Epinefrina

CRITICAL CARE

Third-generation FloTrac/Vigileo does not reliably trackchanges in cardiac output induced by norepinephrinein critically ill patientsX. Monnet1,2*, N. Anguel1,2, M. Jozwiak1,2, C. Richard1,2 and J.-L. Teboul1,2

1 Hopitaux universitaires Paris-Sud, Hopital de Bicetre, service de reanimation medicale, 78, rue du General Leclerc, Le Kremlin-BicetreF-94270, France2 Universite Paris-Sud, Faculte de medecine Paris-Sud, EA 4046, 63, rue Gabriel Peri, Le Kremlin-Bicetre F-94270, France

* Corresponding author. E-mail: [email protected]

Editor’s key points

† FloTrac/Vigileo and otherdevices are available tomeasure cardiac outputby pressure waveformanalysis.

† The performance of thethird-generation FloTrac/Vigileo in measuringcardiac index (CI) wasassessed in critically illpatients undergoingvolume expansionor changes innorepinephrine dose.

† This device wasmoderately reliable fortracking volume-inducedchanges in CI, but poorlyreliable withnorepinephrine dosetitration.

Background. The ability of the third-generation FloTrac/Vigileo software to track changes incardiac index (CI) induced by volume expansion and norepinephrine in critically ill patientsis unknown.

Methods. In subjects with circulatory failure, we administered volume expansion (20subjects) and increased (20 subjects) or decreased (20 subjects) the dose ofnorepinephrine. We measured arterial pressure waveform-derived CI provided by thethird-generation FloTrac/Vigileo device (CIpw) and transpulmonary thermodilution CI (CItd)before and after therapeutic interventions.

Results. Considering the pairs of measurements performed before and after all therapeuticinterventions (n¼60), a bias between the absolute values of CIpw and CItd was 0.26 (0.94)litre min21 m22 and the percentage error was 54%. Changes in CIpw tracked changes in CItd

induced by volume expansion with moderate accuracy [n¼20, bias¼20.11 (0.54) litremin21 m22, r2¼0.26, P¼0.02]. When changes in CItd were induced by norepinephrine(n¼40), a bias between CIpw and CItd was 0.01 (0.41) litre min21 m22 (r2¼0.11, P¼0.04).The concordance rates between changes in CIpw and CItd induced by volume expansionand norepinephrine were 73% and 60%, respectively. The bias between changes in CIpw

and CItd significantly correlated with changes in total systemic vascular resistance(r2¼0.41, P,0.0001).

Conclusions. The third-generation FloTrac/Vigileo device was moderately reliable fortracking changes in CI induced by volume expansion and poorly reliable for trackingchanges in CI induced by norepinephrine.

Keywords: cardiac output, measurement; equipment, monitors; measurement techniques,cardiac output; norepinephrine; shock

Accepted for publication: 24 November 2011

In recent years, efforts have been made to develop devicesthat allow beat-to-beat estimation of cardiac output (CO).Some of these systems compute CO from the arterial pres-sure waveform, using the principle that stroke volume isphysiologically related to arterial pressure, aortic compliance,and arterial tone.1 In particular, some ‘uncalibrated’ devicesestimate aortic compliance and arterial tone from an ana-lysis of the geometric properties of arterial shape and fromsome patient characteristic data. These devices are in con-trast to some ‘calibrated’ systems, which add to this continu-ous estimation of CO an external calibration by a referencetechnique.

The uncalibrated systems have the great advantage of notrequiring a specific system for recalibrating CO measure-ment. Nevertheless, their ability to track changes in CO hasbeen questioned,2 – 9 especially when arterial tone changesto a large extent3 or during hyperdynamic states.7 8 10 In aprevious study, we suggested that the second-generationFloTrac/Vigileow device had a poor ability for trackingchanges in cardiac index (CI) induced by norepinephrine inseptic patients.11 We hypothesized that changes in arterialcompliance and arterial tone induced by the vasopressor dis-torted the arterial pressure wave analysis made by the unca-librated system. In a recent study, a third generation of this

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system has been demonstrated to be as precise, more accur-ate, and less influenced by systemic vascular resistance (SVR)than the previous version.12 The third-generation system wasnot better than the second for detecting significant changesin CI over time,12 but these changes were not induced by sys-tematic therapeutic interventions. Moreover, a recent studysuggested that the third version of the FloTrac/Vigileodevice does not accurately track changes in CO induced

with phenylephrine and ephedrine in the intraoperativesetting.13

In the present study, we tested whether the third-generation FloTrac/Vigileo device allows tracking trends inCI induced either by volume expansion or by changes inthe dose of norepinephrine in critically ill patients.

