Quantifying the Hemodynamic Effects of Ventricular Fibrillation using a Verified Computational Model

TL;DR

This study develops and verifies a computational model to quantify the circulatory effects of ventricular fibrillation, revealing significant reductions in cardiac output and proposing a multiscale framework for future research.

Contribution

It introduces a verified 0D hemodynamic model of VF and a pathway for integrating multiscale cardiac and autonomic models for comprehensive analysis.

Findings

62.4% reduction in cardiac output during VF

Impaired ventricular filling and contractile failure are key effects

Provides a foundation for future multiscale VF modeling

Abstract

Ventricular Fibrillation (VF) is a malignant cardiac arrhythmia and the leading cause of sudden cardiac death, characterized by disorganized, high-frequency ventricular activity that results in the rapid loss of coordinated pump function and circulatory collapse. While the clinical manifestations of VF are well established, the multiscale mechanisms linking cellular electrophysiology to whole-organ mechanical failure remain challenging to study experimentally. Computational modeling therefore provides a critical platform for mechanistic investigation. This work presents a hierarchical computational study of VF beginning with the implementation and verification of a closed-loop, lumped-parameter (0D) hemodynamic model of the cardiovascular system. The verified model is used to quantify the global circulatory consequences of a prescribed VF state, demonstrating a 62.4% reduction in cardiac output and highlighting the dominant role of impaired ventricular filling and contractile failure. Recognizing the limitations of prescribing arrhythmia dynamics, we then propose a pathway toward an integrated, multiscale framework coupling the 0D hemodynamic core with models of cardiac electrophysiology and autonomic regulation to enable simulation of emergent arrhythmogenic behavior and reflex responses. Finally, we introduce an interactive simulator derived from the verified 0D model, designed to support education, hypothesis testing, and future integration of multiscale components. This work establishes a mechanistic baseline and software foundation for next-generation computational studies of VF and cardiovascular control.