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      The estimation of cardiac output by the Nexfin device is of poor reliability for tracking the effects of a fluid challenge

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          Abstract

          Introduction

          The Nexfin device estimates arterial pressure by the volume clamp method through a finger pneumatic cuff. It also allows to estimate cardiac index (CI noninv) by pulse contour analysis of the non-invasive arterial pressure curve. We evaluated the ability of the device to track changes in cardiac index induced by a fluid challenge.

          Methods

          We included 45 patients for whom a volume expansion (500 mL of saline infused over 30 min) was planned. The volume expansion-induced changes in cardiac index measured by transpulmonary thermodilution (CI inv, PiCCO device) and in CI noninv were recorded.

          Results

          In seven patients, the Nexfin could not record the arterial curve due to finger hypoperfusion. Considering both the values obtained before and after volume expansion (n = 76 pairs of measurements), the bias (lower and upper limits of agreement) between CI inv and CI noninv was 0.2 (-1.8 to 2.2) L/min/m 2. The mean change in CI noninv was 10 ± 11%. The percentage error of CI noninv was 57%. The correlation between the changes in CI inv and CI noninv observed during volume expansion was significant ( P = 0.0002) with an r 2 = 0.31.

          Conclusions

          The estimation of CI by the Nexfin device in critically ill patients is not reliable, neither for estimating absolute values of CI nor for tracking its changes during volume expansion.

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          Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure.

          F Michard, S Boussat, D Chemla … (2000)
          In mechanically ventilated patients with acute circulatory failure related to sepsis, we investigated whether the respiratory changes in arterial pressure could be related to the effects of volume expansion (VE) on cardiac index (CI). Forty patients instrumented with indwelling systemic and pulmonary artery catheters were studied before and after VE. Maximal and minimal values of pulse pressure (Pp(max) and Pp(min)) and systolic pressure (Ps(max) and Ps(min)) were determined over one respiratory cycle. The respiratory changes in pulse pressure (DeltaPp) were calculated as the difference between Pp(max) and Pp(min) divided by the mean of the two values and were expressed as a percentage. The respiratory changes in systolic pressure (DeltaPs) were calculated using a similar formula. The VE-induced increase in CI was >/= 15% in 16 patients (responders) and < 15% in 24 patients (nonresponders). Before VE, DeltaPp (24 +/- 9 versus 7 +/- 3%, p < 0.001) and DeltaPs (15 +/- 5 versus 6 +/- 3%, p < 0.001) were higher in responders than in nonresponders. Receiver operating characteristic (ROC) curves analysis showed that DeltaPp was a more accurate indicator of fluid responsiveness than DeltaPs. Before VE, a DeltaPp value of 13% allowed discrimination between responders and nonresponders with a sensitivity of 94% and a specificity of 96%. VE-induced changes in CI closely correlated with DeltaPp before volume expansion (r(2) = 0. 85, p < 0.001). VE decreased DeltaPp from 14 +/- 10 to 7 +/- 5% (p < 0.001) and VE-induced changes in DeltaPp correlated with VE-induced changes in CI (r(2) = 0.72, p < 0.001). It was concluded that in mechanically ventilated patients with acute circulatory failure related to sepsis, analysis of DeltaPp is a simple method for predicting and assessing the hemodynamic effects of VE, and that DeltaPp is a more reliable indicator of fluid responsiveness than DeltaPs.
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            Hemodynamic parameters to guide fluid therapy

