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Reminder that ARDS is a syndrome of hypoxaemia NOT caused via cardiac failure with bilateral infiltrates. Triggers are bacterial infection, viruses, drowning, burns, trauma, TRALI, pancreatitis etc
Just as liver failure can be toxins, cirrhosis, viral infection etc...
When it comes to control of breathing hypoxia is a last ditch effort to restore respiration rate. You’d be a rubbish organism if you waited til the last minute to react to a threat
Hypoventilation is better measured by increasing CO2 - this is a strong trigger to breathe. So are protons. They work centrally. Probably because respiration also an acid base stakeholder and reciprocal CO2 interest.
Other ways of measuring ventilation are actual breath size and lungs stretch - there are muscle spindle fibres in the intercostals with thoracic innervation and pulmonary stretch receptors that are vagal.
These will all kick off dyspnoea in the absence of CO2 or O2 changes.
Furthermore anxiety and perceived imminent exercise will enhance ventilation rate even without changes in CO2. In fact when you exercise your CO2 levels don’t change for ages and if they did you wouldn’t go anywhere fast! So enhanced RR is pro active not reactive.
Additionally cytokines such as TNFa and interleukins have diverse effects on ventilation both via in/direct stimulation of pre Botzinger complex
But also sly inhibition of the usual pathways such as inhibition of the hypoxic response.
Apparently LPS endotoxaemia models for example frequently have vagally mediated increases in IL-1b that mess around in the medulla and blunt breathing. Real issue in septic neonates https://erj.ersjournals.com/content/52/suppl_62/PA4304
So yet another reason covid is just one fireball of sepsis and not a weird new entity.
Septic neonatal mammal paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3150618/
