What is the best way to assess
fluid responsiveness
in a spontaneously breathing patient ?
Prof. Jean-Louis TEBOUL
Medical ICU
Bicetre hospital
University Paris XI
France
Member of the Medical Advisory Board of Pulsion
Three different scenarios
1- Patients in the ER for acute blood losses or body fluid losses
2- Patients in the ER for high suspicion of septic shock
3- Patients in the ICU, already resuscitated for several hours or days
1- Patients in the ER for acute blood losses or body fluid losses
Diagnosis of hypovolemia is almost certain
Presence of clinical signs of hemodynamic instability
good prediction of volume responsiveness
although lacking of sensitivity
No therapeutic dilemma
2- Patients in the ER for high suspicion of septic shock
Most often, no needs for searching sophisticated predictors
of volume responsiveness since volume resuscitation is mandatory
in the first hours (see Rivers et al NEJM 2001)
3- Patients in the ICU, already resuscitated for several hours or days
- with hemodynamic instability requiring therapy
- without certainty of volume responsiveness
- with potential risks of pulmonary edema
and/or excessive cumulative fluid balance
3- Patients in the ICU, already resuscitated for several hours or days
- with hemodynamic instability requiring therapy
- without certainty of volume responsiveness
- with potential risks of pulmonary edema
and/or excessive cumulative fluid balance
How to deal with this therapeutic dilemma?
Fluid challenge ?
Prediction
of volume responsiveness ?
Crit Care Med 2006; 34:1333-1337
Rate of infusion: 500-1000 mL crystalloids or 300-500 mL colloids over 30 mins
Goal: reversal of the marker of perfusion failure that prompted the fluid challenge
(ex: hypotension, tachycardia, oliguria, etc)
Safety limits: CVP of 15 mmHg measured every 10 mins
Crit Care Med 2006; 34:1333-1337
Rate of infusion: 500-1000 mL crystalloids or 300-500 mL colloids over 30 mins
Goal: reversal of the marker of perfusion failure that prompted the fluid challenge
(ex: hypotension, tachycardia, oliguria, etc)
Safety limits: CVP of 15 mmHg measured every 10 mins
Question: benefit/risk ratio ?
Fluid challenge successful in only 50% cases
CHEST 2002, 121:2000-8
Crit Care Med 2006; 34:1333-1337
Rate of infusion: 500-1000 mL crystalloids or 300-500 mL colloids over 30 mins
Goal: reversal of the marker of perfusion failure that prompted the fluid challenge
(ex: hypotension, tachycardia, oliguria, etc)
Safety limits: CVP of 15 mmHg measured every 10 mins
Question: benefit/risk ratio ?
Fluid challenge successful in only 50% cases
Fluid challenge potentially risky
Is a CVP of 15 mmHg a reasonable safety limit?
1) PAOP often > CVP
2) Pulmonary capillary pressure (Pcap) > PAOP
Pcap-PAOP difference is high in ALI/ARDS
Collee et al. Anesthesiology 1987
Radermacher et al. Anesthesiology 1989
Radermacher et al. Anesthesiology 1990
Teboul et al J. Appl Physiol 1992
Benzing et al. Acta Anaesthesiol Scand.1994
Rossetti et al. Am J Respir Crit Care Med 1996
Benzing et al. Br J Anaesth. 1998
Nunes et al. Intensive Care Med. 2003
Her et al. Anesthesiology 2005
Crit Care Med 2006; 34:1333-1337
Rate of infusion: 500-1000 mL crystalloids or 300-500 mL colloids over 30 mins
Goal: reversal of the marker of perfusion failure that prompted the fluid challenge
(ex: hypotension, tachycardia, oliguria, etc)
Safety limits: CVP of 15 mmHg measured every 10 mins
Question: benefit/risk ratio ?
Fluid challenge successful in only 50% cases
Fluid challenge potentially risky
Is a CVP of 15 mmHg a reasonable safety limit?
