Intensive Care Med (2022) 48:1482–1494

https://doi.org/10.1007/s00134-022-06808-9

REVIEW

How can assessing hemodynamics help

to assess volume status?
Daniel De Backer1* , Nadia Aissaoui2, Maurizio Cecconi3,4, Michelle S. Chew5, André Denault6,7,
Ludhmila Hajjar8, Glenn Hernandez9, Antonio Messina3,4, Sheila Nainan Myatra10, Marlies Ostermann11,
Michael R. Pinsky12, Jean‑Louis Teboul13, Philippe Vignon14, Jean‑Louis Vincent15 and Xavier Monnet13

© 2022 Springer-Verlag GmbH Germany, part of Springer Nature

Abstract
In critically ill patients, fluid infusion is aimed at increasing cardiac output and tissue perfusion. However, it may con‑
tribute to fluid overload which may be harmful. Thus, volume status, risks and potential efficacy of fluid administra‑
tion and/or removal should be carefully evaluated, and monitoring techniques help for this purpose. Central venous
pressure is a marker of right ventricular preload. Very low values indicate hypovolemia, while extremely high values
suggest fluid harmfulness. The pulmonary artery catheter enables a comprehensive assessment of the hemodynamic
profile and is particularly useful for indicating the risk of pulmonary oedema through the pulmonary artery occlusion
pressure. Besides cardiac output and preload, transpulmonary thermodilution measures extravascular lung water,
which reflects the extent of lung flooding and assesses the risk of fluid infusion. Echocardiography estimates the
volume status through intravascular volumes and pressures. Finally, lung ultrasound estimates lung edema. Guided by
these variables, the decision to infuse fluid should first consider specific triggers, such as signs of tissue hypoperfusion.
Second, benefits and risks of fluid infusion should be weighted. Thereafter, fluid responsiveness should be assessed.
Monitoring techniques help for this purpose, especially by providing real time and precise measurements of cardiac
output. When decided, fluid resuscitation should be performed through fluid challenges, the effects of which should
be assessed through critical endpoints including cardiac output. This comprehensive evaluation of the risk, benefits
and efficacy of fluid infusion helps to individualize fluid management, which should be preferred over a fixed restric‑
tive or liberal strategy.
Keywords: Cardiac output, Tissue perfusion, Hypovolemia, Hypervolemia, Extravascular lung water, Tissue edema

Introduction in sepsis or in high-risk surgery, and fluid removal in

patients with fluid overload.
In critically ill patients, fluid management ranges from In experimental sepsis, fluid administration prolongs
restoring fluid depletion in hemorrhagic shock, to opti- survival [1]. However, fluids should be administered at
mization of cardiac preload to improve tissue perfusion the correct dose (defined as volume, fluid type and rate
of infusion), as both insufficient and excessive volumes
of fluids are associated with an increased mortality [2].
In septic patients, current guidelines suggest the ini-
*Correspondence: [email protected]
1
tial administration of at least 30 mL/kg of crystalloids
Department of Intensive Care, CHIREC Hospitals, Université Libre de
Bruxelles, Boulevard du Triomphe 201, 1160 Brussels, Belgium
within 3 h [3]. While this formula may be valid for many
Full author information is available at the end of the article patients, individualizing fluid therapy is probably prefer-
able in some patients, especially for the sickest individu-
als in whom the association between amounts of fluids
 1483

