REVIEW

To give or not to give uid challenges!

Kanishka Indraratna
*
Sri Jayewardenepura General Hospital, Sri Lanka
Keywords:
Static parameters
Dynamic parameters
Functional haemodynamics
Stroke volume variation
Transoesophageal echocardiography
s u m m a r y
Fluid challenges are used to improve cardiac output and oxygen delivery. This is done in the presence of
hypovolaemia. Hypovolaemia is generally diagnosed on static haemodynamic parameters, such as
Central Venous Pressure, Pulmonary Capillary Wedge Pressure etc. Only about half of patients admin-
istered uid in this manner, have benetted. Recently interest has been directed at functional haemo-
dynamic parameters. These are based on the relationship between mechanical ventilation and venous
return due to the cyclical changes in intra thoracic pressure. These cause variation in the stroke volume,
systolic blood pressure and pulse pressure during the respiratory cycle. There are factors which can affect
the accuracy and the interpretation of these parameters. Spontaneous respiration, the tidal volumes used
to ventilate, PEEP, lung and chest compliance, heart rhythm, right ventricular function are these factors.
Passive leg raising can be used in the presence of these or in doubt.
This article attempts to set out, how to determine whether a uid challenge will improve the cardiac
output, and also to identify the problems in arriving at that decision.
2012 Elsevier Ltd. All rights reserved.
1. Haemodynamics and functional haemodynamics
Haemodynamics is the physiology concerned with the move-
ment of blood and the forces and pressures associated with that
circulation. Haemodynamics measures oxygen delivery to tissues.
For this, static parameters such as Central Venous Pressure,
Pulmonary Capillary Wedge Pressure, Systemic Vascular Resis-
tance, Cardiac Output are measured. They do not tell us, however,
whether increasing the volume status will improve the cardiac
output and the oxygen delivery or compromise the chances of
survival. Only about 50% of patients responded to uid adminis-
tration based on these parameters.
1
Functional Haemodynamics
attempts to address this dilemma, with the use of dynamic
parameters.
2
Therefore it is necessary to measure the haemody-
namics to know the oxygen delivery and to monitor the functional
haemodynamics to assess whether the oxygen delivery can be
improved.
3
1.1. Cardiac output
DO
2
CI(Hb*1.34*SaO
2
.003PaO
2
)
DO
2
-Oxygen delivery to tissues, CI-Cardiac Index, Hb-
Haemoglobin concentration, SaO
2
-Arterial oxygen saturation,
PaO
2
-Arterial oxygen tension.
The oxygen delivery depends on the cardiac output, amount of
haemoglobin, the saturation and the dissolved oxygen.
The cardiac output is affected by,
1. The pre load, this is the volume status of the patient.
2. The myocardial contractility
3. The after load or the resistance against which the left ventricle
pumps, which is measured by the systemic vascular resistance.
Of the above the Pre load or the uid volume would be focused
upon, as attempting to improve the uid status, and thereby
increasing the cardiac index and thus the oxygen delivery to tissues
is very often the rst line of management when it is required to
improve the cardiac output.
The haemodynamic parameters available to measure the uid
status of a patient are,
Static parameters-A parameter measured under a single loading
condition
Pulmonary capillary wedge pressure
Central venous pressure
Right ventricular end diastolic volume
Left ventricular volume
Global end diastolic volume
* Tel.:94 777578144; fax:94 112778213.
E-mail address: kindraratna@yahoo.co.uk.
Contents lists available at SciVerse ScienceDirect
Trends in Anaesthesia and Critical Care
j ournal homepage: www. el sevi er. com/ l ocat e/ t acc
2210-8440/$ e see front matter 2012 Elsevier Ltd. All rights reserved.
doi:10.1016/j.tacc.2012.02.008
Trends in Anaesthesia and Critical Care 2 (2012) 115e122
However these are all measurements taken under single loading
conditions.
