In summary, the study by Akashiba and colleagues allows us to further
reinforce the concept that nighttime desaturation and vital lung
capacity may contribute to the maintenance of CO2
homeostasis and daytime Paco2 levels
in OSA patients. However, we need to keep in mind that daytime eucapnia
is the end result of a complex conglomerate of factors, for which no
single factor can reliably account for the daytime
Paco2 level in any given patient.
Changes in cardiac output, ventilation-perfusion matching, metabolic
rate and fuel type utilization, sleep stage, circadian regulation,
obesity, intrinsic ventilatory drive, endocrine modulation, respiratory
muscle strength and endurance, and pulmonary mechanics all seem to be
active players in this complex equation, which allows for as many
permutations as the number of individuals experiencing OSA.