Cardiovascular function changes following lung resection: a computational model to compare afterload increase and contractility loss mechanisms.

Functional limitation after lung resection surgery has been consistently documented in clinical studies, and right ventricle (RV) dysfunction has been hypothesized as a contributing factor. However, the mechanisms of RV dysfunction after lung resection remain unclear, particularly whether change in afterload or contractility is the underlying cause. This study reviews the clinical literature on this topic and proposes a lumped parameter model to simulate the effects of lung resection. Our model allowed us to isolate the two mechanisms and compare them. Subsequently, the simulation outputs were compared against the literature. Our rigorous approach included local and global sensitivity analyses to evaluate the effect of model parameters, both individually and collectively. The two mechanisms produced the same trends for all outputs except three: RV systolic pressure (RVSP) and pulmonary artery systolic and diastolic pressure (PASP and PADP) changed in opposite directions. Furthermore, our model indicates that obtaining pressure measurements in the clinic may help quantify the precise combination of the two mechanisms. This study presents the first mathematical model of the effect of lung resection on the cardiovascular system. Further refinement, combined with additional clinical data, will help us predict RV dysfunction and pave the way towards improving outcomes for lung cancer patients.