They, therefore do not indicate whether the patient is normo
volaemic, hypovolaemic or over loaded. They are static parameters.
These static indices of preload have a low predictive ability for
hypovolaemia.
2,4
It has been shown that the CVP does not accu-
rately indicate the preload and also does not predict uid
responsiveness.
2,10,16
An inappropriate uid administration, where the heart is unable
to increase the cardiac output with a uid bolus, can lead to oedema
in both tissues and lungs causing further hypoxia. Therefore it
becomes important to identify those patients who will have
a benecial effect with a uid administration.
5
For this purpose
functional haemodynamics are required.
Functional haemodynamics depend on the heartelung
interaction.
Dynamic parameters - Heartelung interaction on preload indices
Variations in
Stroke volume
Systolic pressure
Pulse pressure
With mechanical ventilation
With mechanical ventilation the pre load will change with each
cycle and therefore, there will be cyclical variations in stroke
volume, systolic pressure and pulse pressure.
18
With mechanical ventilation in a patient with normal left
ventricular function, during inspiration, the intra thoracic pressure
rises. The venous return is therefore decreased, and cardiac output
will fall. In expiration, the intra thoracic pressure falls and the
venous return will increase, thereby increasing the cardiac output.
6
Because of this heartelung interaction during mechanical ventila-
tion, it is possible without administering extraneous uid to obtain
two points on the Frank-Starling curve. One, when the preload is
decreased and the other when it is increased. The changes in the
cardiac output will manifest as variations in Stroke Volume, Systolic
Blood Pressure, and Pulse Pressure with inspiration and expiration.
If these variations are present it means that the patient is on the
steep part of the curve and if there is no variation on the plateau
section. With a uid challenge the cardiac output can increase only
if the patient is on the steep part of the Frank-Starling curve.
As shown in the diagram (Fig. 1), in a person with normal
cardiac function, who will be on the rising steep part of the curve,
when there is a reduction in the venous return from A to B, the
stroke volume will also fall from 1 to 2. This will manifest as a fall
in stroke volume, systolic blood pressure or pulse pressure. In
a person with impaired left ventricular function, who will there-
fore be on the plateau part of the Frank Starling curve, a corre-
sponding change in venous return from C to D, will not show
a reduction in stroke volume. There is hardly any difference
between 3 and 4 in the gure. Therefore a patient with ventricular
dysfunction, who will be on the plateau part of the curve will not
show any changes in stroke volume, systolic blood pressure or
pulse pressure.
The CVP measurement on the other hand, on such a patient, will
just indicate the uid volume of the patient, but not whether it is
adequate or not. It will also not predict, as it is just one measure-
ment under static conditions, how the patient will respond to
a uid challenge.
10
Marik et al. in a literature survey in 2008,
have said the CVP does not indicate the blood volume or the uid
responsiveness.
8
Use of CVP measurements to assess whether or
not a patients cardiac output will increase signicantly in
response to an infusion of intravenous uid cannot therefore be
recommended.
9,10,19
Stroke volume variation can be easily observed with trans-
oesophageal echocardiography.
5,7,11
The picture shows the continuous wave, with trans-
oesophageal echo, at the aortic valve. The variation is easily
observed. The peak velocity at the aortic valve is an accurate
indicator of predicting haemodynamic effects of volume expan-
sion.
17
This is because the stroke volume is the product of the
aortic valve area and the velocity time integral at the aortic valve.
The aortic valve area can be assumed to remain constant during
the respiratory cycle.
17
The peak velocity at the aortic valve is
easily observed with transoesophageal echocardiography as
shown in Fig. 2. There is a variation in the peak velocity (stroke
volume) in Fig. 2.
During mechanical ventilation, at inspiration, the venous
return falls thereby making the stroke volume less, and during
expiration the venous return increases thus making the stroke
volume more. This patient is therefore in the steep part of the
Frank-Starling curve and will be able to increase the cardiac output
following a uid challenge. These patients are termed
responders.
