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J Appl Physiol (July 14, 2005). doi:10.1152/japplphysiol.01040.2004
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Submitted on September 24, 2004
Accepted on June 20, 2005

Ventilation is unstable during drowsiness before sleep onset

Stuart Thomson1, Mary J. Morrell2, Jeremy J. Cordingley2, and Stephen J. Semple1*

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

* To whom correspondence should be addressed. E-mail: s.semple{at}imperial.ac.uk.

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-rem rapid eye movement sleep.chemical feedback. A volume cycled ventilator in the assist control mode was used to maintain CO2 tension (PETCO2) 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 (TTOT) and the pause in gas flow between the end of expiratory air flow and the next breath (TP) 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 TTOT from 5.2 (1.3) to 13.0 (2.1) s and TP from 0.7 (0.4) to 7.5 (2.2) s. 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 PETCO2 awake was 39.6 (2.3) mmHg and on assisted ventilation 38.0 (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.




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