One of the earliest symptoms a COVID-19 patient may experience is a case of “silent hypoxemia.” Patients present with the appearance of normal lung function and few other symptoms, but blood oxygen readings tell a different story. Upon further testing, blood oxygen levels return alarmingly low in these patients, with little certain about the mechanisms that lead to this condition. Recently, a group of scientists at Boston University and the University of Vermont developed a model to explain this phenomenon by taking a closer look at lung function.

In the lungs, oxygen-deficient blood passes by small air sacs called alveoli. At these sites, oxygen is received by blood cells in exchange for carbon dioxide. If some regions of the lungs are unable to exchange carbon dioxide for oxygen, the body diverts blood to more oxygen-rich, aerated regions of the lungs to improve oxygen delivery. In COVID-19 patients, it is hypothesized that this mechanism malfunctions. The researchers tested this hypothesis by creating a mathematical model of the lungs to study the flow of oxygen-rich and oxygen-deficient blood under three different conditions: normal diversion of blood, impaired diversion of blood, and reversed diversion of blood.

These researchers found from their model that impaired or reversed diversion of blood in the lungs may play a role in silent hypoxemia. One key factor was identified: the ratio between the percentage of blood pumped from the heart that could not exchange for oxygen and the percentage of damaged lung tissue. In cases of silent hypoxemia, reports show this ratio hovers around 3.0. Modelling determined it is physiologically plausible for this ratio to manifest partially due to the impaired or reversed diversion of blood into regions unable to exchange for oxygen. Although the extent that this mechanism contributes in a clinical setting is likely limited, they speculated a model combining their purported mechanism and others could provide greater clinical context for this condition.  This study provides a starting point to develop a more comprehensive model to improve treatment and care for patients hospitalized with COVID-19.

Jacob Herrman is a post-doctoral fellow in the Department of Biological Engineering at Boston University. Vitor Mori is a post-doctoral fellow in the Vermont Lung Center at the University of Vermont. Dr. Jason Bates is a professor in the Department of Electrical and Biomedical Engineering at the University of Vermont. Dr. Béla Suki is a professor in the Department of Biological Engineering and a Principal Investigator of the Cell & Tissue Mechanics Lab at Boston University.

Managing Correspondent: Koby Ljunggren

Original Article: Modeling lung perfusion abnormalities to explain early COVID-19 hypoxemia. Nature Communications.

Image Credit: Pixabay

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