Stroke Volume Variation For Prediction of Fluid Responsiveness in Patients Undergoing Gastrointestinal Surgery

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Int. J. Med. Sci. 2013, Vol.

10 148

Ivyspring
International Publisher
International Journal of Medical Sciences
2013; 10(2):148-155. doi: 10.7150/ijms.5293
Research Paper

Stroke Volume Variation for Prediction of Fluid


Responsiveness in Patients Undergoing Gastrointestinal
Surgery
Cheng Li1#, Fu-qing Lin1#, Shu-kun Fu1, Guo-qiang Chen1, Xiao-hu Yang1, Chun-yan Zhu1, Li-jun Zhang2,
Quan Li1 
1. Department of Anesthesiology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, China.
2. Department of Anesthesiology, No.187 Hospital of PLA, Haikou, China.
#Contributed equally.

 Corresponding author: Quan Li, Ph.D., M.D., 301 Yanchang Middle Rd, Shanghai 200072, China. Tel.: 86-21-66307531; Fax:
86-21-66301082; E-mail: [email protected]; [email protected].

© Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/
licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.

Received: 2012.09.25; Accepted: 2012.12.24; Published: 2013.01.03

Abstract
Background: Stroke volume variation (SVV) has been shown to be a reliable predictor of
fluid responsiveness. However, the predictive role of SVV measured by FloTrac/Vigileo sys-
tem in prediction of fluid responsiveness was unproven in patients undergoing ventilation with
low tidal volume. Methods: Fifty patients undergoing elective gastrointestinal surgery were
randomly divided into two groups: Group C [n1=20, tidal volume (Vt) = 8 ml/kg, frequency (F)
= 12/min] and Group L [n2=30, Vt= 6 ml/kg, F=16/min]. After anesthesia induction, 6% hy-
droxyethyl starch130/0.4 solution (7 ml/kg) was intravenously transfused. Besides standard
haemodynamic monitoring, SVV, cardiac output, cardiac index (CI), stroke volume (SV),
stroke volume index (SVI), systemic vascular resistance (SVR) and systemic vascular re-
sistance index (SVRI) were determined with the FloTrac/Vigileo system before and after fluid
loading. Results: After fluid loading, the MAP, CVP, SVI and CI increased significantly,
whereas the SVV and SVR decreased markedly in both groups. SVI was significantly correlated
to the SVV, CVP but not the HR, MAP and SVR. SVI was significantly correlated to the SVV
before fluid loading (Group C: r = 0.909; Group L: r = 0.758) but not the HR, MAP, CVP and
SVR before fluid loading. The largest area under the ROC curve (AUC) was found for SVV
(Group C, 0.852; Group L, 0.814), and the AUC for other preloading indices in two groups
ranged from 0.324 to 0.460. Conclusion: SVV measured by FloTrac/Vigileo system can
predict fluid responsiveness in patients undergoing ventilation with low tidal volumes during
gastrointestinal surgery.
Key words: Stroke volume variation; tidal volume, Functional haemodynamic, Fluid balance,
Gastrointestinal surgery.

Introduction
Precise assessment of volume state is a prereq- clusion pressure (PAOP), intrathoracic blood volume
uisite for adequate volume replacement which may index (ITBI) and left ventricular end-diastolic area
achieve optimal organ perfusion and oxygen supply. index (LVEDAI) often fail to provide reliable infor-
Frequently used standard preload indexes, such as mation and usually predict fluid responsiveness with
central venous pressure (CVP), pulmonary artery oc- conflicting results [1-4]. As an alternative to these static

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Int. J. Med. Sci. 2013, Vol. 10 149