MethodsSubjects

After approval by the Institutional Review Board of our insti-tution, subjects were enrolled if a volume expansion (20 sub-jects) or an increase (20 different subjects) or a decrease (20different subjects) in the dose of norepinephrine was plannedby the attending physician. Subjects’ relatives were informedabout the study at the time of enrolment with the possibilityof refusing participation at that time. Subjects were informedas soon as their mental status allowed, and the possibilitywas given to withdraw their participation in the study.

All subjects had a catheter inserted into the internaljugular vein and a catheter inserted into the femoral artery(PV8215 monitoring kit, Pulsion Medical Systems, Munich,Germany). The arterial line was divided into two branchesthrough a stopcock, one connected to a PiCCO2 device(Pulsion Medical Systems) and the other connected to athird-generation FloTrac/Vigileo device (Edwards Life-sciences, Irvine, CA, USA).

Measurements and study design

Before each therapeutic intervention, we performed a firstset of haemodynamic measurements, including heart rate,systemic arterial pressure, CI measured by transpulmonarythermodilution (CItd), CI measured by pulse-wave analysisby the third-generation FloTrac/Vigileo device (CIpw), andSVR. We used the values of CIpw automatically displayed onthe screen of the FloTrac/Vigileo device averaged over a20 s rolling period. The CItd was measured by the PiCCO2device by injecting 15 ml of iced saline (,108C) throughthe central venous line. The injection was performed in trip-licate and the values of CItd were averaged. Immediatelybefore performing thermodilution boluses, the value of CIpw

Table 1 Subject characteristics at baseline. n¼60. Data areexpressed as mean (SD), median (25–75% inter-quartile) or n (%).SAPS, Simplified Acute Physiologic Score; ARDS: acute respiratorydistress syndrome; MAP, mean arterial pressure; Cltd, cardiac indexmeasured by transpulmonary thermodilution; PaO2/FIO2 , ratio ofthe arterial oxygen tension over the inspired oxygen fraction

Age (yr) 64 (15)

Gender (M/F) 41/19

SAPS II 45 (11)

ARDS (n, %) 34 (57)

Mechanical ventilation (n, %) 60 (100)

Respiratory variables

Tidal volume (ml kg21 of predictedbody weight)

7 (2)

Respiratory rate (breaths min21) 20 (4)

Total positive end-expiratory pressure(cm H2O)

8 (2)

PaO2/FIO2

(mm Hg) 220 (100)

Shock aetiology

Septic (n, %) 48 (80)

Haemorrhagic (n, %) 6 (10)

Drug poisoning (n, %) 6 (10)

CItd (litre min21 m22) 3.4 (1.3)

Systemic vascular resistance(dyn s cm25)

938 (739–1194)

Vasopressors

Norepinephrine (n, %) 56 (93)

Dose of norepinephrine(mg kg21 min21)

0.16 (0.04–0.41)

Dobutamine (n, %) 2 (3)

Table 2 Evolution of haemodynamic parameters during therapeutic interventions. Data are expressed as mean (SD) or as median (25–75%inter-quartile). *P,0.05 vs before intervention, †P,0.05 vs volume expansion. MAP, mean arterial pressure; CItd, cardiac index measured bythermodilution; CIpw, arterial pressure waveform-based cardiac index measured by the FloTrac/Vigileo device; SVR, systemic vascular resistance

Volume expansion (n520) Increase in norepinephrine (n520) Decrease in norepinephrine (n520)

Before After Before After Before After

Heart rate (beats min21) 102 (23) 98 (23) 82 (16)† 88 (23) 87 (16)† 85 (17)

