With respect, this does not sound rooted in factual basis. Anyone who has taken physiology and been educated in anesthesia knows that there are numerous factors

With respect, this does not sound rooted in factual basis. Anyone who has taken physiology and been educated in anesthesia knows that there are numerous factors and feedback loops that decouple your theory of a direct link between ambient pCO2 and "vasopressin levels". I'd like to hear a more detailed explanation on how you feel it overrides compensatory mechanisms in ventilation, with subsequent breakdown in metabolic compensation of acidemia, and how you override negative feedback loops in the RAAS system including inhibition of ANP excretion, unless you theorize it is blunted at the renal level and natriuresis becomes down regulated in this scenario. Or basically if you want to reframe how everyone sitting in a house has subclinical SIADH I would be eager to hear a more detailed explanation.