Journal of Applied Physiology
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J Appl Physiol (June 14, 2002). doi:10.1152/japplphysiol.01082.2001
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Articles in PresS, published online ahead of print June 14, 2002
J Appl Physiol, 10.1152/jap.01082.2001
Submitted on October 29, 2001
Accepted on June 4, 2002

Post-Event Ventilation as a Function of CO2 Load during Respiratory Events in Obstructive Sleep Apnea

Kenneth I Berger1*, Indu Ayappa1, I. Barry Sorkin1, Robert G Norman1, David M Rapoport1, and Roberta M Goldring1

1 Division of Pulmonary and Critical Care Medicine, Department of Medicine, New York University School of Medicine, New York, New York, USA; Chest Service, Bellevue Hospital, New York, New York, USA

* To whom correspondence should be addressed. E-mail: kenneth.berger{at}med.nyu.edu.

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 post-event ventilation to CO2 load during the preceding respiratory event in 14 subjects with OSA (PaCO2 42-56mmHg). Ventilation and expiratory FECO2 and FEO2 were measured on a breath-by-breath basis during daytime sleep. Calculations included CO2 load during each event (metabolic CO2 production minus exhaled CO2) and post-event ventilation in the 10 seconds following an event. In 12/14 subjects, a direct relationship existed between post-event ventilation and CO2 load during the preceding event (p<.05); the slope of this relationship varied across subjects. Thus, the post-event 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 post-event ventilatory response slope and the chronic awake PaCO2 (r = 0.90, p < .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.




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