Cardiovascular function changes following lung resection: a computational model to compare afterload increase and contractility loss mechanisms
Journal:
arXiv
Published Date:
May 2, 2025
Abstract
Functional limitation after lung resection surgery has been consistently
documented in clinical studies, and right ventricle (RV) dysfunction has been
hypothesized as a contributing reason. However, the mechanisms of RV
dysfunction after lung resection remain unclear, particularly whether change in
afterload or contractility is the main cause. This study is the first to employ
a lumped parameter model to simulate the effects of lung resection. The
implementation of a computational model allowed us to isolate certain
mechanisms that are difficult to perform clinically. Specifically, two
mechanisms were compared: afterload increase and RV contractility loss.
Furthermore, our rigorous approach included local and global sensitivity
analyses to evaluate the effect of parameters on our results, both individually
and collectively. Our results demonstrate that contractility and afterload
exhibited consistent trends across various pressure and volume conditions,
pulmonary artery systolic pressure, pulmonary artery diastolic pressure, and
right ventricular systolic pressure showed opposite variations. The results
show that post-operative RV dysfunction may result from a combination of RV
contractility loss and afterload increase. Further exploration and refinement
of this first computational model presented herein will help us predict RV
dysfunction after lung resection and pave the way towards improving outcomes
for lung cancer patients.
