indications and limitations (1.941KB)

26th International Symposium on Intensive Care
And Emergency Medicine
Experiences with S (C)V O2 Michael Bauer
Klinik für Anaesthesiologie und Intensivmedizin
Friedrich-Schiller
Friedrich Schiller-Universität Universität Jena

Oxygen: Oxygen:
limits in uptake and delivery
uptake:
alveoli blood
convective transport:
lungs tissues
microcirculation:
blood cells
pO 2 [mmHg]
150
100
50
mitochondria:
respiratory chain
0
atmosphere
endexspiratory
arterial blood
capillary blood
mitochondria

macrohemodynamics and oxygen transport
MAP
[mmHg]
180
150
• 31 of 36 medical shock patients:
– resuscitated to normal MAP and CVP
120
– have global tissue hypoxia (Scv0 2 < 70% and lactate >2
90
60
30
mmol/L).
Rady, AJEM, 1994
n= 1232
DO2 ml*m-2 *min-1 100 300 500 700 900 1100

Hemodynamics and oxidative metabolism
A. Fick
(1829-1901)
Fick´s principle (1870):
Cardiac output equals peripheral oxygen consumption
divided by arterio-venous difference in oxygen content
i.e. CO = VO 2 / (CaO 2 –CvO 2 )
or CO ≈ VO 2 / 13.4 x Hb x (SaO 2 -SvO 2 )
SvO 2 ≈ SaO 2 –(VO 2 / CO x 13.4 x Hb)
Assuming constant VO 2 , SvO 2 reflects oxygen availability/
demand ratio:
MISMATCH DEFINES SHOCK !

Correlation of of Oxygen - Supply to to - Demand
Ratio with Mixed Venous Oxygen Saturation
2
DO 2 / VO
10.0
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 85 100
S�O 2 %

Correlation of of Oxygen - Supply to to - Demand
Ratio with Mixed Venous Oxygen Saturation
DO 2 / VO 2
10.0
8.2
6.4
4.6
2.8
1.0
25 40 55 70 85 100
S�O 2 %
r= 0.906
y= -9.58 +
0.19*x
n= 1149

avDO 2 ml/dl
8.0
7.0
6.0
5.0
4.0
3.0
2.0
1.0
0
Rudolph, T., et al., 1989
r= -0.707
n= 447
ScvO 2 vs. avDO 2
avDO 2 = 11.4 -0.1*ScvO 2
30 40 50 60 70 80 90 100
ScvO 2 %

Predictive value of ScvO 2
• acute myocardial infarction (Goldman 1968, Muir 1970)
• medical ICU patients (Birman 1984)
• post-op cardiac surgery (Polonen 2000)
• trauma (Kremzar 1997, Rady 1994, Kazarian 1980)
• septic shock (Heiselman 1986, Krafft 1993, Edwards 1991)
• cardiogenic shock (Crearmer 1990)

Factors that influence mixed and central venous SO 2
↑VO2
Stress
Pain
Hyperthermia
Shivering
↓ PaO2
↓ Hb
75%
_ +
↓DO2
↓ Cardiac output
↑ DO2
↑ PaO2
↑ Hb
↑ Cardiac output
↓VO2
Hypothermia
Anesthesia

Evidence for impaired oxygen availability in
Rivers et al. N Engl J Med 2001;345:1368-77.
septic patients

ScvO 2
Base Deficit
80
70
60
50
40
10
6
2
-2
Anaerobic metabolism/ acidosis
* *
*
*
* *
0 3 6 12 24 36 48 60 72
*
*
*
*
*
0 3 6 12 24 36 48 60 72
*
*
*
Lactate
pH
8
6
4
2
0
7.45
7.40
7.35
7.30
7.25
*
*
*
* *
Treatment
Control
0 3 6 12 24 36 48 60 72
*
*
*
*
0 3 6 12 24 36 48 60 72
Hours

„goal goal-directed directed therapy“: therapy“:
the controversy continues
A trial of goal-oriented hemodynamic therapy in critically ill patients
Gattinoni L et al. N Engl J Med 1995 333:1025-1032

„goal goal-directed directed therapy“: therapy“:
the controversy continues
Alia 1999; n=63
Yu 1998; n=66
Yu 1998; n=39
Gattinoni 1995; n=762
Hayes 1994; n=109
Yu 1993; n=70
Lobo 2000; n=42
Wilson 1999; n=138
Bishop 1995; n=115
Boyd 1993; n=107
Tuchschmidt 1992; n=70
Shoemaker 1988; n=70
Schultz 1985; n=70
favors GDT
Sub group analysis
Sub group analysis
Mortality in control group > 20%
- 0.8 - 0.4 0 0.4
Meta-analysis of hemodynamic optimization in high-risk patients
Jack W. Kern, William C. Shoemaker Crit. Care Med 2002; 30: 1686-1692
Established
MODS
GDT: early
onset
Mortality in control groups < 20%

ScvO 2
Concepts to detect „cryptic cryptic shock“ shock
and „early „ early goal directed therapy“ therapy
VO 2
VO 2
ScvO 2 ?
DO 2
DO 2
R. Phillip Dellinger. Crit Care Med 2003; 31:946-955

72
80
75
69
71
66
66
92
71
75
37
88
99
97
97
Percentage
of venous
oxygen
saturation
Reinhart 84
www.berlin-anatomie.de/
deutsch/lehrtafl.htm

The Theproblem: problem: Rationale monitoring options to to
detect microvascular failure/ tissue hypoxia and and
improve oxygen availability to to vital organs in in the thecritically critically ill ill
40 yrs old diabetic
- Unconsciousness (GCS 3)
- Respiratory Insufficiency
pSO 2 84%
-Sinusrhythm (120‘/min)
- Hypotension (MAP 54 mmHg)
- Fever (38,2 °C)
S cvO O cv 2: : 81%
2 81%

Microvascular failure in experimental shock
Sham control
H / R
%
40
35
30
25
20
15
10
5
40
35
30
25
20
15
10
5
0
60 minutes after onset of
resuscitation
0
-100
-200
-300
-400
-500
-600
-700
700
Red cell velocity [µm/s]

The information provided by PDR-ICG:
What makes the difference?
S v O 2
Functional shunt
X
Necrotic Necroticand/or and/or
apoptotic apoptoticinjury injury
PDR-ICG
Impaired Impaired
perfusion perfusion
Loss Lossof of
hepatocellular
hepatocellular
mass/ mass/ function function
Liver Liverinsufficiency/ insufficiency/
extrahepatic extrahepaticsequelae sequelae

Indices of impaired nutritive perfusion
despite „(supra „( supra) ) normal“ S cvO
cv 2
bilirubin [mg/L]
8
6
4
2
0
rhAPC
-1 1 2 3 4 5 6
Tage
24
18
12
6
0
PDR-ICG [%/min]

Why measure plasma dissapearance rate of ICG ?
Hepatosplanchnic region
„The canary of the body“
Extraction
Liver blood flow = of ICG
Clearance

End-points
End points of resuscitation:
resuscitation
DO 2
A critical balance
VO 2