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) over dot / (Q)over dot mismatch"). This study measures acute kinetics of CO 2 during periodic breathing and addresses interapnea ventilatory compensati on for maintenance of CO2 homeostasis in 11 patients with OSA during daytim e sleep (37-171 min). Ventilation and expiratory CO2 and O-2 fractions were measured on a breath-by-breath basis by means of a tight-fitting full face mask. Calculations included CO2 excretion, metabolic CO2 production, and CO 2 balance (metabolic CO2 production - exhaled CO2). CO2 balance was tabulat ed for each apnea/hypopnea event-interevent cycle and as a cumulative value during sleep. Cumulative CO2 balance varied (-3,570 to +1,388 mi). Positiv e cumulative CO2 balance occurred in the absence of overall hypoventilation during sleep. For each cycle, positive CO2 balance occurred despite increa sed interevent ventilation to rates as high as 45 1/min. This failure of CO 2 homeostasis was dependent on the event-to-interevent duration ratio. The results demonstrate that 1) periodic breathing provides a mechanism for acu te hypercapnia in OSA, 2) acute hypercapnia during periodic breathing may o ccur without a decrease in average minute ventilation, supporting the prese nce of temporal (V)over dot / (Q)over dot mismatch, as predicted from our m odel, and 3) compensation for CO2 accumulation during apnea/hypopnea may be limited by the duration of the interevent interval. The relationship of th is acute hypercapnia to sustained chronic hypercapnia in OSA remains to be further explored.