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, Roberta M. Goldring

Research output: Contribution to journalArticlepeer-review

77 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)917-924
Number of pages8
JournalJournal of Applied Physiology
Volume93
Issue number3
DOIs
StatePublished - Sep 2002
Externally publishedYes

Keywords

  • Carbon dioxide
  • Hypercapnia
  • Hypoventilation
  • Pickwickian syndrome
  • Sleep apnea syndromes

Fingerprint

Dive into the research topics of 'Postevent ventilation as a function of CO2 load during respiratory events in obstructive sleep apnea'. Together they form a unique fingerprint.

Cite this