Brief increases in arterial PCO2 (Pa(CO2)) (lasting several minutes) produce a sensation of respiratory discomfort (air hunger). It is not known whether air hunger adapts to chronic changes in Pa(CO2). This study tested whether the level of end-tidal PCO2 (PET(CO2)) required to evoke air hunger would increase with chronic elevation of PET(CO2) (lasting several days). Four ventilator-dependent subjects participated in a 2-wk study during which they were ventilated with air (placebo) or air rich in CO2 (CO2 exposure). Average resting PET(CO2) during control periods was 25 Torr (typical for such patients); PET(CO2) was 15 Torr higher during CO2 exposure. Ventilation and arterial PO2 did not differ between conditions. Periodically, we performed tests in which subjects rated the intensity of air hunger induced by brief increases in PET(CO2). The increase in PET(CO2) required to elicit a given air hunger rating during CO2 exposure also increased by ~15 Torr. That is, subjects' sensation of air hunger fully adapted to the chronic increase in PET(CO2). Arterial pH did not fully return to control values during CO2 exposure. Accommodation in the chemoreceptors and neural pathways that subserve air hunger sensation may explain the adaptation of air hunger.
- acid base
- partial pressure of carbon dioxide
- respiratory sensation
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