MAP (mm Hg) 75 (15) 83 (14)* 61 (13)† 82 (13)* 74 (62) 62 (13)*,†

CItd (litre min21 m22) 3.3 (1.5) 3.8 (1.5) 3.1 (1.1) 3.3 (1.1) 3.7 (1.3) 3.5 (1.3)

CIpw (litre min21 m22) 3.3 (1.3) 3.7 (1.3) 2.7 (0.6) 3.2 (0.8) 3.4 (0.9) 3.0 (0.9)

SVR (dyn s cm25) 940 (861–1283) 927 (844–1169) 916 (677–1153) 1149 (929–1367)* 952 (696–1145) 846 (659–1064)*

Dose of norepinephrine(mg kg21 min21)

0.47 (0.31–0.84) 0.47 (0.31–0.84) 0.07 (0.02–0.19)† 0.21 (0.19–0.45)* 0.13 (0.07–0.20)† 0.03 (0.00–0.12)*,†

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was carried out. The CIpw was recorded immediately beforethermodilution to avoid interference between temperaturedrift and accuracy of CIpw. The total SVR was calculated asSVR¼mean arterial pressure×80/(CItd×body surface area).

After the first set of haemodynamic measurements wascompleted, volume expansion was performed (500 ml ofsaline over 30 min) or the dose of norepinephrine wasincreased or decreased. All other treatments were un-changed during the therapeutic interventions.

A second set of haemodynamic measurements wascarried out again after the therapeutic intervention (i.e. atthe end of fluid administration and 5 min after stabilizationof mean arterial pressure). This set included heart rate, sys-temic arterial pressure, CIpw, CItd, and SVR.

Statistical analysis

All data were normally distributed (Kolmogorov–Smirnovtest) except the dose of norepinephrine and are expressed

as mean [standard deviation (SD)] or median [25–75% inter-quartile range], as appropriate. Comparisons between valuesrecorded before and values after therapeutic interventionswere performed in both groups by paired Student’s t-testor paired Wilcoxon’s test, as appropriate. Comparisonsbetween subjects receiving volume expansion, subjects inwhom the dose of norepinephrine was increased, andsubjects in whom the dose of norepinephrine was decreasedwere performed by a two-tailed Student’s t-test or a Mann–Whitney U-test, as appropriate. Correlations were assessedby the Pearson coefficient and correlation coefficients werecompared using the Fisher transformation.14 This analysiswas also separately performed in subjects in whom SVRchanged in absolute value by more or less than 15% withthe therapeutic interventions.15

We compared the relative changes of CIpw with those ofCItd during the therapeutic intervention by the Bland andAltman analysis (for absolute changes) and by linear regres-sion analysis (for per cent changes). For assessing the trend-ing ability of CIpw, we constructed a four-quadrant plot.16

This allowed calculation of the percentage of total datapoints for which the direction changes of CIpw (increase ordecrease) were concordant with CItd. Since the least signifi-cant change of CItd is 12% when three thermodilution mea-surements are performed,17 we applied a 12% exclusionlimit. We also constructed a receiver operating characteristic(ROC) curve to test the ability of changes in CIpw to detect anincrease in CItd ≥12% induced by volume expansion. We cal-culated the percentage error of CIpw as 2× SD mean21 ofCItd.18 A P value of ,0.05 was considered significant. Thestatistical analysis was performed using MedCalc8.1.0.0 soft-ware (Mariakerke, Belgium).

ResultsSubject characteristics

Subject characteristics at baseline are summarized in Table 1.Circulatory failure was of septic origin in the majority of sub-jects. All subjects received norepinephrine at baseline. Sub-jects deemed as receiving volume expansion received

0 1 2 3 4 5 6 7–2.0

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CI p

w–C

I td (l

itre

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Fig 1 The Bland–Altman plot for the absolute values of CIobtained by transpulmonary thermodilution (CItd) and by thethird-generation FloTrac/Vigileo device (CIpw) considering allpairs of measurements performed during the study. n¼60;straight line, bias; dashed line, +2SD/22SD limits of agreement.