            Paul E Marik, Xavier Monnet, Jean-Louis Teboul (2011)
            The clinical determination of the intravascular volume can be extremely difficult in critically ill and injured patients as well as those undergoing major surgery. This is problematic because fluid loading is considered the first step in the resuscitation of hemodynamically unstable patients. Yet, multiple studies have demonstrated that only approximately 50% of hemodynamically unstable patients in the intensive care unit and operating room respond to a fluid challenge. Whereas under-resuscitation results in inadequate organ perfusion, accumulating data suggest that over-resuscitation increases the morbidity and mortality of critically ill patients. Cardiac filling pressures, including the central venous pressure and pulmonary artery occlusion pressure, have been traditionally used to guide fluid management. However, studies performed during the past 30 years have demonstrated that cardiac filling pressures are unable to predict fluid responsiveness. During the past decade, a number of dynamic tests of volume responsiveness have been reported. These tests dynamically monitor the change in stroke volume after a maneuver that increases or decreases venous return (preload) and challenges the patients' Frank-Starling curve. These dynamic tests use the change in stroke volume during mechanical ventilation or after a passive leg raising maneuver to assess fluid responsiveness. The stroke volume is measured continuously and in real-time by minimally invasive or noninvasive technologies, including Doppler methods, pulse contour analysis, and bioreactance.
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              Passive leg raising predicts fluid responsiveness in the critically ill.

              Xavier Monnet, Mario Rienzo, David Osman … (2006)
              Passive leg raising (PLR) represents a "self-volume challenge" that could predict fluid response and might be useful when the respiratory variation of stroke volume cannot be used for that purpose. We hypothesized that the hemodynamic response to PLR predicts fluid responsiveness in mechanically ventilated patients. Prospective study. Medical intensive care unit of a university hospital. We investigated 71 mechanically ventilated patients considered for volume expansion. Thirty-one patients had spontaneous breathing activity and/or arrhythmias. We assessed hemodynamic status at baseline, after PLR, and after volume expansion (500 mL NaCl 0.9% infusion over 10 mins). We recorded aortic blood flow using esophageal Doppler and arterial pulse pressure. We calculated the respiratory variation of pulse pressure in patients without arrhythmias. In 37 patients (responders), aortic blood flow increased by > or =15% after fluid infusion. A PLR increase of aortic blood flow > or =10% predicted fluid responsiveness with a sensitivity of 97% and a specificity of 94%. A PLR increase of pulse pressure > or =12% predicted volume responsiveness with significantly lower sensitivity (60%) and specificity (85%). In 30 patients without arrhythmias or spontaneous breathing, a respiratory variation in pulse pressure > or =12% was of similar predictive value as was PLR increases in aortic blood flow (sensitivity of 88% and specificity of 93%). In patients with spontaneous breathing activity, the specificity of respiratory variations in pulse pressure was poor (46%). The changes in aortic blood flow induced by PLR predict preload responsiveness in ventilated patients, whereas with arrhythmias and spontaneous breathing activity, respiratory variations of arterial pulse pressure poorly predict preload responsiveness.
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                Author and article information

                Contributors
                Xavier Monnet
                Fabien Picard
                Elsa Lidzborski
                Malcie Mesnil
                Jacques Duranteau
                Christian Richard
                Jean-Louis Teboul
                Journal
                Journal ID (nlm-ta): Crit Care
                Journal ID (iso-abbrev): Crit Care
                Title: Critical Care
                Publisher: BioMed Central
                ISSN (Print): 1364-8535
                ISSN (Electronic): 1466-609X
                Publication date (Print): 2012
                Publication date (Electronic): 29 October 2012
                Volume: 16
                Issue: 5
                Page: R212
                Affiliations
                [1 ]Service de réanimation médicale, Univ Paris-Sud, AP-HP, Hôpitaux universitaires Paris-Sud, Hôpital de Bicêtre, 78, rue du Général Leclerc, 94 270 Le Kremlin-Bicêtre, France
                [2 ]Service de réanimation chirurgicale, AP-HP, Hôpitaux universitaires Paris-Sud, Hôpital de Bicêtre, 78, rue du Général Leclerc, 94 270 Le Kremlin-Bicêtre, France
                Article
                Publisher ID: cc11846
                DOI: 10.1186/cc11846
                PMC ID: 3682316
                PubMed ID: 23107227
                SO-VID: 6674133b-8e1d-401b-a185-e147bcc3971a
                Copyright © Copyright ©2012 Monnet et al.; licensee BioMed Central Ltd.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 6 June 2012
                Date revision received : 4 September 2012
                Date accepted : 23 October 2012
                Categories
                Subject: Research

                ScienceOpen disciplines: Emergency medicine & Trauma
                Data availability:
                ScienceOpen disciplines: Emergency medicine & Trauma

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