administered and mortality is more pronounced [4]. Tai-

loring fluid strategy should consider the severity of illness Take‑home message
as well as cardiac function and other factors influencing
In critically ill patients, fluid management ranges from restoring fluid
the tolerance to fluids [5]. depletion in hypovolemic shock, to optimization of cardiac preload
Fluid management varies according to the differ- to improve tissue perfusion, and fluid removal in patients with fluid
ent stages of shock, with fluid administration occurring overload. This review identifies how the different hemodynamic
monitoring techniques help to individualize fluid management,
mostly during salvage and optimization phases, while which should be preferred to a fixed restrictive or liberal strategy
fluid removal is often considered during stabilization
and de-escalation phases [6]. At each stage, manage-
ment should be informed by monitoring devices which fluid responsiveness and, once infused, to assess fluid
may help indicate the presence of hypovolemia and need effectiveness.
for fluids, the response to fluid infusion and the need for
fluid removal. Fluids may have undesired effects!
Fluid resuscitation may contribute to fluid overload. The
enlargement of the vascular bed due to vasodilation, cap-
Physiological concepts of volume status and fluid
illary leakage, and the transient hemodynamic effects
therapy
of fluid boluses [11] explain why fluid infusion must be
Assessing volume status covers several physiologi-
frequently repeated. In addition, maintenance fluids con-
cal concepts. Intravascular volume can be defined in
tribute to a large part to the total amount of fluid admin-
two distribution states: a larger unstressed volume
istered, especially after the initial optimization phase
which, though present within the vascular space, does
[12]. Accordingly, it will also be important to pay atten-
not result in a measurable vascular distending pres-
tion to non-resuscitative fluids, especially in patients in
sure (affecting vessel geometry below stretching) and
whom the benefits of fluid infusion are minimal.
a vascular stressed volume which distends the vessels
Hypervolemia increases the intravascular pressures
and results in an increase in mean systemic pressure
which promotes edema [13]. The increase in pulmonary
(Pms) [7]. Since all vascular beds have a variable volume
artery pressure also contributes to right ventricular fail-
requirement to reach their unstressed volume before
ure. The increase in central venous pressure (CVP) may
creating a measurable Pms, blood flow distribution
impair organ perfusion pressure either directly (mean
among vascular beds markedly alters the proportion
arterial pressure—CVP) or by increasing interstitial
of blood in the stressed and unstressed compartments.
pressure (mean arterial pressure—interstitial pressure).
For example, the splanchnic circulation has a large
Excess of fluids may contribute to intraabdominal hyper-
unstressed volume, moving blood from splanchnic
tension or the impairment in kidney function [14].
to central compartments to maintain Pms in the early
The harmful effects of fluid overload are clearly recog-
(compensated) phase of hypovolemia. On the other
nized [15, 16]. Of note, cohort studies can hardly sepa-
hand, the decrease in vascular tone (sepsis, anesthe-
rate causation (excessive fluids inducing harm) from
sia,…) markedly decreases Pms even though total blood
association (sicker patients receiving more fluids). Trials
volume is preserved. Hence, total blood volume may be
randomizing patients to restrictive versus liberal fluid
increased due to blood pooling, but the patient may still
resuscitation have failed to demonstrate differences in
be fluid responsive. Accordingly, it is often more useful
outcome [17], but most were deemed to fail as these were
to estimate fluid responsiveness and fluid tolerance, to
based on fixed regimen rather than individualizing fluid
guide fluid administration or withdrawal.
administration according to patient requirements.
In summary, the effectiveness of fluids is inconsistent,
What do we expect from fluid infusion?
and the potentially deleterious effects are serious. Thus,
The primary goal of fluid infusion is to increase cardiac
hemodynamic monitoring should serve to assess both the
output (CO), while the increase in arterial pressure is
beneficial and harmful effects of fluid therapy.
variable and depends on arterial elastance [8]. Basically,
fluid infusion increases Pms, the upstream pressure of
venous return. This leads to a significant increase in Monitoring techniques
venous return and CO only if the ventricles are preload Existing monitoring techniques evaluate volume status by
responsive, as in this case, Pms increases more than the estimating volumes and pressures, as well as the poten-
right atrial pressure [9, 10]. However, estimating Pms at tial consequences of excess volume such as extravascu-
the bedside is not performed routinely. As the response lar lung water (EVLW), and venous stasis. None of these
to volume is inconstant, a key purpose of hemody- variables exactly defines volume status, and all can be
namic monitoring devices should be to help in assessing affected by cardiac function, vascular permeability, and
1484

Fig. 1 Interrelation of intravascular pressures, extravascular lung water and venous stasis indices according to volume status. The relationship
between intravascular pressures and volume is curvilinear and affected by cardiac function. Occurrence of extravascular lung water (EVLW) or
venous stasis is dependent on volume status but may be precipitated at lower volume status in presence of impaired cardiac function, increased
permeability or increased intrathoracic pressures

