In a clinical investigation, Kumar and coworkers reported the hemodynamic events that accompany plasma volume expansion over 3 hours in healthy adult volunteers, and found that increases in stroke volume (SV) may be related to increases in left ventricular (LV)/right ventricular (RV) end-diastolic volume, as they expected, but also to decreases in LV/RV end-systolic volume. The latter finding suggests increased contractility and/or decreased afterload, which do not fit with their perception that clinicians ascribe increases in SV to increases in end-diastolic volume based on Starling's work. Increased ejection fraction and decreased vascular resistances were also observed. The same authors recently reported novel data suggesting that reduced blood viscosity may account for the observed reduction in vascular resistances with saline volume expansion. However, the variances in preload and afterload, along with uncertainty in estimates of contractility, substantially limit their ability to define a primary mechanism to explain decreases in LV end-systolic volume. A focus on using ejection fraction to evaluate the integrated performance of the cardiovascular system is provided to broaden this analytic perspective. Sagawa and colleagues described an approach to estimate the relationship, under clinical conditions, between ventricular and arterial bed elastances (i.e. maximal ventricular systolic elastance [Emax] and maximal arterial systolic elastance [Ea]), reflecting ventricular-arterial coupling. I used the mean data provided in one of the reports from Kumar and coworkers to calculate that LV Emax decreased from 1.09 to 0.96 mmHg/ml with saline volume expansion, while Ea decreased from 1.1 to 0.97 mmHg/ml and the SV increased (i.e. the increase in mean SV was associated with a decrease in mean afterload while the mean contractility decreased). The results reported by Kumar and coworkers invite further studies in normal and critically ill patients during acute saline-induced plasma volume expansion and hemodilution. If reduced viscosity decreases afterload, then this raises the questions by what mechanism, and what is the balance of benefit and harm associated with reduced blood viscosity affecting oxygen delivery? Why the mean Emax might decrease must be evaluated with respect to benefit in reducing ventricular work or a negative inotropic effect of saline.