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 ?