intrathoracic pressures. Furthermore, they explore differ- responsiveness. In the de-escalation phase, they may trig-
ent aspects of volume status and may offer complemen- ger fluid removal.
tary information when combined (Fig. 1). To detect hypervolemia, cardiac preload indices can be
Estimation of cardiac preload is the cornerstone of used. Importantly, presence of edema does not exclude a
measuring volume status. Assessing cardiac preload need for fluids [13]. Likewise, an increase in fluid balance
before and after fluid infusion is important, as it reflects is not systematically accompanied by an increase in blood
the efficacy, and the risk of fluid infusion. Physiologi- volume, other variables should thus be considered. Meas-
cally, ventricular preload depends on the end-diastolic urement of EVLW and indices of venous stasis might be
pressure, volume, and ventricular compliance. Since only useful.
ventricular dimensions and pressure are used as preload
markers in clinical practice, the bedside estimates of Plasma and blood volume measurements
cardiac preload are all imperfect. Given the curvilinear Plasma volume was historically measured using differ-
relationship between end-diastolic pressures and vol- ent dyes or estimated from changes in hematocrit [18,
umes, volumetric measurements are more sensitive for 19]. While these measurements allow characterization
detecting low volume states whereas pressure measure- of total blood volume, the relationship between effective
ments are more sensitive for detecting hypervolemia. The circulating volume and total blood volume is inconsistent
relationship between pressures and volumes is shifted due to concomitant compensatory mechanisms (venous
upwards, and its slope is steeper, in patients with poor constriction in hypovolemia or dilation in inflamma-
diastolic function so that given volume changes are asso- tory states) so that a patient may be fluid responsive (and
ciated with larger increases in pressure. hence fluids potentially indicated) regardless of total
Detecting hypervolemia is also essential. During the blood volume. Measurements of thoracic blood volume
resuscitation phase, signs of hypervolemia may discour- by bioimpedance/bioreactance are discussed in ESM.
age fluid administration, even if there are signs of preload
 1485

Central venous pressure Transpulmonary thermodilution

CVP is often used to guide fluid resuscitation in two Transpulmonary thermodilution allows measurement
different ways [20]. First, CVP may be considered as a of intrathoracic blood volumes, EVLW and CO [26].
marker of the volume status. However, the link between Intrathoracic blood volumes represent mostly the vol-
CVP and volume status is not straightforward, as CVP is ume of heart cavities and hence can be used as a valid
also influenced by venous compliance, intrathoracic and surrogate of cardiac preload (detailed in ESM). As any
pericardial pressures, and cardiac function. Second, CVP static marker of preload, these measurements do not ade-
might be used for indicating preload responsiveness, quately reflect preload responsiveness. Volumetric meas-
even though the ability of CVP to predict the response of urements are not good to detect hypervolemia, but this is
CO to fluid has been challenged [21]. Extreme values can improved by coupling their analysis with CVP.
only be helpful for this purpose. A low CVP suggests that EVLW reflects the extent of lung flooding and is an
volume status is low or normal, and that fluid adminis- independent predictor of mortality [27]. EVLW may be
tration is likely to be well tolerated. On the other hand, a elevated due to increased intravascular pressure at the
high CVP suggests that volume status is high or normal, site of lung filtration or to increased lung capillary per-
or that the right ventricle is failing, and that fluid admin- meability. The increase in intravascular pressure can be
istration is potentially harmful. Median values of CVP related to cardiac dysfunction or to increased central
(7-15 mmHg) are less informative [22]. blood volume. The combination of volumetric, EVLW
Changes in CVP are also informative: increases in CVP and CVP measurements can be helpful to separate the
without improvement in CO indicate that fluids are not different options (Fig. 2).
tolerated [23]. Although far from perfect, CVP should be Another advantage of transpulmonary thermodilution
understood as a complex but informative variable, and its devices is the calibrated estimation of CO with pulse con-
routine measurement in patients with shock should be tour analysis which is perfect for performing tests of fluid
promoted while acknowledging its limitations. responsiveness, like the passive leg raising (PLR) test or
the end-expiratory occlusion test.
Pulmonary artery catheter
The pulmonary artery catheter (PAC) combines left and Echocardiography
right intravascular pressure with CO measurements, Echocardiography can estimate intravascular volumes
allowing a comprehensive characterization of the hemo- and pressures, as well as CO and function [28]. It can also
dynamic profile [24]. Measurements of right ventricular identify fluid responsiveness by different indices [29]. In
volumes are discussed in ESM. critically ill patients, echocardiography may rapidly iden-
The pulmonary artery occlusion pressure (PAOP) may tify hemodynamic phenotypes [30, 31]. It is particularly
help to guide fluid resuscitation. Analogous to CVP, the useful in patients with cardiac mechanical support. Also,
prediction of fluid responsiveness by PAOP has been it can identify patients with volume overload (Fig. 3). An
challenged [21], except for extreme values. Additionally, important advantage of echocardiography is the easy
PAOP may help assessing the risk of lung edema induced identification of acute cor pulmonale, where fluid admin-
by fluid infusion, even though the threshold at which istration is contraindicated [32].
edema occurs depends on vascular remodeling and capil- Echocardiography is thus an excellent tool to evaluate
lary permeability. volume status. An important limitation of echocardiog-
PAOP measurements are influenced by intrathoracic raphy is that estimation of filling pressures is not very
pressure, however, PAOP can be corrected for it [25], and precise [33] and is better suited for semi-quantitative or
transmural PAOP is only influenced by volume status and sequential measurements. Also, transthoracic echocar-
cardiac function. diography may be limited by poor echogenicity in some
The measurement of CO by the PAC is reliable but patients. Another limitation is the intermittent, rather
intermittent. The “semi-continuous” measurements than continuous nature of hemodynamic evaluation.
reflect average CO values of the preceding 3–5 min. Thus,
the PAC is not suitable for evaluation of fluid responsive- Lung ultrasound techniques
ness with tests that are detailed below. On the contrary, Lung ultrasound techniques do not evaluate volume
PAC provides a comprehensive and reliable assessment status but rather the degree of lung edema [34]. B-lines
of tissue oxygenation with mixed venous oxygenation indicate the presence of interstitial lung edema, but
and carbon dioxide-derived indices, that are less reliably quantification is not always easy. Lung echography can
measured in the central venous blood. also be performed in sequential manner to detect the
development of lung edema by counting the number of
1486

