Analytic Review

Journal of Intensive Care Medicine

1-14
Predictors to Intravenous Fluid ª The Author(s) 2017
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Responsiveness DOI: 10.1177/0885066617709434
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Jorge Iván Alvarado Sánchez, MD1,2, William Fernando Amaya Zúñiga, MD3,
and Manuel Ignacio Monge Garcı́a, MD4

Abstract
Management with intravenous fluids can improve cardiac output in some surgical patients. Management with static preload
indicators, such as central venous pressure and pulmonary artery occlusion pressure, has not demonstrated a suitable rela-
tionship with changes in the cardiac output induced by intravenous fluid therapy. Dynamic indicators, such as the variability of
arterial pulse pressure or stroke volume variation, have demonstrated a suitable relationship. Since improvement in cardiac
output does not guarantee an adequate perfusion pressure, in patients with hypotension, it is also necessary to know whether
arterial pressure will also increase with intravenous fluid therapy. In this regard, the functional assessment of arterial load by
dynamic arterial elastance could help to determine which patients will improve not only their cardiac output but also their
mean arterial pressure.

Keywords
cardiac output, critical care, pulse pressure, fluid therapy, hemodynamic monitoring

Introduction Pressure Measures

A positive response to intravenous fluid therapy is usually
defined as an increase in the cardiac output (CO) between
10% and 15%.1 On average, only 50% of patients respond to
intravenous fluid therapy2; therefore, half of the patients may
develop interstitial edema, worsening of gas exchange,
decrease in myocardial compliance, and limitation of oxygen
diffusion in tissues.3 Thus, intravenous fluid therapy should be
individualized.
A positive fluid balance has been associated with increased
mortality and morbidity,4-6 and perioperative therapy directed
with intravenous fluid may reduce hospital stay, morbidity,
days of invasive mechanical ventilation, and serum lactate.7-14
For this reason, it is important to define which hemodynamic
variables determine a positive or negative response to intrave-
nous fluid therapy. Response predictors to intravenous fluids can
be classified as static and dynamic.
Static Indicators of Fluid Responsiveness
Techniques that enable access to preload can be measured in
direct and indirect ways as right ventricular end-diastolic vol-
ume (RVEDV) or left ventricular end-diastolic volume
(LVDEV). Static preload indicators are central venous pressure
(CVP), pulmonary artery occlusion pressure (PAoP), RVEDV,
global end-diastolic volume by thermodilution, and LVEDA by
echocardiogram.
Pressure measures depend on 3 determinants: the breath cycle,
the cardiac cycle, and the anatomical and physiological prop-
erties of the heart. Transmural pressure, the difference between
intravascular and extravascular pressure (pleural pressure), is
the relevant pressure that determines cardiac preload. Conse-
quently, an assessment of preload by pressure measurements
should be carried out at the end of expiration, as pleural pres-
sure is near to 0 and intravascular pressure approaches trans-
mural pressure. In regard to cardiac cycle, the measurement of
the CVP should be made at the end diastole when the tricuspid
1
Department of Physiology, Universidad Nacional De Colombia, Bogota,
Colombia
2
Department of Anesthesiology, Centro Policlı́nico del Olaya, Bogota,
Colombia
3
Department of Anesthesiology, Fundación Santa Fe de Bogotá, Bogota,
Colombia
4
Department of Critical Care, Hospital SAS de Jerez, Jerez de la Frontera,
Cádiz, Spain
Received December 27, 2016. Received revised April 13, 2017. Accepted
for publication April 21, 2017.
Corresponding Author:
Jorge Ivan Alvarado Sanchez, Department of Physiology, National University of
Colombia, Bogota, Colombia; Department of Anesthesiology, Centro Policlı́-
nico del Olaya, Street 15 24G-31 South, Bogota, Colombia.
Email: jialvarados@unal.edu.co
2 Journal of Intensive Care Medicine XX(X)
valve closes and just before the ventricular systole. This point
is represented by the c wave on the CVP curve or, if it is not
visible, by the R wave on the electrocardiogram.15 Anatomical
and physiological properties of the heart affect the CVP values
since changes in ventricular compliance, or conditions like
pulmonary hypertension, can have profound effects on CVP,
regardless of the intravascular volume condition. Similarly, the
CVP can be altered in patients with valve disease.16
Central venous pressure and PAoP. Both CVP and PAoP have
been used for a long time to determine response to intravenous
fluid therapy.17 During recent years, several studies have
revealed the poor predictive value of CVP and PAoP for asses-
sing fluid responsiveness.
Although the performance of CVP for predicting fluid respon-
siveness is poor (18) and there is no correlation between CVP and
changes in blood volume or cardiac index18,19, the Surviving
Sepsis Campaign guidelines for hemodynamic resusctitation has
proposed in the past measuring the CVP for guiding fluid admin-
istration, recommending to give fluids in spontaneously breathing
patients with a CVP < 8 mm Hg or when CVP < 12mm Hg under
mechanical ventilation.20 In an exploration of these cutoff points,
Osman et al found that a CVP of less than 8 mm Hg has a positive
predictive value of 51% and a negative predictive value of 65%.
Also, in patients with a CVP of less than 12 mm Hg and invasive
mechanical ventilation, the positive predictive value was 47%
and the negative predictive value was 67%.2
Guidelines for hemodynamic support of sepsis in adult
patients by The American College of Critical Care Medicine
use a PAoP of 12 to 15 mm Hg for intravenous fluid resuscita-
tion as a cutoff point.21 Osman et al found that a PAoP less than
12 mm Hg does not have enough predictive power in predicting
fluid therapy responsiveness, with a sensitivity of 77%, speci-
ficity of 51%, predictive positive value of 54%, and predictive
negative value of 74%.2 So it’s not recommended being used to
guide a response to a fluid intravenous therapy in the current
Surviving Sepsis Campaign guidelines and other guides.17,22
Volumetric measurements. There are 2 types of measurements in
this group: RVEDV by thermodilution and LVEDA by
echocardiogram.