Table 3 Comparison of changes in CI measured by pulse-wave analysis and transpulmonary thermodilution. Data are expressed as absolutevalues. CItd, cardiac index measured by thermodilution; CIpw, arterial pressure waveform-based CI measured by the FloTrac/Vigileo device

Volume expansion(n520)

Increase in norepinephrine(n520)

Decrease in norepinephrine(n520)

r2 between per cent changes in CItd and CIpw 0.26 2.5×1023 0.16

P-value for the correlation between per centchanges in CItd and CIpw

0.02 0.81 0.07

Bias for the absolute changes in CIpw comparedwith CItd (litre min21 m22)

0.11 0.36 0.17

Upper limit of agreement for the absolutechanges in CIpw (litre min21 m22)

0.98 1.98 0.92

Lower limit of agreement for the absolutechanges in CIpw (litre min21 m22)

21.20 21.25 21.26

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norepinephrine at baseline and this dose was kept un-changed during the study period (Table 2). The second setof measurements was recorded 32 (4) min after the first

set in subjects receiving volume expansion and 35 (10) minafter the first set in subjects in whom the dose of norepin-ephrine was changed.

–20 0 20 40 60 80 100–20

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Fig 2 (A) The Bland–Altman plot for the changes in absolute values induced by volume expansion of CI measured by transpulmonary thermo-dilution (CItd) and by arterial pressure waveform analysis by the third-generation FloTrac/Vigileo device (CIpw). (B) Correlation between the percent changes induced by volume expansion of CI measured by transpulmonary thermodilution (DCItd) and by arterial pressure waveform ana-lysis by the third-generation FloTrac/Vigileo device (DCIpw). (C) Trending ability of the third-generation FloTrac/Vigileo device (DCIpw) against CImeasured by transpulmonary thermodilution (DCItd) during volume expansion based on four-quadrant concordance analysis. n¼20. TheBland–Altman plots: straight line, bias; dashed line, +2SD/22SD limits of agreement. Correlation: dashed line, correlation line.

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Comparison between CItd and CIpw

Considering the pairs of measurements performed beforeand after all therapeutic interventions (n¼60), the biasbetween the absolute values of CIpw and CItd was 0.26(0.94) litre min21 m22 and the percentage error was54% (Fig. 1).

Comparison of CIpw with CItd in subjects receivingvolume expansion

In subjects receiving volume expansion, mean arterial pres-sure, CItd, and CIpw significantly increased by 12 (9)%, 23(23)%, and 19 (22)%, respectively. SVR did not significantlydecrease (Table 2).

The bias between absolute changes in CIpw and CItd

induced by volume expansion was 20.11 (0.54) litre min21

m22. The coefficient of determination (r2) betweenfluid-induced per cent changes in CIpw and CItd was 0.26(P¼0.02) (Table 3 and Fig. 2). The concordance ratebetween changes in CIpw and CItd induced by volume expan-sion was 73% (Fig. 2). After volume expansion, the biasbetween the absolute values of CIpw and CItd was 20.15(0.88) litre min21 m22 and the percentage error was 48%.

The area under the ROC curve constructed for the changesin CIpw for detecting an increase in CItd ≥12% was not sig-nificantly different from 0.5 (Fig. 3).

Comparison of CIpw with CItd in subjects with achange in dose of norepinephrine

In subjects in whom the dose of norepinephrine wasincreased, mean arterial pressure, SVR, CItd, and CIpw

significantly increased by 22 (25)%, 8 (28)%, 9 (21)%, and20 (19)%, respectively (Table 2). In subjects in whom thedose of norepinephrine was decreased, mean arterial pres-sure, SVR, CItd, and CIpw significantly decreased by 15(13)%, 8 (17)%, 9 (18)%, and 12 (12)%, respectively (Table 2).

Considering subjects in whom norepinephrine wasincreased or decreased as one group (n¼40), the biasbetween the absolute changes in CIpw and CItd induced bynorepinephrine decrease/increase was 0.11 (0.68) litremin21 m22. The coefficient of determination (r2) betweenthe norepinephrine-induced per cent changes in CIpw andin CItd was 0.11 (P¼0.04) (Fig. 4). The concordance ratebetween the changes in CIpw and CItd induced by changingthe dose of norepinephrine was 60% (Fig. 4). After the de-crease/increase of norepinephrine dose, the bias betweenthe absolute values CIpw and CItd was 20.30 (1.04) litremin21 m22 and the percentage error was 61%. Results con-cerning separate groups of subjects with an increase and adecrease in the dose of norepinephrine are shown in Table 3.