Fig. 2 Integrative interpretation of volume status and extravascular lung water measurements. Volume status can be estimated by volumetric,
pressure, or combination of both measurements. Extravascular lung water (EVLW) can be measured either by transpulmonary thermodilution, lung
ultrasounds or even estimated by X-rays

B-lines during fluid administration [35] or weaning from vascular permeability while another patient may present
mechanical ventilation [36]. with an increased EVLW associated with hypervolemia.
The different patterns that can be identified using com-
Venous ultrasound techniques bined measurements of blood volume and EVLW are
Venous ultrasound evaluates the degree of venous con- presented in Fig. 2.
gestion (Fig. 3). It combines estimation of the diameter In addition, a patient may still benefit from fluid admin-
of inferior vena cava (and its respiratory variations) with istration despite the presence of some degree of lung or
flow patterns in hepatic veins, portal vein and, eventually, peripheral edema. As the risk benefit profile may not be
renal veins [37]. Indices of venous stasis may be observed advantageous in these patients, it is crucial to determine
in hypervolemia but also in impaired right ventricular whether these patients will be fluid responsive prior to
function or conditions with elevated intrathoracic pres- the administration of fluids. It may also be interesting to
sures. While this approach has mostly been reported consider more specific thresholds for fluid responsive-
after cardiac surgery [38], recent data suggest that it ness in these patients [29].
can also be effective in other patient cohorts [39]. Sono-
graphic evaluation of femoral veins may also be useful When is fluid resuscitation indicated?
[40], as recently reported in patients affected by coro- Several prerequisites thus need to be fulfilled. First, there
navirus disease 2019 (COVID-19) with right ventricular should be a trigger for fluid administration (i.e. signs
dysfunction [41]. of tissue hypoperfusion) for which the increase in CO
induced by fluid administration is considered to be a
How to integrate measurements of blood volume, EVLW potential solution. Second, a careful evaluation of poten-
and fluid responsiveness? tial benefits and risks for fluids should be made. Finally,
It is relevant to consider the patient’s illness and to after these two first steps only, fluid responsiveness
combine measurements to accurately assess the hemo- should be evaluated [42].
dynamic profile. A patient may have a normal blood vol- Selection of the trigger is crucial. Ideally, it should be
ume but an increased EVLW as the result of increased an index of tissue hypoperfusion that rapidly responds
 1487