Right ventricular end-diastolic volume. Right ventricular end-
diastolic volume has been proposed as a preload measurement.
Diebel et al reported that the right ventricular end-diastolic
volume index (RVEDVi) was better than PAoP to predict fluid
response in critically ill and trauma patients.23,24 Cutoff values
below 90, from 90 to 140, and higher than 140 mL/m2 predicted
fluid response in 64%, 27%, and 0%, respectively. Nonetheless,
a positive response to fluids in patients with RVEDVi of more
than 138 mL/m2, and a lack of response in patients with
RVEDVi of less than 90 mL/m2,25 was found by Wagner and
Leatherman. Furthermore, Michard and Teboul did not find a
difference between responders and nonresponders of RVEDVi
in basal values.19
Figure 1. Two different Frank-Starling curves showing the relation
between left ventricular (LV) stroke volume and LV end-diastolic
volume in patients with normal heart and patients with heart failure.
DP indicates changes pressure; DSV, changes in stroke volume.
Left ventricular end-diastolic area. The left ventricular end-
diastolic area index (LVEDAi) better reflects left ventricular
preload in comparison with PAoP.26 The LVEDAi has also
been used to detect blood loss in anesthetized patients.27 In
an animal model, Swenson et al found a relation between
end-diastolic area and changes in CO induced by intravenous
fluid therapy.28 In addition, Tousignant et al found a modest
relation between stroke volume (SV) and LVEDA (r ¼ .6).29
On the other hand, Tarvernier et al demonstrated the superiority
of systolic pressure variation (SPV) over PAoP and LVEDAi in
patients with sepsis.30 Finally, superiority of the aortic flow
variability over LVEDAi was demonstrated by Feissel et al,
as well as a poor relationship between LVEDAi and CI (r2 ¼
.11).31 Hence, it can be concluded that LVEDA is not decisive
enough in response to intravenous fluid therapy.
It is noteworthy that even volumetric measurements of
preload cannot accurately predict fluid responsiveness, since
the change in CO after fluid administration depends not only
on preload but also on the cardiac function curve. Therefore,
the value of static indicators for predicting fluid responsive-
ness is not restricted by a technological limitation but by a
physiological boundary (see Figure 1). For example, an ele-
vated CVP may signify there is an impediment to venous
return (ie, auto-positive end-expiratory pressure [PEEP], car-
diac tamponade, PEEP, tension pneumothorax). Also, CVP
may be normal in left heart failure and that may be elevated
in right heart dysfunction or an obstruction to right ventricular
outflow.32
Dynamic Indexes of Fluid Responsiveness
Dynamic indexes evaluate the cardiovascular system
response to a transient change or perturbation, such as a
brief variation in cardiac preload. According to Cavallaro
et al, dynamic indexes could be divided into 3 groups (see
Alvarado Sánchez et al 3

Table 1. Classification of Dynamic Determinants of Fluid Responsiveness.

Indicator Cutoff Value Sensitivity, % Specificity, % Study

Group 1
33
SPV 10 mm Hg NA NA
1
PPV 13% 94 96
34
SVV 9.5% 79 93
31
DVpeak 12% 100 89
35
DABF 18% 90 94
36
Change in PPV from Vt 6 to 8 ml/kg PBW 3.5% 94 100
36
Change in SVV from Vt 6 to 8 ml/kg PBW 2.5% 88 100
Group 2
37
DPEP 4% 92 89
38
Variation of plethysmography 14% 94 80
39
Collapse index of superior vena cava 36% 90 100
40
cIVC 18% 90 90
Group 3
41
Variability in central venous pressure <1 mm Hg on inspiration NA NA
42
EEO Increase in pulse pressure and cardiac index of at least 5% 87-91 100
43,44
Respiratory systolic variation test 0.24 to 0.51 mm Hg/cm H2O 87.5-93 83-89
45
PLR Descending aortic flow upper than 8% with PLR 90 82
46
Valsalva maneuver PPV 52% 91 95
47
ETCO2 5% with PLR 90.5 93.7
48
VCO2 <11% with PEEP 90 95
49
Mini-fluid challenge >10% VTI with Mini-fluid challenge 95 78

Abbreviations: DABF, aortic blood flow variation; cIVC, distensibility index of inferior vena cava; EEO, end-expiratory occlusion test; ETCO2, end-tidal CO2; NA,
not applied; PEEP, positive end-expiratory pressure; PLR, passive leg raising; PPV, pulse pressure variability; SPV, systolic pressure variability; SVV, stroke volume
variability; VCO2, pulmonary elimination of carbon dioxide; DVpeak, peak velocity variation; Vt, tidal volume; VTI, velocity time index.

Table 1).50 The first group relies on stroke volume varia-
tions (SVVs) or surrogates, such as pulse pressure variation
(PPV) or variations in aortic flow. These indexes are
grounded on the variations in cardiac preload induced by
changes in intrathoracic pressure by intermittent positive-
pressure ventilation. Parameters in the second group are also
based on the effects of mechanical ventilation, although
they are not related to changes in SV. Included in this group
are superior vena cava diameter variability and changes in
the pre-ejection period (PEP). The third group relies on
indexes based on redistribution maneuvers of preload, such
as the passive leg raising (PLR) test.
mechanical ventilation and the systolic pressure of patients
with apnea. Perel et al demonstrated that SPV predicted
response to intravenous fluid therapy better than CVP, PAoP,
mean arterial pressure (MAP), and heart rate (HR).52 However,
if SPV increases due to the Up component, it is due to fluid
overload rather than by hypovolemia.53 Since Denault et al
could not find a relation between the SPV and SV in the left
ventricle, different variables contribute to SPV.54 In addition,
blood systolic pressure relates less to SV than pulse pressure
(PP),55 and this is the reason why this variable has fallen into
disuse.