2
This is a picture of the continuous wave transoesophageal wave
form at the aortic valve of another patient (Fig. 3). As explained
before, with mechanical ventilation, there is cyclical change in the
venous return, however, there is no corresponding variation in the
stroke volume in this patient. This means that this patient is on the
at part of the Frank Starling curve and is unable to increase the
cardiac output in response to a uid challenge. This is a non-
responder.
The above two gures show the peak velocity, at the aortic
valve, with mechanical variation. As discussed before, this is an
indication of the stroke volume. The arterial blood pressure, when
monitored with an arterial cannula and wave form will also show,
whether the systolic blood pressure varies with mechanical venti-
lation. Responders and non-responders can be identied in this
manner too.
As explained above heart-lung interactions enable two points to
be determined on the Frank Starling curve, with the venous return
at two different levels without the administration of extraneous
uid.
However this same heart-lung interaction is subject to inter-
ference by other factors. These will cause difculties in interpre-
tation and may have an effect on the accuracy of the estimations
and assessments.
Respiratory system issues
1. Tidal volume
2. PEEP
Stroke
volume
Venous return
A
B
1
2
C
D
3 4
Fig. 1. Frank Starling curve.
K. Indraratna / Trends in Anaesthesia and Critical Care 2 (2012) 115e122 116
3. Lung compliance
4. Chest compliance
How the respiratory system behaves will have an impact on
the stroke volume variation and other functional haemodynamic
parameters. These are tidal volumes, the amount of PEEP and the
lung and chest compliance.
Tidal volumes - The larger the tidal volumes delivered
by mechanical ventilation, the greater the rise in inspiratory
pressure and therefore the greater the fall in venous return.
However small tidal volumes may not have an inuence on the
intra thoracic pressure, and therefore will not have an impact on
venous return.
12
A patient who did not appear to be a responder
with small tidal volumes can appear to be a responder because of
the use of large tidal volumes. In ARDS, where lowtidal volumes are
used for ventilation, it may still have an impact because the poor
compliance of the lung will cause the generation of large pressures
even with small tidal volumes.
14
Fig. 3. Transoesophageal echocardiography-No stroke volume variation.
Fig. 2. Continuous wave at the aortic valve with transoesophageal echocardiography-stroke volume variation. a, c eshow decreased velocity. beshows increased velocity.
K. Indraratna / Trends in Anaesthesia and Critical Care 2 (2012) 115e122 117
Also hyperination can by constricting the alveolar vessels can
increase the right ventricular afterload and reduce its output,
13
therefore affecting left sided lling and output. Therefore stroke
volume can vary.
It has been found that stroke volume variation is best assessed at
tidal volumes of 8 ml/kg
14,15
.
Fig. 4 shows the peak velocity at the aortic valve when the
patient was ventilated with a tidal volume of 6 ml/kg. On this, there
is no stroke volume variation, and the patient appears as a non-
responder to uid challenges.
In the same patient, the tidal volume was increased to 8 ml/kg
(Fig. 5). The stroke volume variation can be seen clearly now in the
gure. The patient now appears as a responder. It is therefore
important to take into consideration, the tidal volume which is being
used to ventilate the patient, before interpretation and conclusions.
PEEP - Positive End Expiratory Pressure will increase the intra-
thoracic pressure and thereby reduce venous return, causing
a decrease in both right ventricular and left ventricular stroke
volumes. This effect will however be present both in inspiration
and expiration. This will therefore give an exaggerated effect on the
stroke volume variation. A benet of this effect is that, if the stroke
volume variation increases with PEEP, it would predict that the
cardiac index would be reduced by PEEP
20e22
and is uid
responsive
23,24
.
Fig. 6 shows the peak velocity at the aortic valve with trans-
oesophageal echocardiography on a patient on mechanical
Fig. 4. Stroke volume with transoesophageal echocardiography-tidal volume 6 ml/kg.