Fig. 3 Ultrasonographic evaluation of volume status

1488

Fig. 3 continued
 1489

Fig. 3 continued

to therapy (the detailed impact of fluids on tissue per- When there is an indication based on an appropriate
fusion are reported in ESM). Prolonged capillary refill trigger and a potentially positive benefit/risk ratio, then
time, skin mottling, decreased venous oxygen satura- fluid responsiveness should be evaluated prior to fluid
tion, and increased veno-arterial P ­ CO2 gradients are administration whenever feasible.
excellent triggers for fluid resuscitation. Increased
lactate levels are not sufficient in isolation, as hyper- How to predict fluid responsiveness?
lactatemia may take time to resolve and may be also Due to the variability in the slope of the Frank-Starling
affected by other factors. Continuing resuscitation curve, single values of markers of cardiac preload do
efforts in patients who normalized their perfusion indi- not indicate preload responsiveness, except at high and
ces was associated with worse survival [43]. low values. In contrast, a dynamic approach consists in
A low blood pressure is often used as a trigger for observing the effects on CO, or its surrogates, of spon-
fluid resuscitation [44], but the pressure response is taneous or induced changes in cardiac preload [45]. A
highly variable in patients in vasodilatory state who comprehensive review of the dynamic tests and indices
increase their CO after fluid administration [8]. of fluid responsiveness can be found elsewhere [45]. We
The benefit/risk balance of fluids needs to consider will rather focus on how these tests benefit from hemo-
the amount of fluid that has already been adminis- dynamic monitoring devices. They can be separated into
tered (a positive response is less likely to occur if the two categories, methods that mobilize an endogenous
patient has already received several liters of fluid) and amount of fluid mimicking a fluid challenge, and those
the potential risks (right ventricular dysfunction, severe using variations in cardiac preload induced by mechani-
hypoxemia, venous congestion and intra-abdominal cal ventilation.
hypertension).
1490

Methods mimicking fluid challenge measurement errors outweigh the benefit of direct esti-
While the simplest method to detect preload responsive- mation of stroke volume, so that PPV is preferred in
ness is to administer a fluid bolus and measure its effect adults. In children, due to the low elastance of the ves-
on CO, this technique can lead to fluid overload if boluses sels, stroke volume variations performs better than PPV
are repeated. The PLR test reproduces the hemodynamic [58].
effects of approximately 300 mL of fluid load, while being
reversible [45]. Importantly, the effects of PLR cannot Respiratory occlusion tests
be reliably judged by observing changes in blood pres- The respiratory occlusion test consists of interrupting
sure or even pulse pressure which is best related to stroke mechanical ventilation for a few seconds and measur-
volume. ing the CO response. The effects of the test are difficult
Initially, the effects of the PLR test were assessed with to measure on pulse pressure because the variations are
techniques reliably measuring CO (esophageal Doppler, weak and transient. Initially, this test was described with
echocardiography, pulse wave/contour analysis) [46]. In CO measured by pulse wave contour analysis [59].
intubated patients, end-tidal carbon dioxide may also The diagnostic threshold of the end-expiratory occlu-
assess changes in CO during PLR and fluid infusion, pro- sion test is low (5% increase in CO), close to the smallest
vided that ventilation is stable [47, 48]. change detectable by many CO measurement techniques.
Bioreactance may adequately detect changes in CO When echocardiography is used, adding an end-inspir-
during PLR, provided that appropriate versions of the atory pause (which decreases CO in preload depend-
software are used [49], but these results require further ance) to the end-expiratory pause (which increases CO)
validation. The effects of PLR may also be measured as increases the diagnostic threshold, reducing the impact
changes in plethysmography signal amplitude, provided of an error in the measurement of the velocity time inte-
that vasomotor tone does not change simultaneously gral [60]. Changes in the perfusion index of the plethys-
[50]. Echocardiography can also be used for this purpose mography signal may also detect the effects of end-tidal
[51]. One important limitation of these alternative meas- occlusion [61].
urements is reduced precision. Indeed, the changes in
CO during PLR should be larger than the least significant Respiratory variations in vena cava
change of the technique [52]. Accordingly, more precise Respiratory variations of vena cava size reflect respira-
techniques might be more suitable, such as pulse wave tory changes in venous return [62]. Respiratory variations
contour analysis. in superior (SVC) and inferior vena cava (IVC) diameters
can easily be estimated by echocardiography [29]. Ini-
Tests and indices using heart–lung interactions tially described in mechanically ventilated patients [63],
Pulse pressure and stroke volume variation the IVC variations were also applied in spontaneously
Cyclic variations in stroke volume during ventilation may breathing patients but performance was worse, and cut-
reflect preload responsiveness. Several indices have been offs higher than traditionally assumed had to be used [64,
reported to reflect respiratory variations in stroke vol- 65]. The diagnostic prediction of fluid responsiveness of
ume. Arterial pulse pressure variations (PPV) were first respiratory variations of SVC is superior to those of IVC
used [53]. Most bedside monitors display PPV measure- [29], but SVC requires the use of transesophageal echo-
ments. The essential limitation of PPV is that it cannot be cardiography. Given its limitations, IVC variations should
used in many clinical circumstances that create false pos- be used in conjunction with other methods.
itives (spontaneous ventilation, cardiac arrhythmia, right
ventricular failure) and false negatives (low tidal volume, How to perform fluid challenge
low lung compliance, very high respiratory rate) [54]. The Once the likelihood of a significant response of CO to
tidal volume challenge [55] circumvents the limits of PPV fluid has been ascertained, the effects of volume expan-
in the event of a tidal volume < 8 mL/kg [56]. It consists sion should be tested using a fluid bolus. The fluid chal-
of increasing tidal volume transiently from 6 to 8 mL/kg lenge is the safest way to administer fluids. The technique
and measuring the simultaneous changes in PPV [55]. A was described more than 40 years ago by Max Harry Weil
sigh maneuver can also be used in pressure support ven- and refined more recently [23]: a small volume of fluid is
tilation [57]. Theoretically, these tests may lead to false given in a short period of time, safety limits are prede-
positive results in acute cor pulmonale which should thus fined, and critical endpoints for evaluation are settled.
be excluded by echocardiography. Recent studies have helped to better delineate the way a
Techniques that assess stroke volume beat-by-beat, fluid challenge should be assessed, and this has important
such as pulse wave analysis and echocardiography can consequences regarding the techniques used for hemody-
be used to assess stroke volume variations. Unavoidable namic monitoring. Regarding the volume that should be
 1491