Stroke volume variability. This is calculated as the difference

Group I
This group includes SPV, PPV, SVV, aortic blood flow peak
velocity variation, respiratory change in aortic blood flow, and
tidal volume challenge.
Systolic pressure variability. In 1978, Rick and Burke were the
first to suggest that there was a relationship between volume
status in critical patients and swings in systolic arterial pressure
(SAP).51 In 1987, Perel et al divided SPV into 2 components:
Up and Down components. The Up component ensues from the
difference between the maximum systolic blood pressure dur-
ing the inspiratory phase of invasive mechanical ventilation
and the systolic pressure of patients with apnea. The Down
component ensues from the difference between the minimum
systolic pressure during the expiratory phase of invasive
between maximum SV during inspiration and minimum SV
during expiration, divided by the average of both values. It can
be calculated by thermodilution methods or by pulse contour
analysis. Berkenstadt and his colleagues found that a stroke
volume variability (SVV) 9.5% predicted an increase in SV
>5%, with a sensitivity of 79%, a specificity of 93%, and an
AUC of 0.809.34 The SVV correlates with the SVI before and
after intravenous fluid therapy (r ¼ .67 and r ¼ .85, respec-
tively), as does the CI (r2 ¼ .55 and r2 ¼ .59). Both SVV and
PPV depend on the tidal volume used; at low tidal volume, the
SVV decreases.56 Maximum value (SV maximum) is influ-
enced by an initial SV increase in the early inspiratory phase
that is not related to intravenous fluid therapy response. It also
decreases its sensitivity and specificity in patients with
impaired cardiac function.33
4 Journal of Intensive Care Medicine XX(X)
Figure 2. The figure shows how to calculate pulse pressure variation.
PPV indicates pulse pressure variation; PP max, pulse pressure max-
imum; PP min, pulse pressure minimum.
Pulse pressure variation. Arterial PP is directly proportional to
SV and inversely related to arterial compliance.57 The PPV is
usually calculated as the difference of the maximum and min-
imum PP divided by its mean value during a single breath and
averaged during 3 to 5 respiratory cycles (see Figure 2).
Michard et al demonstrated that PPV was a better predictor
to intravenous fluid therapy than SPV. A PPV  13% discri-
minated between responders and nonresponders with a sensi-
tivity of 94% and a specificity of 96%. Moreover, CI changes
induced by intravenous fluid therapy were correlated with
baseline PPV (r2 ¼ .85). So, the higher the PPV, the greater
the increase in CI after fluid administration.1
This variable depends on the tidal volume used, respiratory
frequency used, the HR/respiratory rate (RR) ratio, the driv-
ing pressure (plateau pressure  PEEP), the lung compli-
ance, 58 and PEEP. 59 De Backer et al found that PPV
predicted response to intravenous fluid therapy only when a
tidal volume 8 mL/kg was used, but lower tidal volumes
diminished the sensitivity and specificity of PPV (39% and
65%, respectively).60 Muller and his colleagues explored the
predictive value of PPV in 57 patients with acute circulatory
failure and a low tidal volume; they explored the impact of
driving pressure (plateau pressure  PEEP) and they found
that a PPV of 7% predicted response to intravenous fluid
therapy in this population, with a sensitivity of 61%, specifi-
city of 94%, positive predictive value of 96%, and negative
predictive value of 52% (receiver operating characteristic
[ROC] ¼ 0.77) and that a PPV less than 13% did not predict
the response to fluid administration, especially when driving
pressure is less than 20 cm H2O.61
Vallée et al tried to overcome this limitation by correcting
the PPV adjusted by alveolar pressure variations (P ¼ Pplat 
PEEPtot). Nonetheless, they failed to demonstrate such an
improvement when low tidal volume was used; even if these
corrections were used, they found that PPV adjusted by alveo-
lar pressure variation failed to predict fluid responsiveness,
with an ROC curve area of 0.72.62 The findings by Vallée
et al could be explained by that fact that the driving pressure
is not directly related to the magnitude of variation in pleural
pressure. Furthermore, in patients with acute respiratory dis-
tress syndrome (ARDS),63 it is unlikely that driving pressure
variations reflect changes in pleural pressure, since the trans-
mission of the airway pressure to the pleural space depends on
the ratio of chest wall elastance and the total elastance of the
respiratory system.64 In this regard, Liu et al adjusted the PPV
according to changes in pleural pressure (DPpl), using an eso-
phageal balloon catheter, and found that a relationship where
PPV/DPpl is higher than 2 predicts intravenous fluid therapy
responsiveness with a sensitivity of 92.3% and specificity of
93.2% in patients with ARDS, even if tidal volume was less
than 8 mL/kg.65
Conversely, De Backer et al demonstrated that the ratio
between HR and RR could limit the predictive value of these
indexes. During high RRs, the number of cardiac beats per
respiratory cycle decreases due to a reduction in pulmonary
blood transit time. They found that an HR/RR ratio 3.6
diminishes the predictive performance of PPV.66
Furthermore, PPV depends on induced changes in intrathor-
acic pressure during intermittent positive-pressure mechanical
ventilation. These changes are dependent on the tidal volume
and how the airway pressure is transmitted to the pleural and
pericardial spaces, that is, to lung compliance.58 Therefore, for
the same preload-dependence degree, a patient with low lung
compliance will show a lower PPV, since the airway pressure
transmission to pleural space is reduced.
Other clinical situations should be taken into account
when using PPV as a response predictor to intravenous fluid
therapy (see Table 2). Patients with right ventricular failure
behave as fluid responder patients according to PPV value,
due to afterload increase in the right ventricle. The PPV
presents a 34% false-positive rate in patients with right
ventricular failure,67 so caution should be taken when using
PPV or SVV to predict response to intravenous fluid therapy
in patients with pulmonary hypertension.69 For this reason,
in patients with a right ventricular ejection fraction of less
than 30%, PPV and SVV do not detect hypovolemia.68 In
patients with high diastolic dysfunction or high left ventri-
cular filling, pressure does not predict response to intrave-
nous fluid therapy.77
Tidal volume challenge. Myatra et al hypothesized that raising the
tidal volume from 6 to 8 mL/kg predicted body weight, pre-
dicted tidal volume challenge, increases the intrathoracic pres-
sure, and predicted the magnitude of the heart–lung interaction.