Fig. 5. Stroke volume with transoesophageal echocardiography-tidal volume 8 ml/kg.
K. Indraratna / Trends in Anaesthesia and Critical Care 2 (2012) 115e122 118
ventilation without PEEP. There is no variation in the peak velocity
(Stroke volume as discussed before).
In the same patient a PEEP of 5 was applied (Fig. 7). Now
a variation in the peak velocity is seen. The patient now appears as
uid responsive.
A patient who drops his blood pressure or cardiac output, with
the application of PEEP, can be given uid, if his stroke volume
shows variation, as he is responsive.
23,24
If the patient is in
ventricular failure, PEEP will not induce variation in stroke
volume.
22
Lung compliance - In situations such as ARDS the lung compli-
ance is very low, that the generated pressure is not transmitted to
the intra thoracic pressure. In addition small tidal volumes are used
to ventilate patients with ARDS. Therefore an actual uid respon-
siveness may be masked. However high intra alveolar pressures are
generated in ARDS even with small tidal volumes, because of the
high PEEP used and the low lung compliance. If this pressure is
transmitted to the intra thoracic pressure the venous return is
reduced during inspiration and increased during expiration.
25
Generally the cyclical changes in intra thoracic pressure are suf-
ciently high to predict uid responsiveness in ARDS.
26
Therefore if
stroke volume variation is present in a patient with ARDS, while on
mechanical ventilation, it possibly is an accurate predictor of uid
responsiveness.
27
Chest compliance - The chest compliance will contribute to the
amount of intra thoracic pressure generated during mechanical
ventilation. If the compliance is very high, the pressure generated
will be low, and therefore may not have an impact on venous
return. Stroke volume variation will therefore decrease with the
chest open and increase with closure of chest.
28
Therefore if stroke
Fig. 6. Stroke volume variation with transoesophageal echocardiography without PEEP.
Fig. 7. Stroke volume variation with transoesophageal echocardiography with PEEP 5.
K. Indraratna / Trends in Anaesthesia and Critical Care 2 (2012) 115e122 119
volume variation is not seen, when the chest compliance is very
high i e-open chest during cardiac surgery, it does not necessarily
mean that the patient is a non-responder. Reuter DA et al. found
that Stroke volume variation can be accurately used during open
chest conditions.
29
1.2. Cardio vascular issues
1. Heart rhythm
2. Right ventricular dysfunction
3. Afterload
4. Arterial compliance
Heart rate and rhythm - The diastolic times will differ from beat
to beat when arrhythmias are present. This will affect the effect of
mechanical insufations on stroke volume. Sinus rhythm should be
present during assessment.
30
Right ventricular dysfunction - When there is right ventricular
dysfunction due to myocardial damage or severe pulmonary
hypertension the right ventricular output will be decreased. This
will therefore affect left ventricular lling and thus its stroke
volume.
31
During mechanical ventilation this will manifest as
a stroke volume variation. However giving a uid challenge in this
situation can be fraught with danger as the right ventricle may not
be able to handle any more volume and because of interventricular
dependence it may affect and compromise left ventricular function
as well.
The two transoesphageal echocardiography pictures shows
(Figs. 8 and 9), on top a patient with severe constrictive pericarditis,
with compromise of the right ventricular cavity. The second picture
shows the stroke volume of the same patient. The stroke volume
variationis obvious. However giving uidtothis patient is extremely
dangerous because of the small right ventricular cavity size.
In the presence of right ventricular dysfunction, stroke volume
variation may be seen, because left sided lling is affected. This
does not mean however, that the patient will respond to a uid
challenge.
Afterload - An increased afterload can reduce the left ventricular
stroke volume. However it has been shown that variations in the
afterload does not affect the accuracy of stroke volume variation.
32
Arterial compliance - Variations in systolic pressure and pulse
pressure may be subject to changes and inaccuracies because of
uctuations in arterial compliance. These are difcult to predict and
may vary even in the same patient.
