What is new in respiratory monitoring?

This paper provides a review of a selection of papers published in the Journal of Clinical Monitoring and Computing in 2020 and 2021 highlighting what is new within the field of respiratory monitoring. Selected papers cover work in pulse oximetry monitoring, acoustic monitoring, respiratory system mechanics, monitoring during surgery, electrical impedance tomography, respiratory rate monitoring, lung ultrasound and detection of patient-ventilator asynchrony.

Electric Cell-Substrate Impedance Sensing (ECIS) as a Platform for Evaluating Barrier-Function Susceptibility and Damage from Pulmonary Atelectrauma.

Biophysical insults that either reduce barrier function (COVID-19, smoke inhalation, aspiration, and inflammation) or increase mechanical stress (surfactant dysfunction) make the lung more susceptible to atelectrauma. We investigate the susceptibility and time-dependent disruption of barrier function associated with pulmonary atelectrauma of epithelial cells that occurs in acute respiratory distress syndrome (ARDS) and ventilator-induced lung injury (VILI). This in vitro study was performed using Electric Cell-substrate Impedance Sensing (ECIS) as a noninvasive evaluating technique for repetitive stress stimulus/response on monolayers of the human lung epithelial cell line NCI-H441. Atelectrauma was mimicked through recruitment/derecruitment (RD) of a semi-infinite air bubble to the fluid-occluded micro-channel. We show that a confluent monolayer with a high level of barrier function is nearly impervious to atelectrauma for hundreds of RD events. Nevertheless, barrier function is eventually diminished, and after a critical number of RD insults, the monolayer disintegrates exponentially. Confluent layers with lower initial barrier function are less resilient. These results indicate that the first line of defense from atelectrauma resides with intercellular binding. After disruption, the epithelial layer community protection is diminished and atelectrauma ensues. ECIS may provide a platform for identifying damaging stimuli, ventilation scenarios, or pharmaceuticals that can reduce susceptibility or enhance barrier-function recovery.

Modeling the impact of school reopening on SARS-CoV-2 transmission using contact structure data from Shanghai.

BACKGROUND: Mathematical modeling studies have suggested that pre-emptive school closures alone have little overall impact on SARS-CoV-2 transmission, but reopening schools in the background of community contact reduction presents a unique scenario that has not been fully assessed. METHODS: We adapted a previously published model using contact information from Shanghai to model school reopening under various conditions. We investigated different strategies by combining the contact patterns observed between different age groups during both baseline and "lockdown" periods. We also tested the robustness of our strategy to the assumption of lower susceptibility to infection in children under age 15 years. RESULTS: We find that reopening schools for all children would maintain a post-intervention R0 < 1 up to a baseline R0 of approximately 3.3 provided that daily contacts among children 10-19 years are reduced to 33% of baseline. This finding was robust to various estimates of susceptibility to infection in children relative to adults (up to 50%) and to estimates of various levels of concomitant reopening in the rest of the community (up to 40%). However, full school reopening without any degree of contact reduction in the school setting returned R0 virtually back to baseline, highlighting the importance of mitigation measures. CONCLUSIONS: These results, based on contact structure data from Shanghai, suggest that schools can reopen with proper precautions during conditions of extreme contact reduction and during conditions of reasonable levels of reopening in the rest of the community.

Modeling lung perfusion abnormalities to explain early COVID-19 hypoxemia.

Early stages of the novel coronavirus disease (COVID-19) are associated with silent hypoxia and poor oxygenation despite relatively minor parenchymal involvement. Although speculated that such paradoxical findings may be explained by impaired hypoxic pulmonary vasoconstriction in infected lung regions, no studies have determined whether such extreme degrees of perfusion redistribution are physiologically plausible, and increasing attention is directed towards thrombotic microembolism as the underlying cause of hypoxemia. Herein, a mathematical model demonstrates that the large amount of pulmonary venous admixture observed in patients with early COVID-19 can be reasonably explained by a combination of pulmonary embolism, ventilation-perfusion mismatching in the noninjured lung, and normal perfusion of the relatively small fraction of injured lung. Although underlying perfusion heterogeneity exacerbates existing shunt and ventilation-perfusion mismatch in the model, the reported hypoxemia severity in early COVID-19 patients is not replicated without either extensive perfusion defects, severe ventilation-perfusion mismatch, or hyperperfusion of nonoxygenated regions.

Can Hyperperfusion of Nonaerated Lung Explain COVID-19 Hypoxia?

Early stages of the novel coronavirus disease (COVID-19) have been associated with 'silent hypoxia' and poor oxygenation despite relatively small fractions of afflicted lung. Although it has been speculated that such paradoxical findings may be explained by impairment of hypoxic pulmonary vasoconstriction in infected lungs regions, no studies have confirmed this hypothesis nor determined whether such extreme degrees of perfusion redistribution are physiologically plausible. Here, we present a mathematical model which provides evidence that the extreme amount of pulmonary shunt observed in patients with early COVID-19 is not plausible without hyperperfusion of the relatively small fraction of injured lung, with three-fold increases in regional perfusion to afflicted regions. Although underlying perfusion heterogeneity (e.g., due to gravity or pulmonary emboli) exacerbated existing shunt in the model, the reported severity of hypoxia in early COVID-19 patients could not be replicated without considerable reduction of vascular resistance in nonoxygenated regions.