CO2 homeostasis during periodic breathing in obstructive sleep apnea

The contribution of apnea to chronic hypercapnia in obstructive sleep apnea (OSA) has not been clarified. Using a model (D. M. Rapoport, R. G. Norman, and R. M. Goldring. J. Appl. Physiol. 75: 2302–2309, 1993), we previously illustrated failure of CO2 homeostasis during periodic breathing resulting from temporal dissociation between ventilation and perfusion (“temporal V˙/Q˙mismatch”). This study measures acute kinetics of CO2 during periodic breathing and addresses interapnea ventilatory compensation for maintenance of CO2 homeostasis in 11 patients with OSA during daytime sleep (37–171 min). Ventilation and expiratory CO2 and O2 fractions were measured on a breath-by-breath basis by means of a tight-fitting full facemask. Calculations included CO2excretion, metabolic CO2production, and CO2 balance (metabolic CO2 production − exhaled CO2). CO2 balance was tabulated for each apnea/hypopnea event-interevent cycle and as a cumulative value during sleep. Cumulative CO2 balance varied (−3,570 to +1,388 ml). Positive cumulative CO2 balance occurred in the absence of overall hypoventilation during sleep. For each cycle, positive CO2 balance occurred despite increased interevent ventilation to rates as high as 45 l/min. This failure of CO2 homeostasis was dependent on the event-to-interevent duration ratio. The results demonstrate that 1) periodic breathing provides a mechanism for acute hypercapnia in OSA, 2) acute hypercapnia during periodic breathing may occur without a decrease in average minute ventilation, supporting the presence of temporalV˙/Q˙ mismatch, as predicted from our model, and 3) compensation for CO2 accumulation during apnea/hypopnea may be limited by the duration of the interevent interval. The relationship of this acute hypercapnia to sustained chronic hypercapnia in OSA remains to be further explored.