variables, assessment of stroke volume variation FloTrac/Vigileo system by analyzing the arterial
(SVV) has been used as a indicator for haemodynamic pulse wave following semi-invasive arterial catheter-
monitoring to predict fluid responsiveness in patients ization without pulmonary artery catheterization or
receiving mechanical ventilation [4-11]. calibration with another method, which can monitor
Recently, arterial pulse waveform analysis has CO, CI, SV, SVI and SVV. With a CVP catheter, its
been proposed for monitoring of cardiac output (CO) signal may be interfaced with the Vigileo, allowing for
and SVV (FloTrac/Vigileo; Edwards Lifesciences, the calculation of SVR and SVRI. When used with a
Irvine, CA, USA) [12-15]. The accuracy and reliability of central venous oximetry catheter, the Vigileo also
CO has been evaluated [16, 17], while the accuracy and provides continuous central venous oxygen satura-
clinical applicability of SVV measured with this sys- tion [15].
tem have not been fully evaluated [18-25]. The present The system calculates the arterial pressure using
study was performed to investigate the value of SVV the arterial pulsatility (stand deviation of pressure
in predicting fluid responsiveness in patients receiv- wave over a 20-s interval), resistance and compliance,
ing gastrointestinal surgery in the presence of venti- according to the following general equation:
lation with intermittent positive-pressure ventilation SV=K×Pulsatility, where K is a constant quantifying
(IPPV) mode, and conventional/low tidal volume. arterial compliance and vascular resistance, and pul-
satility is proportional to the standard deviation of the
Materials and methods arterial wave over a 20-s interval. K is derived from
Patient data patient characteristics (gender, age, height and
weight) according to the method described by
The whole protocol was approved by the insti- Langewouter et al [26], as well as the characteristics of
tutional review board committee of the medical fac- waveform (e.g., skewness and kurtosis of individual
ulty of Tenth People`s Hospital of Tongji University, waves). This calibration constant is recalculated every
and written informed consent was obtained from each minute.
patient before study. ASA I-II patients (n=50) aged SVV represents the variation (as a percentage) of
30-78 years who underwent elective gastrointestinal SV during the ventilation cycle and is assessed with
surgery were recruited into the present study, and following equation: SVV (%) = (maximum
then randomly divided into two groups: conventional SV-minimum SV) / mean SV, where the maximum
tidal volume group (Group C, n1=20) and low tidal and minimum SV are mean values of the four extreme
volume group (Group L, n2=30). Patients with pace- values of SV during a period of 30 s, and the mean SV
makers, history of cardiac arrhythmia, severe periph- is the average value for this time period.
eral vascular disease, cardiac support (intra-aortic
balloon pump), and persisting mitral or aortic dys- Study protocol
function after surgery were excluded. All patients Anaesthesia was induced using midazolam (2
received intramuscular atropine (0.5 mg) and pheno- mg iv.), etomidate (0.1-0.3 mg/kg iv.), fentanyl (3
barbital sodium (0.1 g) at 30 min before surgery. μg/kg iv.), and atracurium (0.6-0.8 mg/kg iv.); that
Haemodynamic monitoring was maintained with propofol (1-3 μg/ml plasma
target controlled infusion), remifentanyl (0.1-0.3
Routine haemodynamic monitoring was per- μg/kg/min, iv.), sevoflurane (1-3% inhalation), fen-
formed to measure the heart rate (HR), pulse oxime- tanyl and atracurium (0.3 mg/kg iv.). Following en-
try, electrocardiograph, and arterial blood pressure. dotracheal intubation, all patients received mechani-
Before anaesthesia induction, the left radial artery was cal ventilation with IPPV mode [Group C: tidal vol-
cannulated with a 20-G cannula which was connected ume (Vt)=8 ml/kg, frequency (F) = 12/min, positive
to a FloTrac sensor and a Vigileo monitor (software end expiratory pressure (PEEP) = 0, fractional in-
version 3.06) for continuous monitoring of CO, car- spired oxygen (FiO2) = 0.8, oxygen flow = 2.0 L/min;
diac index (CI) , stroke volume (SV), stroke volume Group L: Vt =6 ml/kg, F=16/min, PEEP = 0, FiO2 =
index (SVI), SVV, systemic vascular resistance (SVR) 0.8, oxygen flow = 2.0 l/min]. Mechanical ventilation
and systemic vascular resistance index (SVRI). After was maintained with an endexpiratory Pco2 at 35-45
anaesthesia induction, a 7.5-F central venous catheter mmHg, peak airway pressure of < 15 cmH2O and
was introduced via right internal jugular vein for pulse oximetry ranging from 98-100%. Bispectral in-
measuring the central venous pressure (CVP). All dex was monitored with the Aspect2000 Monitor
invasive cannulations were performed under local (Aspect Company, America) and ranged from 45 to
analgesia with 1% lidocaine. 55.
Continuous CO was acquired with the Baseline haemodynamic measurements were

