A Comparison of Stroke Volume Variation Measured by Vigileo™/FloTrac™ System and Aortic Doppler Echocardiography

Abstract

BACKGROUND: 

The goal of this study was to compare stroke volume variation (SVV) assessed from a peripheral artery with the Vigileo™/FloTrac™ system (SVV-FloTrac) with SVV derived close to the heart by aortic Doppler (SVV-Doppler).

METHODS: 

Thirty patients undergoing liver transplantation underwent simultaneous SVV-FloTrac and SVV-Doppler measurements before and after intravascular volume expansion.

RESULTS: 

SVV-FloTrac and SVV-Doppler comparison before intravascular volume expansion showed a mean bias of 0.7%, and 95% limits of agreement of −4.2% to 5.5%. The areas under the receiver operating characteristic curves generated to discriminate responders and nonresponders to intravascular volume expansion were not different for SVV-FloTrac and SVV-Doppler.

CONCLUSIONS: 

SVV-FloTrac and SVV-Doppler measurements show acceptable bias and limits of agreement, and similar performance in terms of fluid responsiveness in patients undergoing liver transplantation.

Stroke volume (SV) variation (SVV) measurement is designed to predict the individual response to intravascular fluid administration.^1,2 The Vigileo™/FloTrac™ system (Edwards Lifesciences, Irvine, CA) is based on the analysis of the systemic arterial pressure wave without external calibration to continuously monitor cardiac output (CO) and SVV (SVV-FloTrac).³ It has been shown that SVV-FloTrac is a good indicator of fluid responsiveness.^4–6 However, SVV-FloTrac is measured peripherally and can potentially be affected by reflecting waves, damping, and vascular tone. In contrast, SVV estimated by the measurement of velocity-time integral (SVV-Doppler) or aortic blood flow is measured at the level of the heart and is not affected by arterial wave forms. These indices have also been shown to be sensitive indicators of fluid responsiveness.^7,8 The aims of this study were 1) to determine the agreement between simultaneously measured SVV-FloTrac and SVV-Doppler values and 2) to assess their capacity to predict fluid responsiveness in patients undergoing liver transplantation (LT).

METHODS

Patients

After obtaining IRB approval and informed consent, 30 consecutive patients undergoing LT were included in a prospective observational study. Exclusion criteria were arrhythmias, significant valvulopathy, spontaneous breathing activity, left ventricular ejection fraction <50% before intravascular volume expansion (VE), and unsatisfactory cardiac echogenicity.

Patients were studied immediately after admission to the intensive care unit. They were sedated (propofol and sufentanil) to ensure that there was no evidence of spontaneous breathing effort. Mechanical ventilation was performed in a volume-controlled mode (tidal volume of 8–10 mL/kg, positive end-expiratory pressure of 3 cm H₂O, and an inspiratory/expiratory ratio of 0.5). Respiratory rate was adjusted to maintain an arterial carbon dioxide pressure between 35 and 40 mm Hg. Hemodynamic management was guided by echocardiography.

Hemodynamic Monitoring

An arterial catheter was inserted preoperatively. A dedicated transducer (FloTrac, Edwards Lifesciences) was connected to the radial arterial line on one side and to the Vigileo system (Edwards Lifesciences) on the other. The device calculates SV as k × pulsatility, where pulsatility is the standard deviation of arterial pressure over a 20-s interval, and k is a factor quantifying arterial compliance and vascular resistance. k is derived from a multivariate regression model including 1) Langewouter aortic compliance,⁹ 2) mean arterial blood pressure (MAP), 3) variance, 4) skewness, and 5) kurtosis of the pressure curve. The rate of adjustment of k is 1 min (Software 1.07). SVV is calculated as the variation of beat-to-beat SV from the mean value during the most recent 20 s data: SVV = (SV_max − SV_min)/SV_mean. SVV was recorded as mean values of three repeated measurements (over 1 min).

Doppler echocardiography was performed using an ultrasound device (EnVisor C, Philips Medical System, Eindhoven, The Netherlands) equipped with a phased array transthoracic probe (2.5 MHz). The SV was calculated as the product of the aortic valve area by the velocity time integral of aortic blood flow. The maximum and minimum SV values were identified for 1 min and averaged to obtain SV-Doppler_max and SV-Doppler_min. The mean SV (SV-Doppler_mean) was calculated as (SV-Doppler_max − SV-Doppler_min)/2. SVV-Doppler was calculated as (SV-Doppler_max − SV-Doppler_min)/SV-Doppler_mean. CO-Doppler was calculated as the product of heart rate by SV-Doppler_mean.¹⁰ Data were recorded by a trained observer and analyzed off-line by another investigator blinded to the Vigileo/FloTrac results. SVV-FloTrac and SVV-Doppler measurements were simultaneous.

Central venous pressure and MAP were also recorded. Systemic vascular resistance (SVR) was calculated using the equation: SVR = (MAP − central venous pressure) × 80/CO-Doppler.

Intravascular VE

Two sets of measurements were performed: the first before VE (20 mL × body mass index of 4% albumin over 20 min) and the second immediately after VE.

