ARDS is frequently accompanied by elevated arterial carbon dioxide tension (
), often accentuated by lung-protective ventilation. Although hypercapnia has long been viewed as a tolerable trade-off to limit ventilator-induced lung injury, contemporary clinical data suggest that its clinical interpretation depends on the exposure pattern, including magnitude and duration, the accompanying acid/base status, and the mechanisms underlying CO2 retention. In ARDS, elevated
may reflect reduced effective alveolar ventilation under lung-protective constraints, increased physiologic dead space, or both, and these mechanisms have different bedside implications. In this narrative review, we summarize pragmatic
–pH ranges observed or suggested in cohorts across ARDS severity strata and propose a bedside traffic-light framework that integrates
× pH × exposure time to support individualized decision-making without implying guideline-level thresholds. We also review capnography-derived indices, including the arterial–end-tidal carbon dioxide gradient (
−PETCO2), the normalized arterial–end-tidal carbon dioxide gradient [(
−PETCO2)/
], the end-tidal-to-arterial CO2 ratio (PETCO2/
), the ventilatory ratio, and VE/V̇CO2, which may help estimate and track dead space and V/Q mismatch over time. Prospective studies are needed to determine whether strategies informed by CO2–pH patterns and ventilatory efficiency improve patient-centered outcomes.
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