Studies in man have revealed alveolar hypoventilation and diminution of ventilatory responsiveness to chemical stimuli during non-REM sleep, while results in tracheostomized dogs and intact cats reveal little alteration in alveolar ventilation and chemoventilatory responsiveness. Demonstration that upper airway resistance rises dramatically during sleep has led to the speculation that ventilatory responsiveness declines in man owing to the added resistive load, as described above. Recent results demonstrate this clearly by showing that reduction of upper airway resistance in normals in quiet sleep returns alveolar ventilation nearly to awake values. Accordingly, the relationship between motor output to the diaphragm and the hypercapnia or hypoxia stimulus appears to be essentially unaltered during non-REM sleep, as depicted in Figure 2. In other words, in non-REM sleep the respiratory controller responds normally to an increase in arterial Pco2 or a decrease in arterial Po2. This contrasts with its response during REM sleep when such changes in blood gases evoke attenuated increases in the hypercapnic ventilatory responsiveness, as shown in Figure 2. This change may result from supression of chemoreceptive components or from the depression of motor output by inhibition of nonphrenic, respiratory motoneurons (see REM Atonia section, below). flovent inhaler
Figure 2. Hypercapnic stimulus/ventilatory response relationships for normal man are depicted in normoxic conditions (straight lines). The metabolically determined relationship between ventilation and Pco2 is given by the curved lines. During quiet or non-REM sleep, the stimulus response characteristic below the metabolic curve is steep, resulting in an apneic threshold. This is not apparent during wakefulness or active (REM) sleep. Note also the diminished responsiveness to increases in the hypercapnic stimulus during REM.