33
1.3. Afterload reserve
In addition to improving cardiac output, assessment of how the
vaso motor tone changes in response to changes in volume and
pressure is also important to obtain the best results. This can be
done by assessing the ratio of pulse pressure variation to stroke
volume variation.
33
If the stroke volume variation is greater than
pulse pressure variation, there is vasodilatation and either uid or
a vaso constrictor can be used.
30
1.4. Limitations
Stroke volume variation is easy to assess with the availability
of transoesophageal echocardiography and oesophageal doppler.
Systolic pressure variation, Pulse pressure variation and Stroke
volume variation by pulse contour analysis are affected by arterial
compliance. Transoesophageal echocardiography has the added
advantage of being able to identify the causative problem
by being able to look at both ventricles. However even stroke
volume variation assessed by echocardiography is subject to
certain limitations, which have to be considered during
interpretation.
Stroke volume variation has to be measured only in mechan-
ically ventilated patients. The patient should be in the continuous
mandatory ventilation mode without any spontaneous breathing
during the time of measurement. The tidal volume should be at
least 8 ml/kg. In the presence of arrhythmias, the arrhythmia can
be the cause of the lling problems on the left ventricle. Right
heart dysfunction also causes lling deciencies on the left side of
Fig. 8. Transoesophageal echocardiography of constrictive pericarditis-right ventricle constricted.
K. Indraratna / Trends in Anaesthesia and Critical Care 2 (2012) 115e122 120
the heart making these patients appear as responders when they
are not. It is important to assess right heart function before
interpretation.
2. Limitations of SVV
Mechanical ventilation
SVV has to be assessed on patients who are mechanically
ventilated on CMV mode or without any spontaneous
breathing activity at the time of assessment, with tidal
volumes of more than 8 ml/kg.
Spontaneous ventilation
SVV cannot be used on patients who are breathing
spontaneously
Arrhythmias
SVV is not accurate in the presence of arrhythmia
Right heart failure
Can give misleading and inaccurate information.
PEEP, chest and lung compliance should be considered before
interpretation.
3. Passive leg raising
Elevation of legs to 45

150 ml of blood shifted to intra thoracic compartment

A short response time of 30 s to 1 min
Therefore responsiveness needs to be measured immediately
Echo/doppler pulse contour analysis can be used
Reversible if patient is not responsive
When the limiting factors, for the functional haemodynamic
indices are present, Passive leg raising can be done. This will auto
transfuse about 150 ml of blood into the thoracic cavity. The change
in stroke volume can be measured by transoesophageal echo or
Doppler at the aorta. The response is rapid.
34
If a change is observed
the patient can be deemed to be uid responsive.
35,3
On putting the
legs down the uid returns back as this is a transient and temporary
uid challenge.
4. Conclusion
It is important to remember that uid responsiveness does not
mean that the patient requires uid. Responsiveness means that,
given a uid challenge the cardiac output will increase. The hae-
modynamic indices such as cardiac index, blood pressure, CVP,
SVCO
2
% and other clinical signs as blood pressure, heart rate,
capillary rell, urine output need to be measured and assessed
rst.
2
If these indicate that the patients cardiac output is not
sufcient, functional haemodynamics should be used to assess uid
responsiveness, provided that the patient is mechanically venti-
lated with a tidal volume of at least 8 ml/kg, there is no right
ventricular dysfunction and the patient has a normal cardiac
rhythm. In addition other considerations, such as whether the chest
is open, how much PEEP is on and the lung compliance, have to be
taken into account during interpretation. Transoesophageal echo-
cardiography can be easily used to assess functional haemody-
namics. Those patients determined as responders can be given uid
challenges to improve the cardiac output, but those identied as
non-responders should not be given uid challenges.
Conict of interest statement
The author declared that there is no conict of interest.