1) PAOP often > CVP
2) Pulmonary capillary pressure (Pcap) > PAOP
3) Degree of pulmonary edema poorly evaluated by Pcap
since lung capillary permeability is often altered in ICU pts
Increased
lung capillary
permeability
EVLW
normal
lung capillary
permeability
Pcrit
PVC: 15, PAOP:19
Pulmonary capillary hydrostatic pressure
mmHg
Crit Care Med 2006; 34:1333-1337
Rate of infusion: 500-1000 mL crystalloids or 300-500 mL colloids over 30 mins
Goal: reversal of the marker of perfusion failure that prompted the fluid challenge
(ex: hypotension, tachycardia, oliguria, etc)
Safety limits: CVP of 15 mmHg measured every 10 mins
Question: benefit/risk ratio ?
Fluid challenge successful in only 50% cases
Fluid challenge potentially risky
3- Patients in the ICU, already resuscitated for several hours or days
- with hemodynamic instability requiring therapy
- without certainty of volume responsiveness
- with potential risks of pulmonary edema
and/or excessive cumulative fluid balance
How to deal with this therapeutic dilemma?
Fluid challenge ?
Prediction
of volume responsiveness ?
Volume expansion will increase stroke volume
only if ventricles are preload-dependent
preload-independence
Stroke Volume
preload-dependence
Ventricular preload
How to predict preload-dependence
and hence volume responsiveness?
1- By estimating cardiac preload
- using filling pressures: RAP, PAOP
The lower the ventricular preload,
the more likely the preload-dependency
preload-independence
Stroke Volume
preload-dependence
Ventricular preload
RAP before volume expansion in responders (R) and non-responders (NR)
mmHg
20
responders
nonresponders
10
*
*
0
Calvin
1981
Schneider
1988
Reuse
1990
Wagner
1998
number of pts
28
18
41
25
SB pts (%)
54
33
24
6
Changes in stroke volume (%)
r = 0.45
Baseline PRA (mmHg)
Wagner et al. Chest 1998
PAOP before volume expansion in responders (R) and non-responders (NR)
mmHg
20
responders
nonresponders
10
0
Calvin
1981
Schneider
1988
Reuse
1990
Diebel
1994
number of pts
28
18
41
32
SB pts (%)
54
33
24
31
How to predict preload-dependence
and hence volume responsiveness?
1- By estimating cardiac preload
- using filling pressures: RAP, PAOP
- using dimensions: RVEDVi, LVEDVi
RVEDVi before volume expansion in responders (R) and non-responders (NR)
responders
nonresponders
150
120
*
*
90
60
30
0
Calvin
1981
Schneider
1988
Reuse
1990
Diebel
1992
Diebel
1994
Wagner
1998
number of pts
28
18
41
22
32
25
SB pts (%)
54
33
24
16
31
6
LVEDVi before volume expansion in responders (R) and non-responders (NR)
mL/m2
120
responders
nonresponders
80
40
0
Calvin
1981
Schneider
1988
number of pts
28
18
SB pts (%)
54
33
How to predict preload-dependence
and hence volume responsiveness?
1- By estimating cardiac preload
- using filling pressures: RAP, PAOP
- using dimensions: RVEDVi, LVEDVi
markers of preload:
poor markers
of volume responsiveness
Why ?
Why do ventricular preload indicators not
predict fluid responsiveness ?
1- In the available studies, pts were already resuscitated so that values
of markers of preload were rarely low.
On the other hand, values were rarely high before fluid challenges
It cannot be excluded that low values predict volume responsiveness,
whereas high values well predict the absence of hemodynamic response to volume
2- Because RAP, PAOP, RVEDVi, LVEDVi are not always accurate indicators
of preload
3- Because assessment of preload is not assessment of preload-dependence
normal heart
Stroke volume
preload-dependence
failing heart
preload-independence
.
Ventricular preload
How to detect fluid responsiveness ?
1- By estimating cardiac preload ?
2- By using dynamic tests detecting
cardiac preload reserve ?
2.1- using heart-lung interaction
- SPV, PPV?
. for physiological reasons, these indices must not work
. as confirmed in clinical studies
Systolic pressure variation (mmHg)
Patients with MV
Systolic pressure variation (mmHg)
Patients with SB
Rooke et al Anesth & Analg 1995
Patients breathing without mechanical support










2322,72
%
19,17
15,78
13,50
PPV
before
volume
infusion
1212,50
%
11,11









8,00
7,08
5,88
4,65
3%
2,98













Non
nonresponders
O ui
responders
Soubrier et al. ATS 2005
PPV (threshold: 12 %)
sedated patients
sensitivity
patients with SB
PPV
1 - specificity
How to detect fluid responsiveness ?
