Journal of Applied Physiology
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J Appl Physiol 93: 917-924, 2002. First published June 14, 2002; doi:10.1152/japplphysiol.01082.2001
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Vol. 93, Issue 3, 917-924, September 2002

Postevent ventilation as a function of CO2 load during respiratory events in obstructive sleep apnea

Kenneth I. Berger, Indu Ayappa, I. Barry Sorkin, Robert G. Norman, David M. Rapoport, and Roberta M. Goldring

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

Maintenance of eucapnia during sleep in obstructive sleep apnea (OSA) requires a balance between CO2 loading during apnea and CO2 elimination. This study examines individual respiratory events and relates magnitude of postevent ventilation to CO2 load during the preceding respiratory event in 14 patients with OSA (arterial PCO2 42-56 Torr). Ventilation and expiratory CO2 and O2 fractions were measured on a breath-by-breath basis during daytime sleep. Calculations included CO2 load during each event (metabolic CO2 production - exhaled CO2) and postevent ventilation in the 10 s after an event. In 12 of 14 patients, a direct relationship existed between postevent ventilation and CO2 load during the preceding event (P < 0.05); the slope of this relationship varied across subjects. Thus the postevent ventilation is tightly linked to CO2 loading during each respiratory event and may be an important mechanism that defends against development of acute hypercapnia in OSA. An inverse relationship was noted between this postevent ventilatory response slope and the chronic awake arterial PCO2 (r = 0.90, P < 0.001), suggesting that this mechanism is impaired in patients with chronic hypercapnia. The link between development of acute hypercapnia during respiratory events asleep and maintenance of chronic awake hypercapnia in OSA remains to be further investigated.

carbon dioxide; hypercapnia; hypoventilation; sleep apnea syndromes; Pickwickian syndrome


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