A Systems Engineering Approach to Modeling and Analysis of Chronic Obstructive Pulmonary Disease (COPD)

TL;DR

This paper presents a systems engineering framework modeling COPD as a control system, identifying key physiological parameters affecting disease manifestation and systemic response, with implications for understanding disease mechanisms and stress responses.

Contribution

It introduces a novel systems engineering model of COPD integrating biological control components, enabling systematic analysis of disease-related physiological changes.

Findings

Changes in airway resistance significantly impact the cardio-respiratory system.

Pulmonary hypertension is linked to increased pulmonary resistance.

Hypoxic environments exacerbate systemic stress in COPD patients.

Abstract

Chronic Obstructive Pulmonary Disease (COPD) is a progressive lung disease characterized by airflow limitation. This study develops a systems engineering framework for representing important mechanistic details of COPD in a model of the cardio-respiratory system. In this model, we present the cardio-respiratory system as an integrated biological control system responsible for regulating breathing. Four engineering control system components are considered: sensor, controller, actuator, and the process itself. Knowledge of human anatomy and physiology is used to develop appropriate mechanistic mathematical models for each component. Following a systematic analysis of the computational model, we identify three physiological parameters associated with reproducing clinical manifestations of COPD - changes in the forced expiratory volume (FEV), lung volumes, and pulmonary hypertension. We quantify the changes in these parameters (airway resistance, lung elastance, and pulmonary resistance) as the ones that result in a systemic response that is diagnostic of COPD. A multivariate analysis reveals that the changes in airway resistance have a broad impact on the human cardio-respiratory system, and that the pulmonary circuit is stressed beyond normal under hypoxic environments in most COPD patients.