In Response.

Abstract

We thank Jan Vos et al.1 for their interest in our study recently published in Anesthesia & Analgesia.2 It is important to understand the physiological differences between dynamic arterial elastance (Eadyn) and arterial elastance (Ea). Edyn is not arterial elastance but a functional parameter relating changes in pulse pressure variations (PPVs) to stroke volume variations (SVVs): PPV/SVV. Edyn has been reported as being able to predict changes in arterial pressure after a change in volume. Unlike Ea, Eadyn has a significant central component that is independently influenced by left ventricular dP/dt, because central vascular impedance is not linear. Thus, paradoxically vasopressors may decrease Eadyn and inodilators increase it. Eadyn is primarily a central parameter, whereas Ea is a lumped sum parameter of both central and peripheral tone.3 As these authors correctly pointed out, spontaneously breathing is a known limitation for assessing fluid responsiveness using the functional hemodynamic parameters of PPV or SVV.4 The impact of varying tidal volumes, ventricular interdependence, and the small changes in intrathoracic pressure during spontaneous breathing diminishes the usefulness of these parameters for assessing preload dependency.5,6 However, Eadyn is the instantaneous ratio between PPV and SVV, not the determinants of each; thus, the effects of nonuniform ventilation should have no effect on their ratio. Consequently, it is logical to assume that spontaneous breathing is not a limitation for Eadyn estimation. SVV is the main determinant of PPV. Because aortic impedance remains constant during a respiratory cycle, discrepancies between PPV and SVV should be primarily related to how left ventricular stroke volume dynamically interacts with the arterial system.7,8 It is noteworthy, however, that very low PPV and SVV values resulting from small variations in intrathoracic pressure, as seen during spontaneous breathing, could reduce the reliability of the Eadyn for defining the slope in the PPV–SVV relationship because the changes in both PPV and SVV would be small. Jan Vos et al.1 also point out a possible issue with mathematical coupling in the estimation of Eadyn. With this regard, it is important to differentiate how mathematical coupling can affect the calculation of PPV and SVV and how it can affect the ratio between the 2 (Eadyn). In the article by Cecconi et al.,2 PPV was measured by the Nexfin monitor (BMEYE, Amsterdam, The Netherlands) from the noninvasive assessment of arterial pressure using the Clamp method described by Penáz et al.,9 whereas SVV was computed using the Nexfin-CO algorithm.10 Still, both parameters were obtained from the same arterial pressure signal, and hence, some degree of mathematical coupling cannot be excluded. Importantly, García et al.11 previously confirmed the physiological assumptions and the clinical usefulness of Eadyn for predicting arterial pressure response to fluid administration and found a similar threshold value of <0.89 for the PPV/SVV, and they calculated SVV (esophageal Doppler) and PPV (obtained from an arterial line) independently. Regarding the second point about mathematical coupling, if the PPV/SVV ratio was mathematically coupled, it would not be expected to discriminate between responders and nonresponders. In practice, when using pulse pressure analysis, the reliability of Eadyn relies on the robustness of the algorithm to estimate stroke volume and its changes over a respiratory cycle.12 As long as this estimation is trustworthy enough, this assumption should allow the calculation of a valid Eadyn. This raises another issue regarding the external validity of studies performed with a specific monitor. Because Eadyn relies on the robustness of the algorithm, it is important to study and validate the reliability of Eadyn for different monitors. Finally, although the clinical applicability of Eadyn seems now purely limited by the technological boundaries, the impact of its implementation during hemodynamic resuscitation in a patient’s outcome has yet to be determined.12 Maurizio Cecconi, MD, FRCA, FFICM, MD St. George’s Healthcare NHS Trust and St. George’s University of London Tooting, London, United Kingdom [email protected] Manuel Ignacio Monge García, MD St. George’s Healthcare NHS Trust and St. George’s University of London Tooting, London, United Kingdom Servicio de Cuidados Intensivos y Urgencias Hospital SAS de Jerez Jerez de la Frontera, Spain Michael R. Pinsky, MD Department of Critical Care Medicine University of Pittsburgh Pittsburgh, Pennsylvania Andrew Rhodes, FRCP, FRCA, FFICM, MD St. George’s Healthcare NHS Trust and St. George’s University of London Tooting, London, United Kingdom