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Int. J. Med. Sci. 2013, Vol. 10 150

recorded 10 min after endotracheal intubation. On P=0.004) and SVV (Group C, r=0.843, P=0.000; Group
completion of baseline measurements and prior to L, r=0.742, P=0.000) correlated significantly to ∆SVI,
any surgical intervention, volume replacement was but ∆HR, ∆MAP and ∆SVR had no relationship with
performed with 6% hydroxyethyl starch solution ∆SVI in both groups. SVV before fluid load correlated
(mean molecular weight, 130,000 d/mean degree of significantly to ∆SVI (Group C, r=0.909, P=0.000;
substitution, 0.4; Voluven; Fresenius Kabi; Beijing, Group L, r=0.758, P=0.000), but HR, MAP, CVP and
China) at 7 ml/kg in 30 min. All haemodynamic SVR before fluid load were not related to the ∆SVI in
measurements were re-detected immediately. Blood both groups (Table 3). Results of ROC curve analysis
gas analysis was done during the study period, and are summarized in Table 4, Figure 1 and Figure 2.
red blood cells were transfused to keep hematocrit no The largest AUC was found for SVV (Group C,
less than 90 g/L if necessary. 0.852; Group L, 0.814) as compared to the HR, MAP,
CVP and SVR. The optimal threshold value for SVV
Data Analysis
calculated by the ROC analysis was 9.5%: in patients
All haemodynamic variables were recorded as with SVV of 12.5% at baseline, a SVI increase of ≥25%
mean of three repeated measurements. Body surface as a response to subsequent fluid replacement could
area was calculated with the “du Bois formula” (body be expected with a sensitivity of 100% and a specific-
surface area=body weight [kilograms]0.425× body ity of 57.1% in Group C. In group L, the sensitivity
length [centimeters]0.725×71.84) [27]. Statistical analysis and specificity was 91.3% and 71.4%, respectively.
was performed using SPSS version 13.0 (SPSS; Chi-
cago, IL). A student t test was used for comparison of
haemodynamic data before and after fluid infusion. A Table 1. Biometric variables of patients in both groups at
Pearson`s correlation analysis was employed for baseline.
evaluate the correlation between SVI and other hae- Variable Group C (n=20) Group L (n=30) P
modynamic variables. Prediction of fluid respon- Age (yr) 61±14 62±12 0.487
siveness with SVV and standard preload indexes was Male/female 15/5 21/9
tested by calculating the area under the receiver op- Height (cm) 165±7 164±9 0.695
erating characteristic (ROC) curve (AUC) for a SVI
Weight (kg) 62±13 63±11 0.994
increase of ≥ 25% (AUC =0.5: no predictive value;
Body surface (m2) 1.72±0.20 1.72±0.20 0.993
AUC = 1.0: best predictive value). Furthermore, re-
P<0.05 between two groups.
gression analysis was performed for preload variables
and SVI related to the fluid infusion. A value of
P<0.05 was considered statistically significant. Unless Table 2. Haemodynamic variables in two groups.
otherwise stated, data are presented as mean ±
standard deviation (SD). Variable Group Before fluid After fluid P
load load

Results MAP Group C 69.7±10.2 87.1±12.2 P<0.001


(mm Hg) Group L 69.6±6.2 84.0±10.3 P<0.001
None withdraw from the study. Biometric vari-
HR Group C 60.0±6.0 61.5±5.3 P=0.391
ables were comparable between two groups (Table 1). (beat/min) Group L 61.0±6.1 61.4±5.2 P=0.682
Volume replacement resulted in significant changes in
CVP Group C 3.2±0.9 5.4±1.3 P<0.001
all haemodynamic variables except HR: MAP, CVP, (mm Hg) Group L 3.3±1.1 5.5±1.4 P<0.001
SVI and CI increased, whereas SVRI and SVV de-
SVI Group C 37.2±3.8 49.8±7.0 P<0.001
creased. There were no significant differences in (ml/m2) Group L 34.3±4.3 46.3±6.1 P<0.001
haemodynamic variables between two groups (Table
CI Group C 2.4±0.3 3.0±0.3 P<0.001
2).
(L/min/m2) Group L 2.3±0.3 2.9±0.3 P<0.001
In Group C, the mean increase in SVI as a result
of volume loading was 34±19%, and 14 patients (75%) SVRI Group C 2476±485 2218.2±258 P=0.043
(dyn s/cm5/m2) Group L 2394±433 2123±333 P=0.009
had a SVI increase of ≥25% (mean, 44±13%). In 5 pa-
tients (25%), a SVI increase of ≤25% was observed SVV Group C 12.3±3.0 6.3±1.5 P<0.001
(%) Group L 11.7±2.8 6.0±1.3 P<0.001
(mean, 18±2%). In Group L, the mean increase in SVI
as a result of volume loading was 33±17%, and 24 P value: before fluid load vs after fluid load. MAP=mean arterial pressure;
HR=heart rate; CVP=central venous pressure; SVI=stroke volume index;
patients (80%) had a SVI increase of ≥25% (mean, CI=cardiac index; SVRI=systemic vascular resistance index; SVV=stroke
38±14%). In 6 patients (20%), a SVI increase of ≤25% volume variation.
was observed (mean, 13±4%). Percentage change (∆)
in CVP (Group C, r=0.608, P=0.001; Group L, r=0.578,

