Modelling Capillary O2 Transport Consequences in COVID-19 Induced Sepsis

Abstract

To address the obscure effects of SARS-CoV-2 on the microcirculation, a model of microcirculatory O₂ transport in skeletal muscle segments will be implemented using a capillary PO₂ outlet homogenization constraint and impose decreases in capillary density and tissue O₂ consumption reflecting COVID-19 states in the microcirculation. This will be used to identify quantitative decreases in the regulatory capacity of capillary velocities and inlet saturations in COVID-19 compared to baseline conditions.