They demonstrated that changes in PPV of 3.5% and SVV of
2.5% after performing a tidal volume challenge identified fluid
responders with a sensitivity of 94% and 88%, respectively,
and with a specificity of 100% in both. This maneuver can
be performed easily at the bedside and does not require a CO
monitor. This maneuver should be studied in patients with low
Alvarado Sánchez et al
Table 2. Limitations of Dynamic Indexes of Fluid Responsiveness.
Limitations
PPV and SVV
Lower tidal volumes <8 mL/kg
Driving pressure (plateau pressure  PEEP) less than 20 cm
H2O
Ratio between heart rate and respiratory rate (HR/RR) 3.6
Right ventricular failure
Pulmonary hypertension
Heart rate irregular and spontaneous inspiratory effort
Gray zone
Pressure support ventilation
Impaired cardiac function
cIVC
Spontaneous breathing
PLR
Intra-abdominal pressure 16 mm Hg
Abbreviations: cIVC, distensibility index of inferior vena cava; PEEP, positive
end-expiratory pressure; PLR, passive leg raising; PPV, pulse pressure variabil-
ity; SVV, stroke volume variability.
lung compliance in which the increases in the intrathoracic
pressure don’t happen.36
There are important limitations in this group. If the HR is
irregular, it is impossible to measure blood pressure variation,
SV, and aortic flow. In patients with spontaneous inspiratory
effort, the PPV loses predictive value70 and even has less pre-
dictive value than some static indices.78 The SVV does not
predict intravenous fluid therapy responsiveness in patients
with septic shock on pressure support ventilation.73 Berken-
stadt et al found that with massive blood loss, the PPV, and
SVV can be falsely elevated and may overestimate intravenous
fluid therapy responsiveness.79
It is sometimes difficult to decide whether to give fluids
when the PPV values are close to their cutoff points. For this
reason, some authors have determined a gray zone around the
optimum criterion in which formal conclusions about predic-
tion of fluid response cannot be obtained. For PPV, a gray zone
of between 9% and 13% has been described by Cannesson et al.
Interestingly, 25% of the patients included in their study were
in this area.71 Moreover, Biais et al found that 62% of their
studied patients exhibited a PPV value in the gray zone (4% and
17%).72
Respiratory change in aortic blood flow velocity. Velocity and aortic
blood flow are directly proportional to SV; therefore, their
changes during invasive mechanical ventilation can be used
for predicting fluid responsiveness. Feissel et al studied 19
mechanically ventilated patients with septic shock. They cal-
culated peak velocity variation as DVpeak ¼ 100  maximum
peak speed  minimum speed peak divided by average of both
values. They demonstrated that a DVpeak  12% discriminated
between responders and nonresponders to intravenous fluid
therapy with a sensitivity of 100% and a specificity of 89%.
Moreover, DVpeak prior to intravenous fluid therapy was
related to the fluid-induced changes in CI (r2 ¼ .83).31
5
Descending aortic blood flow measurement by esophageal
Doppler has adequate relation to global CO80 and has good
Study
correlation with a pulmonary artery catheter.81,82 In this regard,
Monnet et al found that aortic blood flow variation (DABF)
60
measured by an esophageal Doppler of 18% predicts intrave-
61
nous fluid therapy responsiveness with a sensitivity of 90% and
a specificity of 94%. They also found that a DVpeak of 13%
66
67,68 also predicts intravenous fluid therapy responsiveness with a
69 sensitivity of 80% and a specificity of 72%, and their areas
70 under the ROC curve are similar (ROC ¼ 0.93 and 0.82,
71,72 respectively).35 In contrast to echocardiography, esophageal
73
Doppler monitoring is easy to apply and requires minimal
33
training.
74,75
76
Group II
This group includes the PEP of the left ventricle, plethysmo-
graphy variation, and superior vena cava and inferior vena cava
collapse indices.
Respiratory change in PEP. The PEP is defined as the interval time
between the start of the Q wave on echocardiography and the
start of the rise curve on invasive blood pressure monitoring. If
SV increases, PEP decreases,83 and positive pressure ventila-
tion increases the PEP by a decrease in venous return and SV.84
Bendjelid et al found an increase in PEP during inspiration and
a decrease during expiration in patients under invasive mechan-
ical ventilation. They also described the respiratory change in
the PEP (DPEP) as: DPEP ¼ 100  PEP expiration  PEP
inspiration divided by the average of both values. They found
that DPEP relates to SV changes induced by intravenous fluid
therapy (r2 ¼ .57) but also found that there is a better correla-
tion with PPV, Down, and SPV (r2 ¼ .83, r2 ¼ .68, r2 ¼ .52,
respectively).37 Feissel et al found that DPEP measured by
plethysmography or invasive blood pressure in patients with
sepsis before intravenous fluid therapy correlates with changes
in CI after therapy (r2 ¼ .73 and r2 ¼ .67, respectively), with
areas under the ROC curves similar to PPV (ROC DPEP by
plethysmography ¼ 0.94, ROC DPEP by invasive blood pres-
sure ¼ 0.97, and ROC PPV ¼ 0.96). A DPEP with an invasive
blood pressure of 4% discriminates between responders on
whether to apply intravenous fluid therapy with a sensitivity
and specificity of 92% and 89%, respectively.85
Variation of plethysmography. Since the plethysmography wave
has a similar behavior to the invasive blood pressure wave on
invasive mechanical ventilation, it was proposed as a response
indicator to volume. Partridge discovered a relation between
variability of plethysmography and systolic blood pressure var-
iation (r ¼ .61).86 Shamir et al discovered the relationship of
plethysmography variability with hypovolemia and a better
relationship between SPV and Down (r ¼ .85).87 Natalini
et al found a response prediction to fluids similar to pulse
variation measured by pulse contour analysis and plethysmo-
graphy (ROC: 0.74 vs 0.72) and an SPV measured by pulse
contour analysis and plethysmography (ROC: 0.64 vs 0.72).88
6 Journal of Intensive Care Medicine XX(X)
The above mentioned studies relate the variability of
plethysmography with SPV, and since the limitations of the
SPV54 are already known, it is clear why it is necessary to
compare this variable with a better indicator such as PPV.
