Rational: Based on a dynamic computational model of the circulation, Burkhoff and Tyberg (5) proposed that a decrease in vascular capacitance and transfer of unstressed volume into stressed volume () is required for the rise in pulmonary venous pressure (Pvp) with left ventricular dysfunction. We argue that the values they used for venous resistance (Rvs), venous compliance (Cvs) and were too low, and changing these values significantly changes the conclusions. We used a computational model of the circulation that was similar to theirs. We used a Rvs that was four times higher (0.06 versus 0.015 mmHg.s.ml^-1), a larger Cvs (110 versus 70 ml.mmHg^-1), and larger (1400 versus 750 ml), but kept other parameters including those for the heart essentially the same. We simulated left ventricular dysfunction by decreasing end-systolic elastance (Eeslv) and examined changes in cardiac output (Q), arterial blood pressure (BP) and Pvp. We then examined the effect of changes in Rvs, heart rate and when Eeslv was depressed with and without pericardial constraint. Results: In contrast to their findings, our model predicts that increasing systemic vascular resistance (SVR), increasing Rvs, or decreasing heart rate produce large increases in Pvp when Eeslv is reduced. Pericardial constraint limits the changes in Pvp. Conclusion: When Rvs and Cvs are increased, baseline must be higher to maintain normal cardiac output. This increased volume can shift between compartments under flow conditions and account for the increase in Pvp with decreased left ventricular function even without recruitment of unstressed volume.