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Int. J. Med. Sci. 2013, Vol. 10 151

Table 3. Pearson correlation analysis of haemodynamic variables before fluid load, changes in baseline haemodynamic
variables and changes in SVI.
Variable Group MAP HR CVP SVR SVV ∆MAP ∆HR ∆CVP ∆SVR ∆SVV
r Group C -0.175 -0.213 -0.071 -0.061 0.909 0.391 -0.109 0.608 0.276 0.843
P 0.461 0.367 0.765 0.800 0.000 0.088 0.646 0.001 0.238 0.000
r Group L -0.091 -0.091 -0.049 -0.145 0.758 0.297 0.067 0.578 0.112 0.742
P 0.631 0.631 0.798 0.445 0.000 0.111 0.725 0.004 0.557 0.000
∆= percentage changes following fluid replacement therapy.

Table 4. ROC for predicting ∆SVI of ≥25%.


Variable Group L Group C
AUC 95%CI SE AUC 95%CI SE
HR 0.441 0.122~0.760 0.163 0.440 0.155~0.724 0.145
MAP 0.407 0.129~0.685 0.142 0.324 0.087~0.561 0.121
CVP 0.404 0.135~0.672 0.137 0.429 0.173~0.684 0.130
SVR 0.460 0.189~0.731 0.084 0.324 0.085~0.563 0.122
SVV 0.814 0.590~1.038 0.114 0.852 0.603~1.101 0.127

Figure 1. Receiver operating characteristic curve of SVV, CVP, MAP, SVR and HR in Group C.

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Int. J. Med. Sci. 2013, Vol. 10 152

Figure 2. Receiver operating characteristic curve of SVV, CVP, MAP, SVR and HR in Group L.

PiCCO system and FloTrac/Vigileo system. PiCCO


Discussion system, which requires transpulmonary thermodilu-
SVV measured by FloTrac/Vigileo system was tion [29], is invasive and requires the venous access and
comparable predictor of changes in SVI following balloon flotation of the catheter through the right side.
volume replacement therapy in patients receiving Accordingly, there are complications associated with
gastrointestinal surgery in the presence of ventilation detection with this system, and some are even fatal
[30-32]. Furthermore, this system requires an elaborate
with conventional tidal volume and was a predictor of
fluid response in these patients undergoing ventila- protocol for intermittent injections into the pulmonary
tion with low tidal volume. The conventional static artery catheter for thermodilution. FloTrac/Vigileo
preload variables assessed in this study, such as CVP, system based on analysis of the systemic arterial wave
failed to predict the fluid responsiveness. is a semi-invasive method, and does not require
To maintain the best volume state is one of im- pulmonary artery catherization or calibration with
portant factors to keep favorable organ perfusion and another method.
provide optimal oxygen supply, the precondition of SVV used for haemodynamic monitoring to
which is to evaluate and predict the volume state ac- guide the fluid supplement in patients receiving me-
curately. Transoesophageal echocardiography has chanical ventilation is based on the heart-lung inter-
been used to evaluate the cardiac function and vol- actions during the mechanical ventilation [33-36]. Res-
ume state [28], but it is expensive, complicate and dif- piratory-induced changes in the left ventricular pre-
ficult to operate and unable to continuously monitor. load result in cyclic changes in the left ventricular SV
Variables, such as blood pressure and urine volume, and arterial pressure. In the presence of hypovolae-
are insensitive because of the influence of vasoactive mia, the left ventricle usually operates on the as-
agents and diuretics. CVP and PAWP can only eval- cending part of the Frank-Starling curve. Thus,
uate volume state indirectly. These variables are often changes in the SV should be more pronounced when
influenced by the general anesthesia agents and vas- compared with that at normovolemia. SVV and the
oactive agents. Thus, it is imperative to develop a surrogate variables systolic pressure variation (SPV)
variable which can evaluate the volume state of pa- and pulse pressure variation (PPV) have been studied
tients easily and accurately. previously in patients receiving brain surgery, criti-
At present, SVV can be monitored with the cally ill patients after cardiac surgery and those suf-

