2 ventricles) could be another mechanism inducing preload variations and as such it could confound results obtained with the DIM technique. On the other hand, HRV is known to be signiﬁcantly reduced during sepsis [2]. We also have a few comments and suggestions to the pro- posed physiological mechanisms. The decrease in left ventricular stroke volume during DIM phase 1 is suggested to be induced by increasing ventric- ular afterload. However, we think that another and perhaps more important mechanism is the reduced intrathoracic pressure reducing left ventricular preload during the initial phase of inspiration—until the increasing right ventricular stroke volume with the delay of pulmonary transit time again increases left ventricular preload substantially. In line with this suggestion, but as a “reversed mechanism,” we also be- lieve that the increasing intrathoracic pressure during passive expiration (DIM phase 4) contributes somewhat to the in- creasing left ventricular (preload and) stroke volume in DIM phase 4 in addition to the suggested overall increase in intrathoracic blood volume. As a last comment, we would like to suggest that the DIM phases 2 and 4 could potentially disclose right ventricular failure: a large maximal value during DIM phase 2 relies on biventricular preload responsiveness whereas a large value in DIM phase 4 relies mostly, if not fully, on left ventricu- lar preload responsiveness. Even though the authors did not encounter any cases of preload unresponsiveness associated with high ΔPPdim (speciﬁcity was 100%) low phase 2 values associated with high phase 4 values could theoretically dis- close right ventricular failure—even when taking interven- tricular dependence into account. References [1] F. Michard, “Changes in arterial pressure during mechanical ventilation,” Anesthesiology, vol. 103, no. 2, pp. 419–428, 2005. [2] C. S. Garrard, D. A. Kontoyannis, and M. Piepoli, “Spectral analysis of heart rate variability in the sepsis syndrome,” Clinical Autonomic Research, vol. 3, no. 1, pp. 5–13, 1993. Cardiology Research and Practice