Am. J. Respir. Crit. Care Med., Vol 149, No. 3, 03 1994, 707-714.
Mechanisms of apnea termination in obstructive sleep apnea. Role of chemoreceptor and mechanoreceptor stimuli
RJ Kimoff, TH Cheong, AE Olha, M Charbonneau, RD Levy, MG Cosio and SB Gottfried
Desmond N. Stoker Sleep Laboratory, Royal Victoria Hospital, Montreal, Quebec, Canada.
Previous work from our laboratory has indicated that mechanoreceptor
feedback from the respiratory muscles may play an important role in arousal
and apnea termination in obstructive sleep apnea (OSA). Other studies have
pointed to a prominent role for chemoreceptor stimuli. We postulated that
mechanoreceptor stimuli from the respiratory system are the primary
determinant of apnea termination, and that chemoreceptor stimuli exert
their effect indirectly through stimulation of ventilation and thus
proprioceptive feedback. To test this, we measured the diaphragmatic
tension-time index (TTdi) during obstructive sleep apneas in seven male
subjects with severe untreated OSA. We compared the maximal TTdi values at
end-apnea during administration of air, O2, and CO2. We reasoned that if
mechanoreceptor stimuli mediate apnea termination, changing the degree of
chemoreceptor stimulation during apneas should not alter the level of
respiratory effort at end-apnea. O2 administration produced a significant
increase in end-apneic arterial oxygen saturation (SaO2) and increased
apnea duration. CO2 administration led to an increase in pre- and
postapneic end-tidal carbon dioxide pressure (PETCO2), and tended to
shorten apneas. However, the mean value for maximal end-apneic TTdi was
0.12 +/- 0.01 (SEM) during room air breathing and was unaltered by O2 (0.12
+/- 0.01) or CO2 (0.11 +/- 0.01) administration. The consistency of
end-apneic TTdi values despite the varying chemical drive supports the
hypothesis that apnea termination in OSA is mediated by mechanoreceptor
feedback from the respiratory system, most likely from the respiratory
muscles. The influence of chemoreceptor information may be mediated
indirectly through an effect on ventilatory effort.
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Copyright © 1994 American Thoracic Society
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