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Int. J. Med. Sci. 2013, Vol. 10 153

fering from septic shock [5-8]. SVV, SPV and PPV are study, tidal volume was set at 6 ml/kg in the IPPV
highly sensitive in predicting the fluid responsiveness mode, and whether SVV can predict the fluid respon-
under these conditions. Thus, dynamic preload vari- siveness was evaluated under this condition in pa-
ables were considered to be important in guiding the tients receiving gastrointestinal surgery, which is
fluid and catecholamine therapy in critically ill pa- more clinically important than the conventional tidal
tients. volume. Results showed that the changes in SVI were
However, SVV depends not only on the cardiac significantly correlated to the changes in SVV and
filling status but the changes in intrathoracic pressure CVP when the ventilation was performed with low
associated with the tidal volume [37, 38]. It has been tidal volume, whereas the changes in SVI were not
demonstrated that accurate prediction of fluid re- related to the changes in HR, MAP and SVR. Changes
sponsiveness by SVV is feasible when tidal volume is in SVI were significantly correlated to SVV before
10-15 ml/kg [5-7]. In contrast, Wiesenack and col- volume replacement, while no relationship was found
leagues did not find the predictive value of SVV in between the changes in SVI and HR, MAP, CVP and
patients receiving cardiac surgery in the presence of SVR before volume replacement under this condition.
ventilation with tidal volume of 10 ml/kg in a study There was no statistical difference compared with
on the volume challenge with colloid solutions [39]. Group C. The ROC suggested that SVV was a better
However, the interpretation of these results is difficult variable for the evaluation of volume state than HR,
as variables reflecting baseline cardiac preload, such MAP, CVP and SVR. SVV of 9.5% or higher could
as ITBI and LVEDAI, and the degree of hypovolae- predict a SVI increase of ≥25% as a response to vol-
mia, were not given [39]. In addition, there was rela- ume replacement with a sensitivity of 91.3% and a
tively wide variation in baseline SVV, suggesting a specificity of 71.4%. These findings were similar to
heterogeneous patient population. However, it re- those in the study of Rex and colleagues in which
mained unclear whether SVV was a reliable predictor PiCCO system was also used for monitoring [11].
of fluid responsiveness during mechanical ventilation The normal range of SVV under controlled ven-
with low tidal volume. tilation is less than 10-13%. With respect to the use of
In the present study, the role of SVV measured SVV assessed by FloTrac/Vigileo system to guide the
by FloTrac/Vigileo system in prediction of fluid re- fluid therapy, the following factors and limitations
sponsiveness was first evaluated in patients receiving have to be emphasized: 1) Mechanical ventilation:
gastrointestinal surgery in the presence of ventilation only patients mechanically ventilated in fixed respir-
with IPPV and conventional tidal volumes (8 ml/kg). atory frequency and tidal volume of ≥6 ml/kg can use
Results suggest that the changes in SVI were signifi- SVV. It is infeasible for patients with spontaneous
cantly correlated with the changes in SVV and CVP, breath or irregular tidal volume. 2) PEEP: SVV will
while the changes in SVI were not related to the increase with the increase in PEEP. 3) Airway pres-
changes in HR, MAP and SVR. Changes in SVI were sure and intrathoracic pressure. 4) Arrhythmias: the
significantly correlated to the SVV before volume re- occurrence of arrhythmias or alterations of myocardi-
placement, while no correlation was found between al contractility (including that after pharmacologic
the changes in SVI, HR, MAP, CVP, and SVR before treatment) may render these SVV estimates unrelia-
volume replacement. Both CVP and SVV can evaluate ble. 5) Vasoactive agents: Vasoactive agents, espe-
the volume state, but only SVV can predict the fluid cially β-receptor blockers, vasoconstrictors and vaso-
responsiveness under this condition. AUC can reflect dilators, influence SVV significantly. 6) General an-
the diagnostic value of variables [40]. The analysis of esthetics: General anesthetics, such as sevoflurane,
ROC curve suggested that SVV was a better variable propofol, fentanyl, and etomidate, can influence SVV
in the evaluation of volume state than the HR, MAP, via the circulatory inhibition. 7) The interference with
CVP, and SVR. SVV of 9.5% or higher could predict a arterial waveform, surgical operation, artery catheter
SVI increase of ≥25% as a response to volume re- and other during the surgery may influence the ac-
placement with a sensitivity of 100% and a specificity curacy of SVV. Thus, in fully sedated patients with
of 57.1%, which is in accordance with the results from mechanical ventilation, sinus rhythm, or pacing in a
the PiCCO system [9-11,41]. fixed mode and unchanged catecholamine manage-
Mechanical ventilation is a basic way for oxygen ment are prerequisites for proper use of this haemo-
supply under the general anesthesia, but it may cause dynamic monitoring tool.
ventilation induced lung injury (VILI). Ventilation Some limitations of this study have to be ad-
with low tidal volume is one of important methods to dressed. First, the assessment of SVV with
avoid or reduce VILI [42]. The normal tidal volume of FloTrac/Vigileo system has not yet been proven by
mammalians is 6.3 ml/kg [43]. Thus, in the present direct comparison with other techniques. However,