Cannesson et al found a good relationship with PPV (r2 ¼
.83), and they determined that a variability of plethysmography
above 15% discriminates between patients with PPV higher
than 13% and those with PPV less than 13%, with a sensitivity
of 87%, specificity of 100%, positive predictive value of 100%,
and negative predictive value of 94%.89 It is important to con-
sider that in this study accuracy decreased when variability
increased; moreover, it evidenced no response to fluids, only
the relationship between 2 variables (PPV and plethysmogra-
phy variability). Thus, Feissel et al researched this further,
discovering that prior to intravenous fluid therapy, PPV relates
to plethysmography variability (r2 ¼ .71), PPV changes corre-
late with changes in plethysmographic variability after intrave-
nous fluid therapy (r 2 ¼ .52), and changes in CI after
intravenous fluid therapy was correlated with PPV (r2 ¼ .76)
and plethysmography variability (r2 ¼ .5). Additionally, intra-
venous fluid therapy decreased the PPV and plethysmography
variability and also correlates with an increased CI (r2 ¼ .64).
Before intravenous fluid therapy, PPV 12% and plethysmo-
graphy variability 14% discriminate between responders and
nonresponders to intravenous fluid therapy with a sensitivity of
100% and 94%, respectively, and a specificity of 70% and
80%, respectively, and areas under the ROC curve were 0.99
for PPV and 0.96 for plethysmography variability.38 From this
study, we can therefore conclude that the proportion of changes
between PPV and CI after intravenous fluid therapy is closer
than the proportion between plethysmography variability and
CI. Landsverk et al demonstrated a great variation—inter- and
intraindividual—between PPV and plethysmography variabil-
ity.90 It is important to note that pharmacologic hypotension
can simulate the effects of hypovolemia with normal blood
pressure figures on the plethysmography wave.91 Based on
current evidence, the use of plethysmography variability, as a
response predictor to intravenous fluid therapy, is not
recommended.
Superior and inferior vena cava collapse index. Venous return is
determined by the pressure gradient between mean systemic
pressure and right atrial pressure.92 Intravenous fluid adminis-
tration increases mean systemic pressure above right atrial
pressure, thereby increasing the pressure gradient and, there-
fore, the venous return. In a patient under positive pressure
ventilation, pleural pressure and right atrial pressure increase,
thus pressure gradient decreases93 and consequently the venous
return decreases. Twenty percent of this pressure is transmitted
to the abdomen.94 Cyclical effects of mechanical ventilation on
venous return are influenced by the transmural pressure of the
superior and inferior vena cava, which is determined by intra-
vascular pressure and extramural pressure (intrathoracic or
intra-abdominal). The relationship between transmural pres-
sure and vein diameter is not direct.95 Positive pressure venti-
lation decreases transmural pressure of the superior vena cava,
with a subsequent decrease in superior vena cava diameter, and
a collapse of the superior vena cava leads to a decrease of SV in
the right ventricle and pulmonary artery blood flow.96,97
Vieillard-Baron et al found that, in 66 patients with circulatory
failure secondary to sepsis, a collapse index of the superior
vena cava of 36% (difference of superior vena cava maximum
diameter in exhalation and minimum diameter in inspiration
divided by maximum diameter in expiration) discriminates
between responders and nonresponders to intravenous fluid
therapy, with a sensitivity of 90% and specificity of 100% and
areas under the ROC curve similar to PPV (ROC ¼ 0.993 and
0.94, respectively). It is important to note that in this study, 6
false positives of PPV were found as a result of cor pulmo-
nale.39 Positive pressure ventilation increases pleural pressure
that is transmitted to the left atrium and abdomen, increasing
the transmural pressure and inferior vena cava diameter
(cIVC). Barbier et al assessed 23 patients with circulatory fail-
ure associated with sepsis, measured the distensibility index of
the inferior vena cava (cIVC ¼ maximum diameter at inspira-
tion  minimum diameter at expiration divided by minimum
diameter at expiration) before and after intravenous fluid ther-
apy, and found that a cIVC  18% can predict intravenous fluid
therapy responsiveness with a sensitivity and specificity of
90%, as well as a good correlation between cIVC before ther-
apy and increased CI after therapy with intravenous fluids (r ¼
.9).40 Feissel et al used a different index but reached the same
conclusion. They studied 36 patients with circulatory failure
secondary to sepsis and measured change in diameter of infer-
ior vena cava (DcIVC ¼ maximum diameter  minimum dia-
meter divided by average maximum and minimum diameters
vena cava  100) and discovered that DcIVC  12% predicts
intravenous fluid therapy responsiveness with a positive pre-
dictive value of 93% and a negative predictive value of 92%,
and a good correlation between increased CO secondary to
therapy and DcIVC before therapy was observed.98
The inferior vena cava diameter (cIVC) could correlate
with fluid removal after dialysis or during continuous hemo-
filtration in patients with spontaneous breathing and heart
failure99-101; in addition, it could predict PVC in patients with
mechanical ventilation or spontaneous breathing.102-105 Mul-
ler et al queried whether a relation between blood volume and
cIVC diameter exists and whether it may be used as a predic-
tion factor of fluid responsiveness in patients with sponta-
neous breathing. They studied 40 patients with acute
circulatory failure and spontaneous breathing and discovered
that the best cutoff value was 40%, with the area under the
ROC curve of 0.77, a positive predictive value of 72%, and a
negative predictive value of 83% (ROC 0.77). However, a
cIVC value below 40% cannot exclude fluid responsiveness,
so it has a high rate of false positives.74 Airapetian et al stud-
ied the predictive value of the inferior vena cava diameter in
59 patients with spontaneous breathing and acute circulatory
failure. They observed that neither the inferior vena cava
diameter nor inferior vena cava variability predicts fluid
responsiveness. An inspiratory variation of inferior vena cava
of 42% may predict an increase in fluid responsiveness with a
Alvarado Sánchez et al
high specificity (97%) but low sensitivity (31%) and negative
predictive value (59%).75
This group may have several limitations. Patients should be
ventilated in pressure-regulated volume control modes; so
patients should be sedated and perhaps even receive neuromus-
cular relaxation. The volume tidal used, and whether or not
PEEP is used, can influence the predictive value of this
test.56,60 Situations where intra-abdominal pressure increases
can increase the false-positive rate of this test (obesity, trauma,
laparostomized patients), and finally, it requires validation in
patients with myocardial dysfunction.106
Group III
This group includes CVP variation, end-expiratory occlusion
(EEO) tests, PLR tests, respiratory systolic variation tests,
changes in end-tidal CO 2 (ETCO 2 ), and the mini-fluid
challenge.
