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Division of Pulmonary and Critical Care Medicine and Bellevue Hospital Chest Service, Department of Medicine, New York University School of Medicine, New York, New York 10016
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 
/
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 CO2
excretion, metabolic CO2
production, 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 temporal
/ 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.
carbon dioxide; blood; hypercapnia (physiopathology); respiration; sleep apnea syndromes (physiopathology); pulmonary gas exchange (physiology)
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