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2727thth ESICM, ESICM, BruxellesBruxelles 20072007
IsIs therethere somethingsomethinggoinggoing wrongwrong??
EarlyEarly recognitionrecognition of hemodynamicof hemodynamicimpairmentimpairment
Prof. Dr. Michael BauerProf. Dr. Michael BauerDeptDept. of . of AnaesthesiologyAnaesthesiology and Intensive and Intensive CareCare MedicineMedicine
Friedrich Friedrich SchillerSchiller--UniversityUniversity, Jena, Jena
OxygenOxygen: limits in : limits in uptakeuptake and deliveryand delivery
uptake:alveoli blood
convective transport:lungs tissues
microcirculation:blood cells
pO2[mmHg]150
100
50
0
atmosphere
endexspiratoryarterial blood
capillary blood
mitochondria
mitochondria:respiratory chain
DO2 ml*m-2*min-1100 300 500 700 900 1100
n= 123230
60
90
120
150
180
MA
P
[mm
Hg]
macrohemodynamicsmacrohemodynamics and oxygen transportand oxygen transport
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
Why is mixed (or central) venous saturation a good
surrogate for hemodynamic impairment?
HemodynamicsHemodynamics and and oxidativeoxidative metabolismmetabolismFick´s principle (1870):
Cardiac output equals peripheral oxygen consumptiondivided by arterio-venous difference in oxygen content
i.e. CO = VO2 / (CaO2 – CvO2)or CO ≈ VO2 / 13.4 x Hb x (SaO2 - SvO2)
SvO2 ≈ SaO2 – (VO2 / CO x 13.4 x Hb)
Assuming constant VO2, SvO2 reflects oxygen availability/ demand ratio:
MISMATCH DEFINES SHOCK !
A. Fick (1829-1901)
TheThe conceptconcept of of oxygenoxygen supplysupply dependencydependency::anaerobicanaerobic metabolismmetabolism
Correlation of Oxygen - Supply to - Demand Ratio with Mixed Venous Oxygen SaturationCorrelation of Oxygen - Supply to - Demand Ratio with Mixed Venous Oxygen Saturation
S O2 %
DO
2/ V
O2
25 705540 85 1001.0
2.8
4.6
6.4
8.2
10.0
r= 0.906y= -9.58 + 0.19*xn= 1149
72%
Factors that influence mixed venous SO2Factors that influence mixed venous SO2
HypothermiaSedation
↑PaO2↑ Hb ↑Cardiac output
↓ PaO2↓ Hb ↓ Cardiac output
StressPainHyperthermiaShivering
↓VO2↑ DO2↓DO2↑VO2
_+
PredictivePredictive valuevalue of ScvOof ScvO22• 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)
Rivers et al. N Engl J Med 2001;345:1368-77.
ScvO2 as a surrogate to direct therapy
0 12 24 36 48 60 723 6
40
50
60
70
80 * ** *
* *
ScvO
2
0 12 24 36 48 60 723 6
0
2
4
6
8 **
* *
Lact
ate * Control
Treatment
0 12 24 36 48 60 723 6
-2
2
6
10 **
**
*
* **
Bas
e D
efic
it
0 12 24 36 48 60 723 6
7.25
7.30
7.35
7.40
7.45
** *
*pH
Hours
A man´s got to know his limitations !
Dirty Harry ; Clint Eastwood, WB 1973
66
92
66
9969
Mixed andMixed and
CentralCentral--venousvenous
SaturationSaturation
72
Does ScvO2 reliably reflect SvO2?
t (min)
veno
us s
atur
atio
n [%
]
20 30 40 50 60100
SvO2
50
60
70
80
90
100
40
ScvO2
Simultaneous registration of SvO2 and ScvO2Simultaneous registration of SvO2 and ScvO2
Lee J et al. (1972) Anaesthesiology 36: 472
%
Ssv
cO2
% SvO2
100
80
60
40
20
0 60 20 4 0 80 100
r= 0.73
r= 0.88
Shock
Normal
Simultaneous registration of SvO2 and ScvO2Simultaneous registration of SvO2 and ScvO2
In In patientspatients withwith severesevere sepsissepsis oror septicsepticshockshock a a goalgoal of 70% of 70% forfor centralcentral venousvenous
oxygenoxygen saturationsaturation correspondscorresponds to a to a mixedmixed venousvenous oxygenoxygen saturationsaturation
betweenbetween 60 and 65%60 and 65%
R. Phillip Dellinger. Crit Care Med 2003; 31:946-955
VO2 DO2
VO2
DO2
ScvO2
ScvO2 ?