Variability in CVP. Magder et al explored whether a dynamic
response of CVP could predict intravenous fluid therapy
responsiveness. They determined that a decrease in CVP 1
mm Hg on inspiration predicts intravenous fluid therapy
responsiveness with a positive predictive value of 77% to
84% and a negative predictive value of 81% to 93% in patients
with spontaneous breathing.41 However, Heenen et al in studies
carried out with 21 intensive care unit patients with different
pathologies found that only in 3 patients CVP did not diminish
during inspiration, and one of them responded to intravenous
fluid therapy (negative predictive value 66%). Of the 18
patients, 8 had a decrease of 1 mm Hg in CVP during inspira-
tion and responded to therapy (positive predictive value of
44%); therefore, it was concluded that variability in CVP does
not predict intravenous fluid therapy responsiveness.78
End-expiratory occlusion test. During inspiration in mechanical
ventilation, the right ventricular preload decreases. Therefore,
an EEO test, consisting of the suspension of mechanical venti-
lation at the end of expiration for a duration of 15 seconds,
should increase right ventricular preload and, if the patient is
preload dependent, also SV. Monnet et al showed that an
increase in PP (as a surrogate for SV) or CI of more than 5%
during the test predicted fluid response with a sensitivity of
87% and a specificity of 100%, with areas under the ROC curve
of 0.95.42 Moreover, this study was conducted in patients under
assist–control mode ventilation and in patients with arrhyth-
mia, so EEO could be useful even during spontaneous mechan-
ical ventilation or in patients with atrial fibrillation.
Furthermore, EEO tests can detect hypovolemia regardless of
whether PEEP is used.107 In patients with a lung compliance of
less than 30 mL/cm H2O, the EEO test was better than PPV for
predicting intravenous fluid therapy responsiveness.58 On the
other hand, Guinot et al were unable to find such similar results
in surgical patients.108 For this reason, the usefulness of the
EEO test should be assessed in patients with right-sided heart
7
failure, intra-abdominal hypertension, and ventricular
interdependence.
Respiratory systolic variation test. This is a technique where intu-
bated and sedated patients undergo pressure-controlled ventila-
tion. Then, 4 successive respiratory cycles with a progressive
increase in inspiratory pressure of 5, 10, 15, and 20 cm H2O are
produced. These values are compared with corresponding min-
imum invasive systolic pressures, and a slope is drawn between
the first and fourth cycles. Perel et al found high levels of
respiratory systolic variation in responding patients, which was
a better relationship with CI than EDAi, PAoP, and CVP. The
CI change percentage correlates with decrease in systolic blood
pressure variation after intravenous fluid therapy (r ¼ .748).
The area under the ROC curve of the test was 0.896. Values
0.24 mm Hg/cm H2O predict CI increase of 15% approxi-
mately, with a sensitivity of 87.5% and a specificity of 83%.43
Preisman et al found an appropriate relationship with SVI (r ¼
.7). Additionally, systolic respiratory variation values higher
than 0.51 mm Hg/cm H2O predict intravenous fluid therapy
responsiveness with a sensitivity of 93%, specificity of 89%,
and area under the ROC curve of 0.96.44
Passive leg raising test. This is a reversible test that simulates a
transient infusion of fluids by displacing the blood flow from
the lower limbs and abdominal compartment toward the
intrathoracic compartment. This test mobilizes on average
300 mL of blood from the lower limbs,109 and 450 mL on
average if the test starts in a semi-sitting position.110 This sud-
den increase in cardiac preload will be translated to a signifi-
cant increase in SV if the patient is fluid responsive. Therefore,
the PLR mimics the response to a transient, reversible, and
small infusion. Boulain et al were the first to report the useful-
ness of the PLR to test fluid responsiveness.111
Importantly, PLR requires a rapid method for measuring CO
or SV, so methods such as the thermodilution are not suitable.
Lafanechère et al conducted the PLR and measured CO
changes using an esophageal Doppler; they established that
an increase in aortic blood flow 8% during a PLR predicted
the fluid responsiveness with a sensitivity of 90% and a speci-
ficity of 82%.45 Monnet et al observed that in 31 patients with
spontaneous breathing activity and/or arrhythmias, the PLR
predicted fluid responsiveness with a sensitivity of 97% and
a specificity of 94%.70 Lamia et al showed that an increase in
SV or velocity time index (VTI) measured by transthoracic
echocardiography during the PLR predicts response to fluids
in nonintubated patients,112 and similar results were found by
Préau et al in patients with sepsis and pancreatitis.113
Nonetheless, this test has some limitations that must be
taken into account. For instance, in patients with intra-
abdominal hypertension, the PLR could show a false-
negative response. Mahjoub et al demonstrated that patients
with intra-abdominal pressure 16 mm Hg have a false-
negative rate of 48%.76 Another important limitation is that
to measure SV by transthoracic echocardiogram and transeso-
phageal echocardiogram, aortic diameter is required. Also, to
8 Journal of Intensive Care Medicine XX(X)
measure aortic area, aortic diameter can be changed by increas-
ing the SV,114 and as some esophageal devices display constant
aortic diameter, the false-negative rate may increase and
response to fluids could be underestimated.115
Valsalva maneuver. This is an expiration against a closed glottis
which abruptly reduces venous return by increasing intrathor-
acic pressure and decreases left ventricular SV and PP if the
patient is preload dependent. The Valsalva maneuver, similar
to the PLR, is a reversible and transient “preload challenge.”