Statistical Analysis

Results were expressed as mean ± sd if data were normally distributed or median (25%–75% interquartile range) if not. SVV-FloTrac and SVV-Doppler were compared using the Bland and Altman method.¹¹ Relationships between baseline SVV-FloTrac, baseline SVV-Doppler, and change in CO-Doppler induced by VE were evaluated using the Spearman Rank test. Assuming that a 15% change in CO was required for clinical significance, patients were separated into responders (R) and nonresponders (NR) by change in CO-Doppler ≥15% and <15% after VE.^12–14 SVV-FloTrac and SVV-Doppler before VE in R and NR were compared with a nonparametric Mann–Whitney test. Receiver operating characteristic (ROC) curves were generated for SVV-FloTrac and SVV-Doppler varying the discriminating threshold of each parameter, and areas under the ROC curves (95% confidence interval [CI]) were calculated and compared.¹⁵ Statistical analysis was performed using Statview (software 5.0; SAS Institute, Cary, NC) and Medcalc (software 8.1.1.0; Mariakerke, Belgium).

RESULTS

Fourteen patients were R and 16 were NR. Characteristics of the patients are shown in Table 1. CO-Doppler, SVV-FloTrac, SVV-Doppler, SVR, and norepinephrine doses before VE in R and in NR are shown in Table 2. Before VE, the mean bias between SVV-Doppler and SVV-FloTrac was 0.7%, and the 95% limits of agreement was −4.2% to 5.5% (Fig. 1). Baseline SVV-FloTrac and baseline SVV-Doppler correlated significantly with the change in CO-Doppler induced by VE (r² = 0.67, P < 0.0001 and r² = 0.64, P < 0.0001, respectively).

Table 1: Patient Characteristics

Table 2: Hemodynamic Variables Before Intravascular Volume Expansion in Responders and in Nonresponders

Figure 1.: Bland-Altman plots between SVV-Doppler (stroke volume variation obtained with aortic Doppler) and SVV-FloTrac (stroke volume variation obtained with Vigileo™/FloTrac™) before fluid challenge (baseline). The unbroken lines show the mean difference and the dotted lines show the 2sd limits of agreement.

A 10% SVV-FloTrac threshold discriminated R and NR with a sensitivity of 93% (95% CI: 66–99) and a specificity of 94% (95% CI: 70–99). A 9% SVV-Doppler threshold discriminated R and NR with a sensitivity of 100% (95% CI: 77–100) and a specificity of 88% (95% CI: 62–98).

The area under the ROC curves, showing the ability of SVV-FloTrac and SVV-Doppler before VE to discriminate R and NR after VE, were not different (0.94 [0.79–0.99] vs 0.95 [0.80–0.99]), respectively.

DISCUSSION

The main finding of this study is that SVV derived from a peripheral pulse (with the Vigileo/FloTrac system) is comparable with SVV derived close to the heart (by aortic Doppler) in patients undergoing LT with vasopressor support.

Pinsky^16,17 has advised caution in the clinical use of SVV, reasoning 1) that the pulse contour technique has not been validated to monitor rapid changes in SV, as may occur over a single breath and 2) that the extent to which ventilation may alter the determinants of arterial input impedance used to calculate SV is not known.

Our results may be surprising for several reasons. First, we already demonstrated that the generation of the Vigileo/FloTrac system used in this study underestimated SV in patients undergoing LT with low SVR.¹⁸ Second, all patients received significant doses of vasopressor, which may have had an impact on the arterial pressure wave form and have affected the accuracy of SVV-FloTrac measured peripherally to a greater extent than the accuracy of SVV-Doppler measured close to the heart. The good agreement between SVV-Doppler and SVV-FloTrac may be explained by the fact that the patients included in the study exhibited normal SVR and that the accuracy of the Vigileo/FloTrac system is acceptable in such patients.¹⁸ Furthermore, it has been shown that the SVV-FloTrac is able to predict fluid responsiveness in patients undergoing cardiac surgery or LT, and the best cutoff value of 10% we report in this study is also in accordance with previous studies.^4–6

To our knowledge, ours is the first clinical study showing that rapid changes in left ventricular SV can be accurately assessed from a peripheral artery. In 20 patients undergoing abdominal aortic surgery, De Castro et al.¹⁹ found a moderate correlation between SVV measured by PiCCO™ monitor (Pulsion Medical Systems, Munich, Germany) and SVV determined by transesophageal echocardiography. Recently, Marquez et al.²⁰ found that arterial pulse power (LiDCOplus™) documented dynamic changes in SV induced by the venous occlusion and release maneuver moderately well in seven patients undergoing cardiac surgery.

A cutoff of 15% is usually used to cope with the intrinsic variability of CO measurements and to define a clinically relevant change.^12–14 However, defining this threshold determines the results obtained by the ROC analysis, and different thresholds would provide different results.

Our study has some limitations. SVV assessed by transthoracic echocardiography was considered the reference. Despite taking caution in interpreting the measurements, the transthoracic approach may pose difficulties in the postoperative period of abdominal surgery or LT. Because we studied a specific population of liver-transplanted patients with a left ventricular ejection fraction >50% and with vasopressor support, our results cannot be extrapolated to another population.

In conclusion, SVV derived from a peripheral artery by the Vigileo/FloTrac system and SVV derived close to the heart by aortic Doppler measurements show an acceptable bias and limits of agreement and similar performance in terms of identifying fluid responsiveness in patients undergoing LT with vasopressor support.

ACKNOWLEDGMENTS

The authors thank Françoise Masson for statistical support and Ray Cooke for revising the English.