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J Appl Physiol 99: 2036-2044, 2005. First published July 14, 2005; doi:10.1152/japplphysiol.01040.2004
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HIGHLIGHTED TOPICS
Physiology and Pathophysiology of Sleep Apnea

Ventilation is unstable during drowsiness before sleep onset

Stuart Thomson,1 Mary J. Morrell,2 Jeremy J. Cordingley,2 and Stephen J. Semple1

1Department of Respiratory Medicine, Charing Cross Hospital Campus, and 2Clinical and Academic Unit of Sleep and Breathing, Royal Brompton Hospital, National Heart and Lung Institute, Imperial College, London, United Kingdom

Submitted 24 September 2004 ; accepted in final form 20 June 2005

Ventilation is unstable during drowsiness before sleep onset. We have studied the effects of transitory changes in cerebral state during drowsiness on breath duration and lung volume in eight healthy subjects in the absence of changes in airway resistance and fluctuations of ventilation and CO2 tension, characteristic of the onset of non-rapid eye movement sleep. A volume-cycled ventilator in the assist control mode was used to maintain CO2 tension close to that when awake. Changes in cerebral state were determined by the EEG on a breath-by-breath basis and classified as alpha or theta breaths. Breath duration and the pause in gas flow between the end of expiratory airflow and the next breath were computed for two alpha breaths which preceded a theta breath and for the theta breath itself. The group mean (SD) results for this alpha-to-theta transition was associated with a prolongation in breath duration from 5.2 (SD 1.3) to 13.0 s (SD 2.1) and expiratory pause from 0.7 (SD 0.4) to 7.5 s (SD 2.2). Because the changes in arterial CO2 tension (PaCO2) are unknown during the theta breaths, we made in two subjects a continuous record of PaCO2 in the radial artery. PaCO2 remained constant from the alpha breaths through to the expiratory period of the theta breath by which time the duration of breath was already prolonged, representing an immediate and altered ventilatory response to the prevailing PaCO2. In the eight subjects, the CO2 tension awake was 39.6 Torr (SD 2.3) and on assisted ventilation 38.0 Torr (1.4). We conclude that the ventilatory instability recorded in the present experiments is due to the apneic threshold for CO2 being at or just below that when awake.

apneic threshold for CO2; sleep-related rise in PCO2; arterial to end-tidal PCO2 gradient



Address for reprint requests and other correspondence: S.J.G. Semple, Dept. of Respiratory Medicine, Charing Cross Hospital, Fulham Palace Rd., London W6 8RF, UK (e-mail: s.semple{at}imperial.ac.uk)




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