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Int. J. Med. Sci. 2013, Vol. 10 154

our findings are strongly supported by some studies 10. Hofer CK, Müller SM, Furrer L, Klaghofer R, Genoni M, Zollinger A.
Stroke volume and pulse pressure variation for prediction of fluid re-
in which SVV was assessed with PiCCO system and sponsiveness in patients undergoing off-pump coronary artery bypass
found to be a favorable predictor of fluid respon- grafting. Chest. 2005; 128: 848-54.
11. Rex S, Brose S, Metzelder S, Hüneke R, Schälte G, Autschbach R,
siveness [9-11, 41]. Second, our patients were hypovo- Rossaint R, Buhre W. Prediction of fluid responsiveness in patients
lemic at baseline because of pre-operative fasting, during cardiac surgery. Br J Anaesth. 2004, 93: 782-8.
12. Sander M, Spies CD, Grubitzsch H, Foer A, Müller M, von Heymann C.
gastrointestinal preparations and application of gen- Comparison of uncalibrated arterial waveform analysis in cardiac sur-
eral anesthetics. The predictive value of SVV was not gery patients with thermodilution cardiac output measurements. Crit
evaluated in normovolemic or even hypervolemic Care. 2006; 10: Rl64.
13. Penttila J, Snapir A, Kentala E, Koskenvuo J, Posti J, Scheinin M, Scheinin
patients with SVV within or below the normal range. H, Kuusela T. Estimation of cardiac output in a pharmacological trial
However, it seems likely that the present setting is using a simple method based on arterial blood pressure signal wave-
form: a comparison with pulmonary thermodilution and echocardio-
close to most common clinical situations, with graphic methods. Eur J Clin Pharmacol. 2006; 62: 401-7.
hypovolemia as the major cause of arterial hypoten- 14. Opdam HI, Wan L, Bellomo R. A pilot assessment of the FloTrac cardiac
output monitoring system. Intensive Care Med. 2007; 33: 344-9.
sion. Moreover, during measurements and fluid trial, 15. Manecke GR. Edwards FloTrac sensor and Vigileo monitor: easy, accu-
manipulations were not allowed, ie, table-tilting ma- rate, reliable cardiac output assessment using the arterial pulse wave.
neuvers, catheter insertion, or surgical interventions Expert Rev Med Devices. 2005; 2: 523-7.
16. Button D, Weibel L, Reuthebuch O, Genoni M, Zollinger A, Hofer CK.
were strictly avoided. These conditions rarely apply Clinical evaluation of the FloTrac/Vigileo system and two established
to clinical situations, when the decision on fluid re- continuous cardiac output monitoring devices in patients undergoing
cardiac surgery. Br J Anaesth. 2007; 99: 329-36.
placement therapy has to be made. 17. Cannesson M, Attof Y, Rosamel P, Joseph P, Bastien O, Lehot JJ. Com-
In conclusion, SVV assessed with the parison of FloTrac cardiac output monitoring system in patients under-
going coronary artery bypass grafting with pulmonary artery cardiac
FloTrac/Vigileo system shows comparably good output measurements. Eur J Anaesthesiol. 2007; 24: 832-9.
performance in predicting fluid responsiveness in 18. Su BC, Tsai YF, Cheng CW, Yu HP, Yang MW, Lee WC, Lin CC. Stroke
patients receiving gastrointestinal surgery in the volume variation derived by arterial pulse contour analysis is a good
indicator for preload estimation during liver transplantation. Transplant
presence of ventilation with conventional tidal vol- Proc. 2012; 44: 429-32.
ume. Moreover SVV was proved to be a reliable var- 19. Khwannimit B, Bhurayanontachai R. Prediction of fluid responsiveness
in septic shock patients: comparing stroke volume variation by
iable for the prediction of fluid responsiveness in pa- FloTrac/Vigileo and automated pulse pressure variation. Eur J Anaes-
tients receiving gastrointestinal surgery in the pres- thesiol. 2012; 29: 64-9.
20. Zhang Z, Lu B, Sheng X, Jin N. Accuracy of stroke volume variation in
ence of ventilation with low tidal volume. predicting fluid responsiveness: a systematic review and meta-analysis. J
Anesth. 2011; 25: 904-16.
Competing Interests 21. Kungys G, Rose DD, Fleming NW. Stroke volume variation during acute
normovolemic hemodilution. Anesth Analg. 2009; 109: 1823-30.
The authors have declared that no competing 22. Lahner D, Kabon B, Marschalek C, Chiari A, Pestel G, Kaider A,
interest exists. Fleischmann E, Hetz H. Evaluation of stroke volume variation obtained
by arterial pulse contour analysis to predict fluid responsiveness in-