Fig. 4 Optimized fluid management. The optimal fluid management is based on defining the indication (trigger), predicting fluid responsiveness
and evaluating the response to fluids both in terms of increase in perfusion but also taking into account tolerance to fluids. CRT​ capillary refill time,
CO cardiac output, CVP central venous pressure, EVLW lung edema (estimated by various ways including transpulmonary thermodilution or lung
ultrasounds, VS venous stasis

administered, evaluating the changes in CO after admin- a non-significant change in CVP [20]. Tolerance to fluids
istration of 4 mL/kg of crystalloids over 10 min allows the may also take into account some other factors such as
identification of the maximal number of fluid respond- lung edema or venous stasis (Fig. 4).
ers [66], compared to slower rates or smaller amounts of The mini-fluid challenge consists of the administra-
fluids [66, 67]. Ideally, the effects of a fluid bolus should tion of 50–100 mL crystalloids over 1 min, to predict a
be assessed on CO or surrogates. Other variables such as subsequent response to a larger bolus [68, 69]. While the
heart rate or arterial pressure often fail to identify some mini fluid challenge may limit fluid administration, this
CO responders. Importantly, measurements should be maneuver should be considered with caution. First, the
obtained at the end of fluid infusion, as the effects may initial bolus of fluid may not predict the response to the
vanish 5–10 min after the end of infusion. subsequent bolus, due to the curvilinear aspect of the
Regarding the safety limits, CVP is one of the most Starling relationship. Second, the amount of fluid may be
commonly used indices [44]. Interpretation of a fluid insufficient to elicit changes in preload and hence in CO,
challenge should consider changes in preload, best leading to a false negative response.
tracked by changes in CVP. It is usually accepted that a In summary, the fluid challenge technique should be
positive fluid challenge corresponds to an increase in standardized. A small amount of fluid is given in a short
CO by 10% or more with minimal changes in CVP, a period of time, evaluating the initial response in terms of
negative fluid challenge to an absence of change in CO increases in stroke volume and CO, the tolerance to flu-
despite an increase in CVP by 3 mmHg and an indefinite ids during the administration and the dissipation of the
response to a non-significant change in CO coupled with initial effect [23].
1492