1- By estimating cardiac preload ?
2- By using dynamic tests detecting
cardiac preload reserve ?
2.1- using heart-lung interaction
- SPV, PPV?
NO
- Inspiratory decrease in RAP?
J Crit Care 1992, 7:76-85
RAP
positive respiratory
response
negative respiratory
response
RAP decrease by ≥ 1 mmHg
at inspiration
RAP decrease by < 1 mmHg
at inspiration
RAP
mmHg
mmHg
20
Inspiration
Inspiration
20
0
0
hemodynamic response
to volume challenge
no hemodynamic response
to volume challenge
(L/min)
Changes in CO after volume loading
2.4
1.8
1.2
0.6
0.0
- 0.6
negative respiratory
response
positive respiratory
response
Magder et al J Crit Care 1992
Limitation : to be sure that the inspiratory effort is sufficient
How to detect fluid responsiveness ?
1- By estimating cardiac preload ?
2- By using dynamic tests detecting
cardiac preload reserve ?
2.1- using heart-lung interaction
- SPV, PPV?
NO
- Inspiratory decrease in RAP?
2.2- using passive leg raising
Passive Leg Raising
Venous blood shift
(Rutlen et al. 1981, Reich et al. 1989)
45 °
Increase in right ventricular preload (Thomas et al 1965)
Reversible effects
Increase in left ventricular preload (Rocha 1987, Takagi 1989, De Hert 1999, Kyriades 1994 )
Chest 2002; 121: 1245-52
PAOP (mmHg)
RAP (mmHg)
30
20
25
15
20
15
10
10
5
5
0
0
PLR
Base
post-PLR
PLR
Base
post-PLR
Passive Leg Raising
Venous blood shift
(Rutlen et al. 1981, Reich et al. 1989)
45 °
PLR could be used as a test to detect volume responsiveness
Increase in right ventricular preload (Thomas et al 1965)
rather than as a therapy
Increase in left ventricular preload (Rocha 1987, Takagi 1989, De Hert 1999, Kyriades 1994 )
Transient effect (Gaffney 1982)
Chest 2002; 121: 1245-1252
Hypothesis
The increase in pulse pressure during PLR
predicts the increase in stroke volume
afler volume loading
Chest 2002; 121: 1245-52
Fluid-induced
changes in
Stroke Volume
(%)
n = 39
r = 0.74
PLR-induced changes in Pulse Pressure (mmHg)
Hypothesis : a better surrogate of stroke volume than PP could do better
Real-time CO monitoring is mandatory
Hypothesis : a better surrogate of stroke volume than PP could do better
Hypothesis
PLR-induced increase in mean aortic blood flow
provides a better prediction
of volume responsiveness than
PLR-induced increase in pulse pressure
Base 1
PLR
Base 2
Post VE
500 mL
saline
responders
40
nonresponders
30
20
10
0
-10
Base 1
PLR
Base 2
Post VE
80
PLR-induced changes
PLR-induced changes
in aortic blood flow
in pulse pressure
% change from Baseline
60
40
*
*
20
10
0
-20
-40
NR
R
NR
R
100
PLR-induced changes in ABF
sensitivity
80
60
PLR-induced changes in PP
patients
with spontaneous
breathing
n = 19
40
PPV
20
0
0
20
40
60
80
100
100 - specificity
Monnet et al. Crit Care Med 2006
Hypothesis : a better surrogate of stroke volume than PP could do better
Hypothesis
PLR-induced increase in Pulse Contour CO
provides a better prediction
of volume responsiveness than
PLR-induced increase in pulse pressure
% increase in Pulse Contour CO during PLR
100
90
80
70
60
50
40
30
*
20
cut-off = 12 %
10
Se = 70 %
Sp = 92 %
0
-10
nonresponders
responders
Ridel ATS 2006
Conclusion
In spontaneously breathing patients
Prediction of volume responsiveness is a difficult issue
markers of preload
unreliable
PPV, SPV, SVV
Inspiratory decrease in RAP
Response to passive leg raising
valuable
but need to be confirmed
Thank you for your attention