
Polonen Anesth. Analg 2000
Goal oriented hemodynamic therapy in
cardiac surgical patients n = 411
Goals:
SvO2 > 70% and lactate  2mmol/l from
admission to the ICU and 8 hrs thereafter
hospital stay (days)
goal oriented
6
p<0,005
n.s.
ICU stay
morbidity at hospital
discharge
(Polonen et al., Anesthesia and Analgesia 2000)
control
7
1,1%
p<0,001
6,1%
Failure of Vital Signs
• 31 of 36 medical shock patients:
– Resuscitated to normal MAP and CVP
– Have global tissue hypoxia (Scv02 < 70%
and lactate >2 mmol/L).
Rady, AJEM, 1994
SCVO2 Can Predict Occult Shock in
CHF
60
50
40
SCVO2 % 30
20
10
0
Control
Low Lactate
High Lactate
Patients enrolled in decompensated CHF with EF<30%
No difference in vital signs or clinical category of HF between groups.
Ander Am J Card 98
ScvO2 is superior to CVP to reflect
reduced central blood volume
before
blood loss
CVP
mm Hg
ScvO2
%
(Madsen et al., Scand J Clin Lab Invest 1993)
3
*
(6 – 1)
75
**
(69 – 78)
after
blood loss
1
(5 – -3)
60
(49 – 67)
SCVO2 Monitoring in Trauma
• 26 consecutive patients with injury suggestive
of blood loss.
• HR, BP, Urine output, CVP and SCVO2
measured.
• Blood loss estimated.
• SCVO2 most sensitive indicator blood loss
• SCVO2 <65% associated with increased injury,
blood loss and transfusion requirements.
Scalea J Trauma 1990
Continuous central venous ScvO2 monitoring
can reliably indicate ROSC during CPR
(n = 100)
Patients with ROSC had higher initial mean and
maximal ScvO2.
No ROSC in patients without ScvO2 > 30%
A ScvO2 > 75% was 100% predictive of ROSC.
(Rivers et al., Ann Emerg. Med. 1992)
Complications in patients with high vs. low
ScvO2 after major surgery
Evolution of ScvO2, base excess,
and lactate in 65 patients with septic
shock
Parks M et al. CLINICS 2006;61(1):47
Does it matter wether we
measure central venous
or mixed venous oxygen
saturation ?
100
Shock
% SsvcO2
80
r= 0.73
60
Normal
r= 0.88
40
20
0
20
Lee J et al. (1972) Anaesthesiology 36: 472
40
60
% SO2
80
100
SvO2 closely correlates with ScvO2
Gemischt-venös
Zentral-venös
80
Normoxie
Blutung
Volumentherapie (HAES)
Hyperoxie
20
Normoxie
40
Hypoxie
% Sat
60
Blutung
0
0
30
60
90
120
Zeit (min)
Reinhart K et al, Chest, 1989; 95:1216-1221
150
180
210
240
100
ScvO2
90
%
80
70
SvO2
60
50
40
0
10
20
30
t (min)
40
50
60
100
90
%
80
70
60
50
SvO2
ScvO2
40
0
10
20
Zeit (min)
30
40
R.A. O2 and C.V. O2
- %Saturation
All Determinations
C.V. O2 (r= 0.90)
R.A. O2 (r= 0.95)
M.V. O2- % Saturation
Scheinmann MM et al. 1969 Circulation 40: 165
80
60
r= 0.9761
p< 0.001
n= 131
ScvO2 % Sat
40
20
0
-20
-40
-60
-80
-80
-60
-40
Reinhart K et al, Chest, 1989; 95:1216-1221
-20
0
20
SvO2 % Sat
40
60
80
Changes in SvO2 and ScvO2 in
general anesthesia during
neurosurgery
Conclusion: Despite some large differences between absolute values, in patients with varying
hemodynamic situations, the trend in ScvO2 may be used as a surrogate variable for the trend in SvO2.
Dueck MH et al. Anesthesiology 2005; 103:249
Changes in mixed venous
oxygen saturation are well
matched by changes in
central venous oxygen
saturation !
Differences between SvO2 and ScvO2 in
different patient groups
 SO2
n = number of
measurements
high risk surgical
n = 18
7,25 %
220 313
septic shock
n = 11
7,90 %
148 534
severe head injury
n=3
10,7 %
26 281
Reinhart K et al., unpublished
Differences between mixed venous and
hepato-venous O2 saturation in patients
with septic shock
SvO2 - ShO2 [%]
40
30
20
10
Normalbereich
0
-10
60
62
64
66
68
70
72
SvO2 [%]
74
76
78
80
82
Percentage of splanchnic O2 consumption
from total body O2 consumption
in septic shock patients
60% (n=34)
In patients with severe
sepsis or septic shock a goal
of 70% for central venous
oxygen saturation
corresponds to a mixed
venous oxygen saturation
between 60 and 65% !!!
Does it matter wether we
measure central venous
oxygen saturation
continuously or
discontinuously ?
Blood gas analyses in patients with
severe sepsis and septic shock
All patients with severe sepsis or septic shock between April 2004 and May 2005 (n=221)
Total amount all
patients; all days
Average amount
during ICU stay
(range)
Average amount per
patient and day1
Average costs per
patient (Euro)
1:
average ICU length of stay 21.5 days
Central venous
blood gas analysis
16,936
76.9 (1-393)
3.5
approx. 300,00
Limitations of mixed and
central venous oxygen
saturation for the
assessment of tissue
oxygenation
Hepatic venous O2-saturation
MEGX-test
ICG-clearance
Hepatic venous blood flow
(splanchnic blood flow)
pHi
rCO2
Transcutaneous liver near infrared spectroscopy
(TOI) in 20 children during surgical hemorrhage
• TOILiver provided a better trend
monitor of central venous oxygen
saturation than gastric intramucosal
pH.
• Because of its limited sensitivity and
specificity to indicate deterioration of
SvO2, liver tissue oxygenation
measured by transcutaneous NIRS
does not provide additional practical
information for clinical management.
Weiss M et al. Pediatric Anesthesia 2004; 14: 989
Correlation between central venous oxygen
saturation and near-infrared spectroscopic
cerebral oxygenation (cTOI) in 43 critically ill
children
Nagdyman N. et al. Intensive Care Med (2004) 30:468
Inadequate tissue
oxygenation may exist on
the regional and organ
level despite normal
central and mixed venous
oxygen saturation
Summary
• ScvO2 and SvO2 are superior to conventional hemodynamic
monitoring parameters in the assessment of the adequacy of
global tissue oxygenation
• Continuous monitoring of ScvO2 and SvO2 in the framework
of hemodynamic goals and treatment algorithms have
resulted im improved patient outcome
• ScvO2 closely parallels SvO2 saturation
• In patients with shock ScvO2 is 7 – 10% (mean) higher than
SvO2
• These differences between ScvO2 and SvO2 saturation result
from changes in the regional blood flow and oxygen
supply/demand ratio
• Normal or high ScvO2 and SvO2 do not rule out tissue
hypoxia on the organ or regional level