LowLow and and „„supranormalsupranormal““ ScvOScvO22
““supranormalsupranormal”” ScvOScvO22: : Can it rule out persistent tissue hypoxia?Can it rule out persistent tissue hypoxia?
n=205 pts., electivecardiac surgery, mortality 4,4%
< 65%: 54 pts65-75%: 71 pts>75%: 80 pts
time [h]
ScvO
2 [%
] 80
70
60
0 6 12 18 24
Perz, Uhlig, Reinhart, Bauer, in prep.
time [h]
Lact
ate
[mm
ol/l]
Mortality rate in subgroups
< 65%: 4 (7,4%)65-75%: 0 (0)>75%: 5 (6,3%)
““supranormalsupranormal”” ScvOScvO22: : Can it rule out persistent tissue hypoxia?Can it rule out persistent tissue hypoxia?
0 6 12 18 24
8
6
4
2
0
Perz, Uhlig, Reinhart, Bauer, in prep.
The problem: Interpreting „high“ ScvO2 in hyperdynamic sepsisThe problem: Interpreting „high“ ScvO2 in hyperdynamic sepsis
40 yrs old diabetic
- Unconsciousness (GCS 3)
- Respiratory Insufficiency
pSO2 84%
-Sinusrhythm (120‘/min)
- Hypotension (MAP 54 mmHg)
- Fever (38,2 °C)
ScvO2: 81% ScvO2: 81%
MicrovascularMicrovascular failurefailure in experimental in experimental shockshockSham control
resuscitated shock
5
10
15
20
25
30
35
40
0-1
00-2
00-3
00-4
00-5
00-6
00-7
00 700
0
5
10
15
20
25
30
35
4060 minutes after onset of resuscitation
Red cell velocity [µm/s]
%
X
The information provided by PDR-ICG:What makes the difference?
Loss ofhepatocellularmass/ function
Loss ofhepatocellularmass/ function
Necrotic and/orapoptotic injury
Necrotic and/orapoptotic injury
Liver insufficiency/extrahepatic sequelaeLiver insufficiency/
extrahepatic sequelae
Impairedperfusion
Impairedperfusion
Functional shunt
SvO2 PDR-ICG
Indices of Indices of impairedimpaired nutritivenutritive perfusionperfusiondespitedespite „„((suprasupra) normal) normal““ SScvcvOO22
8
6
4
2
0
-1 1 2 3 4 5 6days
bilir
ubin
e[m
g/L]
24
18
12
6
0
PDR
-ICG
[%/m
in]
rhAPC
ScvO2 > 75-80 %
ScvO2- factor time
is discontinuous equivalent to continuous monitoring?
Time elapsed between intermittentScvO2 measurements in 85 septic
shock patients (Jena)
- 0.8 - 0.4 0 0.4
Favours GDT
EstablishedOrgan failure
GDT: early onset(prior to MODS)
Mortality of control > 20%
Mortality of control < 20%
Meta-analysis of hemodynamic optimization in high-risk patientsJack W. Kern, William C. Shoemaker Crit. Care Med 2002; 30: 1686-1692
TheThe questionquestion of of timingtiming: : TheThe „„golden golden hourhour““ of of shockshock revisitedrevisited
Alia 1999; n=63Yu 1998; n=66Yu 1998; n=39Gattinoni 1995; n=762Hayes 1994; n=109Yu 1993; n=70
Lobo 2000; n=42Wilson 1999; n=138Bishop 1995; n=115Boyd 1993; n=107Tuchschmidt 1992; n=70Shoemaker 1988; n=70Schultz 1985; n=70
Subgroup analysis
Subgroup analysis
May explain futility of hemodynamic
optimization trials to a large extent!
• ScvO2 closely parallels SvO2 (7 – 10% higher than SvO2)
• ScvO2 is superior to conventional hemodynamic parameters in theassessment of the adequacy of global tissue oxygenation
• Continuous monitoring of ScvO2 in the framework of hemodynamic goals and treatment algorithms has resulted im improved patient outcome
• Normal or high ScvO2 and SvO2 do not rule out tissue hypoxia on the organ or regional level (need for additional parameters)
Take home message
In a nutshellIn a nutshell
ScvO2 ? yes EGDT
no
invasivemonitoringyes
suspectedtissue hypoxia ?