Incorporation of ventricular viscoelasticity in a lumped parameter pressure-volume model to predict healthy and diseased right ventricular function

The myocardium exhibits viscoelastic behavior, and we recently demonstrated that right ventricular (RV) viscosity and elasticity increase with pulmonary hypertension (PH). Acute in vivo reduction of RV viscoelasticity improves RV and vascular function. However, the treatment induces multifactorial changes in cardiovascular system, preventing isolation of the independent effects of RV viscoelasticity. Multiscale computational models can separate such factors, including hemodynamic load, myocyte contractility, ventricular geometry, and passive tissue mechanics. But such models typically neglect myocardial viscosity. Thus, our goal was to develop a lumped-parameter model that incorporates both RV elasticity and viscosity to predict pressure–volume (PV) behavior. We hypothesized that RV viscosity impacts PV relations in healthy and diseased states. We modeled the cardiopulmonary circulation by revising a previous lumped-parameter framework [4]. Healthy and hypertensive states were simulated by altering input parameters ( Table 1 ). RV viscoelasticity was incorporated using a modified Kelvin–Voigt formulation, where the passive stress (σpassive) is given by < where Here, [Formula: see text] is volume rate of change, C is passive stiffness, and η is RV viscosity. The active stress is modeled by a Hill model. We simulated 4 conditions: 1) healthy RV; 2) diseased RV with increased viscoelastic passive stress and reduced active stress due to viscous resistance; 3) diseased RV with normal viscoelastic passive stress but reduced muscle contraction; 4) diseased RV with combined effects of 2) and 3). Systolic and diastolic parameters were derived from the PV relation but are not shown. We first observed marked changes in the PV loop with incorporating viscosity (data not shown). Moreover, PV loop was distinctly altered by RV viscoelasticity and contractility (Fig. 1). Overall, conditions 2-4 induced RV dilation and increased end-systolic pressure (ESP) compared to the healthy RV. The effect was most prominent with weakened contractility but normal RV viscoelasticity (dark blue). The stroke volume was the largest among the diseased conditions, suggesting that an impaired inotropy alone allows the RV to continue to manage the high arterial afterload. But the chamber dilation is the maximum in this condition. In contrast, if we keep the inotropy at the control level and increase RV viscoelasticity, it resulted in smaller changes in ESP and dilation and more stroke volume reduction (orange). This suggests that while the mechanical dysfunction prevents RV dilation, it reduces the systolic function, probably due to the Frank-Starling mechanism. Lastly, the combined effects resulted in a PV relation representative of severe RV failure. This work is the first to incorporate RV viscoelasticity in a PV model. We found marked changes in RV function with the addition of viscosity and the separate effects of RV viscosity and inotropy. The improved computational model offers a new, powerful tool to study different etiologies of RV dysfunction. [Table: see text] This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.