Abstract
Acute respiratory distress syndrome (ARDS) represents an acute diffuse inflammation of the lungs triggered by different causes, uniformly leading to a noncardiogenic pulmonary edema with inhomogeneous densities in lung X-ray and lung CT scan and acute hypoxemia. Edema formation results in “heavy” lungs, inducing loss of compliance and the need to spend more energy to “move” the lungs. Consequently, an ARDS patient, as long as the patient is breathing spontaneously, has an increased respiratory drive to ensure adequate oxygenation and CO2 removal. One would expect that, once the blood gases get back to “physiological” values, the respiratory drive would normalize and the breathing effort return to its initial status. However, in many ARDS patients, this is not the case; their respiratory drive appears to be upregulated and fully or at least partially detached from the blood gas status. Strikingly, similar alteration of the respiratory drive can be seen in patients suffering from SARS, especially SARS-Covid-19. We hypothesize that alterations of the renin-angiotensin-system (RAS) related to the pathophysiology of ARDS and SARS are involved in this dysregulation of chemosensitive control of breathing.
Highlights
Per definition, acute respiratory distress syndrome (ARDS) is characterized by an inhomogeneously distributed, noncardiogenic pulmonary edema and acute hypoxemia
The increased respiratory drive can lead to severe hyperventilation with breathing efforts that create large negative pressure swings that lead to self-inflicted lung injury (P-SILI), promoting a shift to the H-type of COVID-19 pneumonia (Cruces et al, 2020; Gattinoni et al, 2020a; Smit et al, 2020)
Apart from this clinical alteration, it has been shown that plasma levels of angiotensin II of severe acute respiratory syndrome (SARS)-CoV2 infected patients were elevated (Liu et al, 2020; Wu et al, 2020), and plasma levels correlated to the viral load as well as to the degree of lung injury (Liu et al, 2020)
Summary
Acute respiratory distress syndrome (ARDS) is characterized by an inhomogeneously distributed, noncardiogenic pulmonary edema and acute hypoxemia. The increased respiratory drive can lead to severe hyperventilation with breathing efforts that create large negative pressure swings that lead to self-inflicted lung injury (P-SILI), promoting a shift to the H-type of COVID-19 pneumonia (Cruces et al, 2020; Gattinoni et al, 2020a; Smit et al, 2020) Apart from this clinical alteration, it has been shown that plasma levels of angiotensin II of SARS-CoV2 infected patients were elevated (Liu et al, 2020; Wu et al, 2020), and plasma levels correlated to the viral load as well as to the degree of lung injury (Liu et al, 2020). MasR are robustly expressed in GABAergic neurons in the basolateral amygdala (BLA), and ACE2 overexpression increases the spontaneous postsynaptic inhibitory currents in this region (Wang et al, 2016)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