References
1. Marik PE, Cavallazzi R, Vasu T, Hirani A. Dynamic changes in arterial waveform
derived variables and uid responsiveness in mechanically ventilated patients:
a systematic review of the literature. Critical Care Medicine 2009;37:2642e7.
2. Michard F, Teboul JL. Predicting uid responsiveness in ICU patients: a critical
analysis of the evidence. Chest 2002;121:2000e8.
3. Pinsky MR, Payen D. Functional haemodynamic monitoring, foundations and
future. In: Pinsky MR, Payen D, editors. Functional haemodynamic monitoring.
Springer; 2006. p. 3. Update in intensive care medicine, Series ed., Vincent J.L.
Fig. 9. The stroke volume variation in constrictive pericarditis.
K. Indraratna / Trends in Anaesthesia and Critical Care 2 (2012) 115e122 121
4. Preisman S, Kogen S, Berkenstadt H, Perel A. Predicting uid responsiveness in
patients undergoing cardiac surgery: functional haemodynamic parameters
including respiratory systolic variation test and static preload indicators. British
Journal of Anaesthesia 2005;95:746e55.
5. Eyre L, Breen A. Optimal volaemic status and predicting uid responsiveness.
continuing education in anaesthesia. Critical Care and Pain 2010;10(2):59e62.
6. Magder S. Clinical usefulness of respiratory variations in arterial pressure.
American Journal of Respiratory Critical Care Medicine 2004;169:151e5.
7. Feinberg MS, Hopkins WE, Davila-Roman VG, Barziala B. Multiplane trans-
oesophageal echocardiographic doppler imaging accurately determines cardiac
output measurements in critically ill. Chest 1995;107:769e83.
8. Marik PE, Baram M, Vahid B. Does central venous pressure predict uid
responsiveness. Chest 2008;134:172e8. July 2008.
9. Smith T, Grounds RM, Rhodes A. Central venous pressure. Uses and limitations.
In: Pinsky MR, Payen D, editors. Functional haemodynamic monitoring. Springer;
2005. p. 99. Update in intensive care medicine, Series ed. Vincent J.L.
10. Kumar A, Anel R, Bunnel E. Pulmonary artery occlusion pressure and central
venous pressure fail to predict ventricular lling volume, cardiac performance
or the response to volume infusion in normal subjects. Critcal Care Medicine
2004;32:691e9.
11. Darmon PL, Hillel Z, Mogtader A, Mindich B, Thys D. Cardiac output by trans-
oesophageal using continuous wave doppler across aortic valve. Anaesthesiol-
ogy 1994;80:796e805.
12. Reuter DA, Baverlein J, Goepfert MS, Weiss FC. Inuence of tidal volume on left
ventricular stroke volume variation measured by pulse contour analysis in
mechanically ventilated patients. Intensive Care Medicine 2003;29(3):476e80.
13. Teboul JL, Monnet X, Richard C. Arterial pulse variation during positive pres-
sure ventilation and passive leg raising. In: Pinsky MR, Payen D, editors.
Functional haemodynamic monitoring. Springer; 2005.
14. De Backer D, Heenan S, Piagnerelli M, Koch M, Vincent JL. Pulse pressure
variation to predict uid responsiveness;inuence of tidal volume. Intensive
Care Medicine 2005;31:517e23.
15. Suehiro K, Okutani R. Inuence of tidal volume for stroke volume variation to
predict uid responsiveness in patients undergoing one lung ventilation July 9
2011.
16. Godje O, Peyerl M, Seebauer T, Lamm P, Mair H, Reichart B. Central venous
pressure, pulmonary capillary wedge pressure and intra thoracic blood
volumes as preload indicators in cardiac surgery patients. European Journal of
Cardiothoracic Surgery 1998;13(5):533e9.
17. Feissel M, Michard F, Mangin I, Ruyer O, Faller JP, Teboul JL. Respiratory
changes in aortic blood velocity as an indicator of uid responsiveness in
ventilated patients with septic shock. Chest 2001;119:867e73.
