Journal of Applied Physiology | 2021
Commentaries on Viewpoint: Nondyspnogenic acute hypoxemic respiratory failure in COVID-19 pneumonia
Abstract
TO THE EDITOR: Barreto-Filho et al. (1) proposed a potential mechanism of dysregulation of ventilatory control in patients affected by COVID-19 (disease caused by the newly discovered SARS-CoV-2) and a lack of awareness during acute hypoxemic respiratory failure. Although the physiopathology of COVID-19 is largely unknown, the fact that SARSCoV-2 may affect the control of minute ventilation raises important considerations that need to be addressed. The SARS-CoV-2 invasion of central and peripheral respiratory neural networks may cause different effects on the control of respiratory frequency (fR) and tidal volume (VT), with important implications for patients who recovered from the COVID-19 disease. Indeed, although VT appears to be mainly influenced by chemical stimuli, fR seems to be substantially regulated by central command and group III/ IV muscle afferent feedback inputs (2,3). Consequently, the chemosensitivity damage induced by SARS-CoV-2 might be more evident in VT rather than fR responses. Moreover, the inflammatory damage induced by the SARS-CoV-2 in the central respiratory neurons may also be extended to the subregion of the medial parabrachial complex, an area known to be involved in the control of expiratory and inspiratory duration (4). Lastly, the SARS-CoV-2 invasion of skeletal muscle tissues may cause neuromuscular damage (5) and affect the neural activity of group III/IV muscle afferents, which, in turn, may contribute to the dysregulation of fR (2). Therefore, it is highly advised to consider the effects of SARS-CoV-2 on fR and VT separately. Further studies are certainly required to better understand the effects of SARSCoV-2 on the ventilatory control system.