Effects of changes in SVR on the agreementof CIpw with CItd

Considering the aggregate of all therapeutic interventions,changes in SVR ranged from 231% to +73%. The biasbetween changes in CIpw and CItd significantly correlatedwith changes in SVR (r2¼0.41, P,0.0001).

In the subset of subjects in whom SVR (absolute value)changed by less than 15% (n¼33), the bias between the ab-solute changes in CIpw and CItd was 20.12 (0.43) litre min21

m22. In these subjects, there was no significant correlationbetween SVR and bias between CItd and CIpw (P¼0.29).

In the subset of patients in whom the SVR (in absolutevalue) increased by more than 15% (n¼27), the biasbetween the absolute changes in CIpw and CItd was 0.22(0.89) litre min21 m22. In these patients, the coefficient ofdetermination (r2) between SVR and the per cent changesin CItd and CIpw was 0.49 (P,0.0001).

DiscussionThe third-generation FloTrac/Vigileo device was not reliablefor detecting trends in CI, especially when induced by nor-epinephrine. The higher the total SVR, the higher was thebias between CI measured by FloTrac/Vigileo and by trans-pulmonary thermodilution.

Monitoring CO in critically ill patients is recommendedwhen shock persists despite adequate fluid resuscitation.19

A recent study also suggests that changes in arterial pressureare unable to reliably monitor the changes in CI induced byvasopressors,20 reinforcing the message that CO should bemeasured in critically ill patients after initial fluid resuscita-tion. Among the several techniques that are currently avail-able for measuring CI, the estimation of CI computed fromarterial pressure waveform analysis has the advantage of pro-viding beat-to-beat estimation of CI. In fact, three elementsinfluence the relationship between the shape of the periph-eral arterial wave and stroke volume: arterial compliance,

0 20 40 60 80 1000

20

40

60

80

100

100-specificity

Sen

sitiv

ity

Fig 3 An ROC curve constructed for testing the ability of thechanges in CI by the third-generation FloTrac/Vigileo device todetect an increase in CI obtained by transpulmonary thermodilu-tion ≥12% induced by volume expansion.


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–60 –40 –20 0 20

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Fig 4 (A) The Bland–Altman plot for changes in absolute values induced by changes in the dose of norepinephrine on CI measured by trans-pulmonary thermodilution (CItd) and by arterial pressure waveform analysis by the third-generation FloTrac/Vigileo device (CIpw). (B) Correlationbetween per cent changes induced by changes in the dose of norepinephrine on CI measured by transpulmonary thermodilution (DCItd) and byarterial pressure waveform analysis by the third-generation FloTrac/Vigileo device (DCIpw). (C) Trending ability of the third-generation FloTrac/Vigileo device (DCIpw) against CI measured by transpulmonary thermodilution (DCItd) during changes in the dose of norepinephrine based onfour-quadrant concordance analysis. n¼40. The Bland–Altman plots: straight line, bias; dashed line, +2SD/22SD limits of agreement. Correl-ation: dashed line, correlation line.

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arterial vasomotor tone, and pulse-wave amplification phe-nomenon.1 Thus, estimation of CI by arterial pressure wave-form analysis is based upon a geometric analysis of theshape of the arterial pressure curve which is then adjustedwith a factor taking into account the arterial complianceand tone and the pulse-wave amplification phenomenon.The devices currently available on the market are fundamen-tally different. The ‘calibrated’ devices, namely the PiCCO(Pulsion Medical Systems), EV1000 (Edwards Lifesciences),and LidCOplus (LidCO) devices calibrate the estimation ofCO made from the arterial pressure curve by an external cali-bration of CI by a reference method (transpulmonary thermo-dilution for the PiCCO and EV1000 and lithium dilution for theLidCOplus). This external calibration requires periodic injec-tion of an indicator and the use of a specific material formeasuring dilution. In contrast, some ‘uncalibrated’ devices,like the FloTrac/Vigileo (Edwards Lifesciences), LidCOrapid(LidCO), or Pulsioflex (Pulsion Medical Systems), continuouslyestimate arterial compliance and tone and pulse-wave amp-lification from a complex geometric analysis of the arterialwave and from some biometric data.