18. Michard F, Teboul JL. Using heart lung interactions to assess uid responsive-
ness during mechanical ventilation. Critical Care 2000;4:282e9.
19. Marick PE, Monnet X, Teboul JL. Haemodynamic parameters to guide uid
therapy. Annals of Intensive Care 2011;1:1.
20. Michard F, Chemla D, Richard C. Clinical use of respiratory changes in arterial
pressure to monitor haemodynamic effects of PEEP. American Journal of
Respiratory Critical Care Medicine 1999;159:935e9.
21. Kublitz JC, Annecke T, Kemming GI, Fork S, Kronas N, Goetz AE, et al. The
inuence of positive end expiratory pressure on stroke volume variation and
central blood volume during open and closed chest conditions. European
Journal of Cardiothoracic Surgery 2006;30(1):90e5.
22. Pizov R, Cohen M, Weiss Y, Segal E, Cotev S, Perel A. Positive end expiratory
pressure induced haemodynamic changes are reected in the arterial pressure
waveform. Critical Care Medicine 1996;24(8):1381e7.
23. Yogo H, Isona S, Ikeda A, Kasuya Y, Nishiro T. Positive end expiratory
pressure induced pulse pressure changes predict stroke volume variation in
anaesthetized patients. European Journal of Anaesthesiology 2011;28:58.
24. Edward Life Sciences. Stroke volume variation. can we use uid to improve
haemodynamics? 2007.
25. Lamia B, Chemla D, Richard C, Teboul JL. Clinical review-Interpretation of
arterial pressure wave in shock states. Critical Care 2005;9:601e6.
26. Teboul JL, Monnet X. Meaning of pulse pressure variation during ARDS. In:
Vincent JL, editor. Annual update in intensive care and emergency medicine 2011.
p. 322e31.
27. Huang CC, Jui-Ying F, Han C. Prediction of uid responsiveness in acute
respiratory distress syndrome patients ventilated with low tidal volume and
high positive end expiratory pressure. Critical Care Medicine 2008;36:2810e6.
28. Rex S, Schalte G, Schroth S, De Waal EE, Metzelder S, Overbeck Y, et al. Limi-
tations of arterial pulse pressure variation and left ventricular stroke volume
variation in estimating cardiac preload during open heart surgery. Acta
Anaesthesiology Scandal 2007;51(9):1258e67.
29. Reuter DA, Goepfert MS, Goersch T, Schmoeckel M, Kilger E, Goetz AE.
Assessing uid responsiveness during open chest conditions. British Journal of
Anaesthesia 2005;94(3):318e23.
30. Sorbara C, Romangoli S, Rossi A, Romano SM. Circulatory failure;bedside func-
tional haemodynamic monitoring. In: Atlee JL, Gullo A, Singara G, Vincent JL,
editors. Peri operative critical care cardiology. 2nd ed. 2007. p. 89e108.
31. Viellard-Baron A. Pulse pressure variation in managing uid requirements.
Beware the pitfalls. In: Vincent JL, editor. Year book of intensive care and
emergency medicine 2006. p. 185e91.
32. Kubitz JC, Annecke T, Fork S, Kemming GI, Kronas N, Goetz AE, et al. Validation
of pulse contour derived stroke volume variation during modication of
cardiac afterload. British Journal of Anaesthesia 2007;98(5):591e7.
33. Pinsky MR. Functional haemodynamic monitoring, applied physiology at the
bedside. In: Vincent JL, editor. Intensive care medicine annual update. Springer;
2002. p. 537e52.
34. De Backer D. Can passive leg raising be used to guide uid administration?
Critical Care 2006;10(6):170.
35. Monnet X, Rienzo M, Osmann D, Angel N, Richard C. Passive leg raising predicts
uid responsiveness in the critically ill. Critical Care Medicine 2006;34:1402e7.
K. Indraratna / Trends in Anaesthesia and Critical Care 2 (2012) 115e122 122