Monge Garcı́a and colleagues conducted a study in 30 patients
under spontaneous ventilation and sinus rhythm; the PPV and
SPV were measured during a standardized 10-second Valsalva
maneuver of 30 cm H2O before and after administration of
colloids. Since then, it was discovered that a relationship
between PPV and SPV preinfusion values induced for the Val-
salva maneuver and changes induced in the SVI (r2 ¼ .71 and
r2 ¼ .6, respectively). A PPV during a Valsalva maneuver
52% predicted the response to intravenous fluid therapy with
a sensitivity of 91% and a specificity of 95%. They concluded
that changes in blood pressure during the Valsalva maneuver
could help to predict response to intravenous fluid therapy.46
This respiratory maneuver is inexpensive and demands little
time to carry out. However, it requires patient’s cooperation,
and, variables such as age, comorbidities, and heart condition,
could alter the quality of the test.116
Changes in ETCO2. Since the amount of expired CO2 is mainly
determined by pulmonary blood flow (ie, CO), metabolic CO2
production, and alveolar ventilation, changes in ETCO2 should
predominantly reflect variations in pulmonary blood flow and
thus, indirectly, changes in CO, if patients are in stable respira-
tory and metabolic conditions. Exhaled CO2 can be measured
at the end of exhalation (ETCO2) or per minute (VCO2).
Monge Garcı́a et al studied 37 mechanically ventilated patients
with acute circulatory failure and observed that an increase in
ETCO2  4% during a PLR test predicted an increase in CO 
15% after fluid administration, with adequate relation between
changes in CO and changes in ETCO2 secondary to a PLR test
(r2 ¼ .79), with a sensitivity of 90.5% and a specificity of
93.7%.47 Similar results were found by Monnet et al using a
different methodology. They discovered that a PLR-induced
increase in ETCO2  5% predicted a fluid responsiveness with
a sensitivity of 71% and a specificity of 100%, and a significant
correlation was found between the changes in CI induced by
fluid administration and the changes in ETCO2 induced by the
PLR test (r ¼ .79), with adequacy area under the ROC curve
(ROC ¼ 0.93).117 Tusman et al observed in surgical patients
under controlled mechanical ventilation that a decrease of
VCO2 secondary to application of PEEP predicts response to
intravenous fluid therapy. Changes in the CO after administra-
tion of intravenous fluids correlate with decreased VCO2 sec-
ondary to application of PEEP prior to the administration of
intravenous fluids (r2 ¼ .71). However, they found that there
was not enough value for predicting therapy responsiveness
with this maneuver.48 Measurement of CO2 is a simple way
for predicting fluid responsiveness; it can be found in most of
operating rooms and intensive care units, and furthermore, it is
less expensive than other monitoring tools.
Mini-Fluid Challenge
This maneuver can be used in medical conditions that make it
impossible to use the PLR test, such as intracranial hyperten-
sion, brain trauma, brain stroke, deep vein thrombosis, lower
limb or pelvis fracture, and lower limb amputation, as well as to
avoid the deleterious effects of an unnecessary fluid challenge.
This maneuver consists of administering 100 mL of colloid or
crystalloid over 1 minute; there are different methods that can
be used to see results with this maneuver. Muller et al were the
first to describe this maneuver; they administered to 39 sedated
patients, who were mechanically ventilated and had acute cir-
culatory failure, without spontaneous breathing, first 100 mL
over 1 minute. After measuring the subaortic VTI with trans-
thoracic echocardiography at 1 minute, they then infused 400
mL at a constant rate over 14 minutes. This fluid challenge was
performed with a 6% hydroxyethyl starch 130/0.4. They dis-
covered a 10% increase in VTI after rapid infusion of 100 mL
of hydroxyethyl starch accurately predicted a 15% increase in
VTI after 500 mL infusion (a surrogate for SV), with a sensi-
tivity of 95%, a specificity of 78%, positive predictive value of
0.83, and negative predictive value of 0.93. A correlation
between VTI at 1 minute and VTI after 400 mL of colloid was
good (r ¼ .81).49 Guinot et al studied 34 patients under spinal
anesthesia and spontaneous breathing; while monitored with
impedance cardiography, they measured hemodynamic vari-
ables before and after fluid challenge with 100 mL of crystal-
loid, and before and after volume expansion. They were
defined responders like those who increase in SAP  15%;
they found the SV variation in response to mini-fluid challenge
predicted the increase in SAP. The cutoff value was 5%, with a
sensitivity of 100%, specificity of 71%, positive predictive
value of 83%, and negative predictive value of 100%.118 In
another study, these same authors found that in 73 patients with
spontaneous breathing, an increase of 7% in the SV with mini-
fluid challenge predicted fluid responsiveness with an AUC of
0.93, a sensitivity and specificity of 89%, a positive predictive
value of 83%, and a negative predictive value 93%.119 Xiao-
ting et al explored the value of ETCO2 in replacing the CI for
evaluating fluid responsiveness during the PLR test and mini-
fluid challenge. They found that in 48 patients with sepsis,
changes in ETCO2  5% during the PLR test predicted fluid
responsiveness with 75.8% sensitivity and 93.4% specificity
but did not find similar results with mini-fluid challenge; the
changes in ETCO2  3% with the mini-fluid challenge pre-
dicted fluid responsiveness with 33.3% sensitivity and 93.4%
specificity.120 This study has some limitations, for example, CI
was measured using a PiCCO device, this has 2 methods to
determine CI: pulse contour method and transpulmonary ther-
modilution technique. In this study, it is clear which method
they used. For example, if they were using the transpulmonary
thermodilution technique, this technique is not fast enough to
Alvarado Sánchez et al
detect changes with the mini-fluid challenge or PLR test. Sec-
ond, there are discrepancies between PP contour and transpul-
monary thermodilution techniques, especially after fluid
challenges or alterations in norepinephrine infusion rates.