References .
traoperatively. Br J Anaesth 2009; 103: 346-51.
23. Derichard A, Robin E, Tavernier B, Costecalde M, Fleyfel M, Onimus J,
1. Bendjelid K, Romand JA. Fluid responsiveness in mechanically venti- Lebuffe G, Chambon JP, Vallet B. Automated pulse pressure and stroke
lated patients: a review of indices used in intensive care. Intensive Care volume variations from radial artery: evaluation during major ab-
Med. 2003; 29: 352-60. dominal surgery. Br J Anaesth. 2009; 103:678-84.
2. Michard F, Teboul JL. Predicting fluid responsiveness in ICU patients: a 24. de Waal EE, Rex S, Kruitwagen CL, Kalkman CJ, Buhre WF. Stroke
critical analysis of the evidence. Chest. 2002; 121: 2000-8. volume variation obtained with FloTrac/Vigileo fails to predict fluid
3. Reuse C, Vincent JL, Pinsky MR. Measurements of right ventricular responsiveness in coronary artery bypass graft patients. Br J Anaesth.
volumes during fluid challenge. Chest. 1990; 98: 1450-4. 2008; 100: 725-6.
4. Feissel M, Michard F, Mangin I, Ruyer O, Faller JP, Teboul JL. Respira- 25. Hofer CK, Senn A, Weibel L, Zollinger A. Assessment of stroke volume
tory changes in aortic blood velocity as an indicator of fluid respon- variation for prediction of fluid responsiveness using the modified
siveness in ventilated patients with septic shock. Chest. 2001; 119: 867-73. FloTrac and PiCCOplus system. Crit Care. 2008; 12:R82.
5. Berkenstadt H, Margalit N, Hadani M, Friedman Z, Segal E, Villa Y, 26. Langewouters GJ, Wesseling KH, Goedhard WJ. The pressure dependent
Perel A. Stroke volume variation as a predictor of fluid responsiveness in dynamic elasticity of 35 thoracic and 16 abdominal human aortas in vitro
patients undergoing brain surgery. Anesth Analg. 2001; 92: 984-9. described by a five component model. J Biomech. 1985; 18: 613-20.
6. Reuter DA, Felbinger TW, Schmidt C, Kilger E, Goedje O, Lamm P, 27. Du Bois D, Du Bois EF. A formula to estimate the approximate surface
Goetz AE. Stroke volume variations for assessment of cardiac respon- area if height and weight be known.1916. Nutrition. 1989; 5: 303-11.
siveness to volume loading in mechanically ventilated patients after 28. Tousignant CP, Walsh F, Mazer CD. The use of transesophageal echo-
cardiac surgery. Intensive Care Med. 2002; 28: 392-8. cardiography for preload assessment in critically ill patients. Anesth
7. Reuter DA, Kirchner A, Felbinger TW, Weis FC, Kilger E, Lamm P, Goetz Analg. 2000; 90: 351-5.
AE. Usefulness of left ventricular stroke volume variation to assess fluid 29. Della Rocca G, Costa MG, Pompei L, Coccia C, Pietropaoli P.Continuous
responsiveness in patients with reduced cardiac function. Crit Care Med. and intermittent cardiac output measurement: pulmonary artery cathe-
2003; 31: 1399-404. ter versus aortic transpulmonary technique. Br J Anaeth. 2002; 88: 350-6.
8. Marx G, Cope T, McCrossan L, Swaraj S, Cowan C, Mostafa SM, Wen- 30. Bossect T, Schnitt DV, Mohr FW. Pulmonary artery rupture-fatal com-
stone R, Leuwer M. Assessing fluid responsiveness by stroke volume plication of catheter examination (thermodilution catheter). Z. Kardiol.
variation in mechanically ventilated patients with severe sepsis. Eur J 2000; 89: 54.
Anaesthesiol. 2004; 21: 132-8. 31. Abreu AR, Campos MA, Krieger BP. Pulmonary artery rupture induced
9. Liu SQ, Qiu HB, Yang Y, Li JQ, Shen JF. Assessment of stroke volume by a pulmonary artery catheter: a case report and review of the litera-
variation and intrathoracic blood volume index on the responsiveness to ture. J Intensive Care Med. 2004; 19: 291-6.
volume loading in mechanically ventilated canine with hemorrhagic 32. Huang L, Elsharydah A, Nawabi A, Cork RC. Entrapment of pulmonary
shock. Zhonghua Wai Ke Za Zhi. 2006; 44: 1216-9. artery catheter in a suture at the inferior vena cava cannulation site. J
Clin Anesth. 2004; 16: 557-9.

