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A further analysis of why pulmonary venous pressure rises after the onset of LV dysfunction

¹Division of Critical Care, McGill University Health Centre, Montreal, Quebec, Canada; and ²Department of Medicine, University of Vermont, Burlington, Vermont

Submitted 6 May 2008 ; accepted in final form 1 October 2008

Based on a dynamic computational model of the circulation, Burkhoff and Tyberg (Am J Physiol Heart Circ Physiol 265: H1819–H1828, 1993) concluded that the rise in pulmonary venous pressure (Pvp) with left ventricular (LV) dysfunction requires a decrease in vascular capacitance and transfer of unstressed volume to stressed volume (). 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 conclusion. We used a computational model of the circulation that was similar to theirs, but we made Rvs four times higher (0.06 versus 0.015 mmHg·s·ml^–1), Cvs larger (110 versus 70 ml/mmHg), and larger (1,400 versus 750 ml); all other parameters, including those for the heart, were essentially the same. We simulated left ventricular dysfunction by decreasing end-systolic elastance (Eeslv) as they did and examined changes in cardiac output, arterial blood pressure, and Pvp. We then examined the effect of changes in Rvs, heart rate, and when Eeslv was depressed with and without pericardial constraint. In contrast to their findings, with our parameters the model predicts that decreasing Eeslv substantially increases Pvp. Furthermore, increasing systemic vascular resistance or decreasing Rvs or heart rate produces large increases in Pvp when Eeslv is reduced. Pericardial constraint limits the changes in Pvp. In 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.

venous return; venous resistance; pulmonary venous pressure; heart failure; cardiac output

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