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This Article Full Text Full Text (PDF) All Versions of this Article: 559/2/663    most recent jphysiol.2004.066084v2 jphysiol.2004.066084v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by O'Donoghue, F. J. Articles by McEvoy, R. D. Search for Related Content PubMed PubMed Citation Articles by O'Donoghue, F. J. Articles by McEvoy, R. D.

¹ Adelaide Institute for Sleep Health, Repatriation General Hospital, Daw Park, South Australia 5041, Australia
² Flinders University of South Australia, Bedford Park, South Australia 5042, Australia
³ University of Adelaide, Adelaide, South Australia 5005, Australia

Sleep hypoventilation is common in hypercapnic chronic obstructive pulmonary disease (COPD) and may contribute to daytime hypercapnia. The contributions of respiratory drive and respiratory mechanics to alterations in minute ventilation (_I) during sleep in this group have not been assessed. We assessed _I, breathing pattern, upper airway and total lung resistance (UAR, R_L), intraoesohageal diaphragmatic EMG (EMG_oes), intrinsic positive end-expiratory pressure (PEEP_i), dynamic compliance (C_dyn), pressure–time product of oesophageal pressure (PTP_oes), tension–time index of the diaphragm (TTI_di), end-expiratory lung volume (EELV) and respiratory drive (assessed as the slope of P_oes versus time in the isovolumetric interval before PEEP_i is overcome). Measurements were made in wakefulness and non-rapid eye movement (NREM) sleep, on 76%N₂/24%O₂ and on 76%He/24%O₂ (heliox). Satisfactory data for analysis were obtained in 10 patients; five had measurements on heliox. _I fell from (mean (S.E.M.)) 8.84(0.46) to 6.64(0.91 l min^–1, P = 0.011) between wakefulness and stage II sleep, due to a fall in tidal volume. No changes were seen in PEEP_i, C_dyn, EELV, PTP_oes, TTI_di, EMG_oes or respiratory drive. UAR increased (3.11(0.8) to 10.24(2.96) cmH₂O l^–1 s (P = 0.013) but R_L was unchanged. UAR was reduced on heliox (5.20(1.67) to 3.45(1.35) cmH₂O l^–1 s, P = 0.049) but _I during sleep did not increase. PTP_oes (350.2(51.0) to 259.4(46.3) cmH₂O s min^–1, P = 0.016), TTI_di (0.13(0.02) to 0.10(0.02) P = 0.04), and respiratory drive (20.48(4.69) to 15.02(4.57) cmH₂O s^–1, P = 0.01) were all reduced. This suggests respiratory drive alters to maintain a preset _I in sleep, irrespective of load, at least while the fatigue threshold of respiratory muscles is not exceeded.

(Received 18 April 2004; accepted after revision 23 June 2004; first published online 2 July 2004)
Corresponding author R. D. McEvoy: Adelaide Institute for Sleep Health, Repatriation General Hospital, Daw Park, South Australia 5041, Australia. Email: doug.mcevoy{at}rgh.sa.gov.au

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