Which strategy for fluid management? Author details

1
Department of Intensive Care, CHIREC Hospitals, Université Libre de Bruxelles,
Instead of using a fixed fluid regimen, being restrictive or Boulevard du Triomphe 201, 1160 Brussels, Belgium. 2 Assistance publique des
liberal, it may be more appropriate to individualize fluid hôpitaux de Paris (APHP), Cochin Hospital, Intensive Care Medicine, médecine
management according to patient’s condition and hemo- interne reanimation, Université de Paris and Paris Cardiovascular Research
Center, INSERM U970, 25 rue Leblanc, 75015 Paris, France. 3 Humanitas Clinical
dynamic measurements. This approach combines the and Research Center-IRCCS, Rozzano, MI, Italy. 4 Department of Biomedi‑
potential benefits of fluids and prevent useless adminis- cal Sciences, Humanitas University, Pieve Emanuele, MI, Italy. 5 Department
tration of fluids. of Anaesthesia and Intensive Care, Biomedical and Clinical Sciences, Linköping
University, Linköping, Sweden. 6 Department of Anesthesiology, Montreal
Individualization of fluid management consists of giv- Heart Institute, Université de Montréal, Montreal, QC, Canada. 7 Critical Care
ing the appropriate dose of fluid during the salvage and Division, Montreal Heart Institute, Université de Montréal, Montreal, QC, Can‑
stabilization phases [6], refraining from fluid infusion in ada. 8 Departamento de Cardiopneumologia, InCor, Faculdade de Medicina
da Universidade de São Paulo, São Paulo, Brazil. 9 Departamento de Medicina
patients with no preload responsiveness. Fluids should Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile,
also be avoided in patients in whom the risk of fluid infu- Santiago, Chile. 10 Department of Anaesthesiology, Critical Care and Pain, Tata
sion seems too high. The degree of vasodilation may Memorial Hospital, Homi Bhabha National Institute, Mumbai, India. 11 Depart‑
ment of Intensive Care, King’s College London, Guy’s & St Thomas’ Hospital,
also be taken into account, as an early administration of London, UK. 12 Department of Critical Care Medicine, University of Pittsburgh,
noradrenaline, which increases the stressed blood vol- Pittsburgh, PA, USA. 13 AP-HP, Service de médecine intensive-réanimation,
ume [70], may potentiate the effects of fluid, and help Hôpital de Bicêtre, DMU 4 CORREVE, Inserm UMR S_999, FHU SEPSIS, CARMAS,
Université Paris-Saclay, 78 rue du Général Leclerc, 94270 Le Kremlin‑Bicêtre,
reducing the amount of fluid infused [71]. France. 14 Medical‑surgical ICU and Inserm CIC 1435, Dupuytren Teaching
During the de-escalation phase [6], fluid removal Hospital, 87000 Limoges, France. 15 Department of Intensive Care, Erasme Univ
should be adapted to the patient’s hemodynamic status. Hospital, Université Libre de Bruxelles, Brussels, Belgium.
Indeed, the most important risk of fluid removal is that it Declarations
exceeds its goal, and that the reduction in central blood
volume is excessive, decreasing CO and blood pressure. Conflicts of interest
DDB: Edwards Lifesciences, Philips, Baxter Nadia Aissaoui No conflict of inter‑
In a recent randomized trial [72], the achieved negative est. MC: Edwards Lifesciences, Directed Systems. MSC: Edwards Lifesciences.
fluid balance was well below the predefined target, dem- AD: Edwards Lifesciences, Masimo. LH: No conflict of interest. GH: No conflict
onstrating that patient’s condition limited the feasibility of interest. AM: Vygon, Edwards, Philips and Getinge. SM: No conflict of inter‑
est. MO: Fresenius Medical, Baxter, Biomerieux. MRP: Edwards LifeSciences,
of achieving a negative fluid balance. During forced fluid Baxter, Intelomed, Exostat. J-LT: Getinge. PV: Baxter. J-LV: No conflict of interest.
removal, the rate of fluid removal had to be decreased XM: Gettinge.
or even stopped in 12% of the patients [73]. Both insuf-
ficient [74] and excessive rates [75] of fluid removal have
been associated with increased mortality, indicating the Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in pub‑
need to individualize this therapy. What could be the rel- lished maps and institutional affiliations.
evant warning factors to predict poor tolerance to fluid
removal? Excluding patients with preload responsiveness Received: 22 April 2022 Accepted: 25 June 2022
Published: 10 August 2022
prior to fluid removal may be an option to select candi-
dates for safe fluid removal [76] but further studies are
needed to better characterize the variables that should be
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