Therefore, PP contour should be recalibrated after fluid chal-
lenge, and in this study, it is not clear whether it was recali-
brated after the fluid challenge.121,122 Mallat et al studied 49
patients who were mechanically ventilated (tidal volume <8
mL kg1 of ideal weight) and had circulatory failure, but not
cardiac arrhythmias. They measured hemodynamic variables
before and after 100 mL of colloid infusion during 1 minute
and then after the additional infusion of 400 mL during 14
minutes. They found that a reduction in PPV and SVV after
the mini-fluid challenge predicted fluid responsiveness; a
reduction of 2% in SVV and PPV predicted fluid responsive-
ness with a sensitivity of 86% and specificity of 89% and 85%,
respectively. The AUCs for PPV and SVV were excellent (0.91
and 0.92, respectively). Also, they found a small gray zone,
which included between 8% and 12% of patients.123
Since the aim of fluid resuscitation is to achieve an adequate
CO and sufficient MAP in order to maintain tissue oxygena-
tion, in patients with hypotension, it becomes important not
only to determine fluid responsiveness but also to determine
whether arterial pressure will also improve with fluids. How-
ever, the response of arterial pressure to fluid administration is
not easily predictable, because arterial pressure is the result of
interactions between blood ejected by the heart and the arterial
system. Therefore, even if a patient is able to increase CO with
fluids, MAP will also change, depending on the arterial system.
Recognition of patients who require intravenous fluid ther-
apy and its administration is only possible in patients with
tisular hypoperfusion. Rivers et al found that therapy aimed
at restoring venous saturation, reduction of lactate, and increase
of MAP above 65 mm Hg reduced early mortality.124 Admin-
istration of intravenous fluids in patients with circulatory fail-
ure does not imply an increase in MAP; this factor just could be
predicted whether arterial tone was known.
Arterial elastance is defined as the relationship between PP
and SV. On the basis of the functional hemodynamic concept,
Pinsky described dynamic arterial elastance (Eadyn) as the
relationship between PPV and SVV. He proposed that patients
with an adequate arterial tone should exhibit an Eadyn between
0.8 and 1.2. Values below 0.8 imply that patient has low arterial
pressure and, that consequently, intravenous fluid therapy
would not increase MAP, even if CO does. Instead, a value
above 0.8 implies that MAP, along with CO, will increase after
intravenous fluid administration125 (see Figure 3).
Monge Garcia et al have demonstrated the usefulness of this
concept in critically ill patients with hypotension having acute
circulatory failure. They found that in 25 patients, an Eadyn
value 0.89 predicted the MAP response after intravenous
fluid administration with a sensitivity of 94% and a specificity
of 100. Additionally, volume expansion–induced increases in
MAP were strongly correlated with baseline Eadyn (r2 ¼ .83)
and an adequate area under curve (r2 ¼ .83).127 However,
because both SVV and PPV were obtained from PP analysis,
9
Figure 3. Algorithm showing how to manage patients with hemo-
dynamic instability based on predictors of intravenous fluid respon-
siveness and dynamic arterial elastance. Adapted from Pinsky.126
a mathematical coupling factor could not be excluded. More
recently, the same group corroborated their previous findings in
a larger population using 2 independent biological signals:
SVV from esophageal Doppler and PPV obtained from an
arterial line. They found that an Eadyn  0.73 predicted a
subsequent 10% MAP increase with a sensitivity of 90.9% and
a specificity of 91.5% (AUC ¼ 0.94).128 Moreover, the useful-
ness of Eadyn for predicting arterial response after fluid admin-
istration has been recently demonstrated even in spontaneously
breathing patients. In this way, Cecconi et al showed in 26
patients that an Eadyn  1.06 allowed to discriminate
preload-dependent patients with spontaneous ventilation and
positive pressure response (MAP increase 10%) after intra-
venous fluid therapy, with a sensitivity and specificity of 88.2%
and area under the ROC curve of 0.92.129 Moreover, Eadyn has
shown to be also useful for predicting MAP decrease after
reducing vasopressor support in patients with sepsis or surgical
patients.130,131 However, although the theoretical basis of
Eadyn now seems well established, further studies are required
before its implementation in future hemodynamic resuscitation
protocols.
Conclusions
Dynamic preload indicators predict intravenous fluid therapy
responsiveness better than static preload indicators. The
increase in CO does not guarantee a proportional increase in
MAP. In this regard, Eadyn may be helpful in predicting
MAP increase in preload-dependent patients after fluid
administration.
Authors’ Note
JIAS was a great help in regard to the design, analysis, interpretation,
and writing process of this work. Furthermore, this author agrees with
all aspects of the publication and finally approved the final version to
10
be published. WFAZ collaborated in the conception of the work, in the
acquisition of reference articles, analysis of these, and writing. In
addition, this author approved the final version to be published and
agrees with all aspects of work. MIMG collaborated in the analysis,
interpretation, and writing process of this work. This author approved
the final version to be published; also, he agrees with all aspects of
work.
Declaration of Conflicting Interests
The author(s) declared the following potential conflicts of interest
with respect to the research, authorship, and/or publication of this
article: Manuel Ignacio Monge Garcia has received honoraria and/or
travel expenses from Edwards Lifesciences and Deltex Medical.
Funding
The author(s) received no financial support for the research, author-
ship, and/or publication of this article.
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