In examining the mechanical properties of the respiratory system during sleep in healthy humans, we observed that the inspiratory pressure-flow relationship of the upper airway was often flow limited and too curvilinear to be predicted by the Rohrer equation. The purposes of this study were 1) to describe a mathematical model that would better define the inspiratory pressure-flow relationship of the upper airway during sleep and 2) to identify the segment of airway responsible for the sleep-related flow limitation. We measured nasal and total supralaryngeal pressure and flow during wakefulness and stage 2 sleep in five healthy male subjects lying supine. A right rectangular hyperbolic equation, V = (alpha P)/(beta + P), where V is flow, P is pressure, alpha is an asymptote for peak flow, and beta is pressure at a flow of alpha/2, was used in its linear form, P/V = (beta/alpha) + (P/alpha). The goodness of fit of the new equation was compared with that for the linearized Rohrer equation P/V = K1 + K2V. During wakefulness the fit of the hyperbolic equation to the actual pressure-flow data was equivalent to or significantly better than that for the Rohrer equation. During sleep the fit of the hyperbolic equation was superior to that for the Rohrer equation. For the whole supralaryngeal airway during sleep, the correlation coefficient for the hyperbolic equation was 0.90 +/- 0.50, and for the Rohrer equation it was 0.49 +/- 0.25. The flow-limiting segment was located within the pharyngeal airway, not in the nose.(ABSTRACT TRUNCATED AT 250 WORDS)
Elderly subjects are known to be prone to periodic breathing in sleep. Because periodic breathing may be associated with changes in upper airway caliber, we hypothesized that oscillations in upper airway caliber contribute to the increased prevalence of sleep-related periodic breathing in the elderly. We tested this hypothesis by measuring upper airway resistance, ventilatory variables, and the pattern of variation of these variables in groups of body size-matched young and elderly healthy individuals during wakefulness and stage 2 non-rapid-eye-movement sleep. No major differences existed between the two groups during either wakefulness or sleep in mean upper airway resistance or ventilation values. However, ventilation was more variable during sleep in the elderly; this variability was oscillatory in the majority of elderly subjects at an average rate of 0.04 breaths/cycle or one cycle approximately every 24 s. Oscillations in upper airway resistance during sleep were associated with reciprocal oscillations in tidal volume and/or minute ventilation at the same frequency. Those subjects who had significant oscillations in upper airway resistance had more apneas and hypopneas than those subjects without such oscillations. Oscillations in resistance and ventilation occurred in the supine but not in the lateral body position. We conclude that the wide oscillations in upper airway resistance present during sleep in supine healthy elderly subjects produce a fluctuating mechanical limitation of ventilation, which may contribute to periodic breathing.
Oscillatory ventilatory pattern occurs more frequently in sleep despite the stabilizing factor of sleep-induced reduction in CO2 chemosensitivity. In nine young normal humans, we have tested the hypothesis that, despite a sleep-induced reduction in chemosensitivity, the transient central chemoreceptor-mediated change inspiratory ventilation (VI) caused by a standardized disturbance to chemoreflex ventilatory control is similar in quiet sleep and wakefulness. The equivalent VI response to a single-breath hyperoxic hypercapnic stimulus (i.e., inhaling a single breath of 0.01 liter of CO2 in O2--a direct measure of "closed-loop" dynamic response) was determined using pseudorandom binary CO2 stimulation and the prediction-error method of transfer function estimation. From these data, the response of VI to a single-breath increase of 1 Torr in end-tidal PCO2 was also derived, from which "dynamic" central chemosensitivity was calculated. Despite a 43% reduction in dynamic central chemosensitivity, the peak and the area under the closed-loop VI response are similar in wakefulness and quiet sleep, whereas sleep increases the duration of the response by 48%. Thus hyperoxic ventilatory stability is not reduced in quiet sleep relative to wakefulness. We propose that changes in dynamics of pulmonary gas exchange in sleep substantially offset the decreased chemosensitivity, thereby maintaining the gains and time constants of the central chemoreceptor-mediated component of the closed-loop ventilatory control system similar to those during wakefulness.
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