Reliability of uncalibrated pressure waveform analysisfor measuring CO has been demonstrated in severalstudies.12 21 – 24 Nevertheless, concerns have been raisedabout the validity of the technique when the arterialtone changes to a large extent,3 during hyperdynamicstates,7 8 10 and when vasopressors are administered, aswe recently showed with the second-generation FloTrac/Vigileo device.11 To address this problem, a third version ofthe FloTrac/Vigileo software has been developed. Comparedwith the previous version, estimation of arterial complianceand tone and pulse-wave amplification has been madefrom a human database containing more recordings fromseptic and liver transplant patients.12 In a recent study, inseptic shock patients, De Backer and colleagues12 foundthat the third-generation FloTrac/Vigileo device is more ac-curate, as precise as, and less influenced by total SVR thanthe previous version. Consistent with this study, we foundthat the percentage error for CIpw recorded for all pairs ofmeasurements was improved compared with resultsobtained with the second-generation system11 (54% vs61%, respectively).

In contrast to De Backer and colleagues, we focused onthe ability of the uncalibrated devices to follow changes inCI induced by some systematic therapeutic changes. Eventhough it was conducted in subjects with total SVR in thesame range as those in the study of De Backer and collea-gues,12 the present study suggests that the most recentversion of the FloTrac/Vigileo system does not provide a sat-isfactory track of therapy-induced changes in CO. First, eventhough changes in CItd and CIpw were more significantly cor-related when induced by volume expansion than by norepin-ephrine, the third-generation FloTrac/Vigileo did not providea correct estimation of the response to a standardized fluidchallenge, as defined by an increase in CItd ≥15%. Secondand more importantly, our results suggest that the newFloTrac/Vigileo device was not reliable for tracking trends in

CI induced by changing the dose of norepinephrine. More-over, by showing that the accuracy of the third-generationFloTrac/Vigileo device correlated with total SVR, we suggestthat its estimation of CI is still distorted by a change in vas-cular tone. The ability to track norepinephrine-inducedchanges in CI seems to be improved compared with the pre-vious version of the system. Indeed, in our previous study,11

we did not find significant correlation between changes inCIpw and CItd induced by norepinephrine changes, whilethis correlation was significant in the present study(r¼0.35, P,0.05). This suggests substantial but insufficientimprovements in the device software. Importantly, thepresent results are in accordance with two recent studiesconducted in other clinical settings. In neurosurgical patientsrequiring high-dose vasopressor support, Metzelder and col-leagues25 showed that the introduction of the third-generation FloTrac/Vigileo software algorithm did notimprove the insufficient precision for CI measurementsobserved with the second software version. In a generalpopulation of anaesthetized subjects, Meng and colleagues13

reported that the newest FloTrac/Vigileo generation accur-ately tracked changes in CO when preload changed but didnot accurately track changes in CO induced with phenyleph-rine and ephedrine.

We acknowledge some limitations to our study. First, wecould not perform a direct comparison between the secondand third generations of the FloTrac/Vigileo system sincethe previous version is no longer provided by the manufac-turer. Secondly, as a reference for measuring CI, we usedtranspulmonary thermodilution rather than classical thermo-dilution with the pulmonary artery catheter.26 Nevertheless,the accuracy of transpulmonary thermodilution in measuringCO has been repeatedly demonstrated.15 23 27 – 33 Thirdly, wedid not test other systems that compute CI from the pressurewaveform without external calibration, so our conclusionsmight not apply to these devices.

In conclusion, estimation of CI made from the third-generation FloTrac/Vigileo device was only moderately reli-able for detecting the changes in CI induced with volume ex-pansion and did not allow tracking trends in CI provoked bychanging the dose of norepinephrine in critically ill patients.As a clinical consequence, this study suggests that thisdevice should be reserved for patients who are not receivingvasopressors.

Declaration of interestJ.-L.T. and X.M. are members of the Medical Advisory Board ofPulsion Medical Systems.

FundingThis study was supported solely by institutional and depart-mental sources.

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