http://www.medsci.org
Int. J. Med. Sci. 2013, Vol. 10 155

33. Morgan BC, Martin WE, Hornbein TF, Crawford EW, Guntheroth WG.
Hemodynamic effects of intermittent positive pressure respiration. An-
esthesiology. 1966; 27: 584-90.
34. Brower R, Wise RA, Hassapoyannes C, Bromberger-Barnea B, Permutt S.
Effect of lung inflation on lung blood volume and pulmonary venous
flow. J Appl Physiol. 1985; 58: 954-63.
35. Taylor RR, Covell JW, Sonnenblick EH, Ross J Jr. Dependence of ven-
tricular distensibility on filling of the opposite ventricle. Am J Physiol.
1967; 213: 711-8.
36. Buda AJ, Pinsky MR, Ingels NB Jr, Daughters GT 2nd, Stinson EB, Al-
derman EL. Effect of intrathoracic pressure on left ventricular perfor-
mance. N Engl J Med. 1979; 301: 453-9.
37. Reuter DA, Bayerlein J, Goepfert MS, Weis FC, Kilger E, Lamm P, Goetz
AE. Influence of tidal volume on left ventricular stroke volume variation
measured by pulse contour analysis in mechanically ventilated patients.
Intensive Care Med. 2003; 29: 476-80.
38. Michard F, Teboul JL, Richard C. Influence of tidal volume on stroke
volume variation. Does it really matter? Intensive Care Med. 2003; 29:
1613.
39. Wiesenack C, Prasser C, Rödig G, Keyl C. Stroke volume variation as an
indicator of fluid responsiveness using pulse contour analysis in me-
chanically ventilated patients. Anesth Analg. 2003; 96: 1254-7.
40. Hanley JA, McNeil BJ. The meaning of use of the area under a receiver
operating characteristic (ROC) curve. Radiology. 1982;143: 29-36.
41. Reuter DA, Goepfert MS, Goresch T, Schmoeckel M, Kilger E, Goetz AE.
Assessing fluid responsiveness during open chest conditions. Br J
Anaesth. 2005; 94: 318-23.
42. Koner O, Celebi S, Balci H, Cetin G, Karaoglu K, Cakar N. Effects of
protective and conventional mechanical ventilation on pulmonary func-
tion and systemic cytokine release after cardiopulmonary bypass. Inten-
sive Care Med. 2004; 30:620-6.
43. Tenney SM, Remmers JE. Comparative quantitative morphology of the
mammalian lung: diffusing area. Nature. 1963;197: 54-6.

http://www.medsci.org

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