Patients with moderate or severe respiratory muscle weakness characteristically show dips in oxygen saturation (SaO2) related to periods of rapid eye movement (REM) sleep (23, 24) (Figure 7). The episodic desaturation is usually due to hypopnea and less often to apnea and is associated particularly with phasic REM sleep, when brief periods of rapid, irregular eye movements are accompanied by reduced activity of skeletal muscles (24) (Figure 8). The hypopneas and/or apneas may appear to be either "central" (Figure 8) or "obstructive," or sometimes a mixture of both. The precise pattern of such events depends on the relative activation of the respiratory pump and upper airway dilator muscles (24). Obstructive ap-neas are more likely in weak patients who are also overweight (25). In patients with severe respiratory muscle weakness, some apneas that appear to be central may in fact be obstructive, incorrect classification being due to failure of external sensors to detect chest wall movements of reduced amplitude (26).
Hypercapnia in patients with slowly progressive weakness probably develops first during sleep. Continuous monitoring during sleep (e.g., with a transcutaneous Pco2 electrode) shows a gradual rise in Pco2 during REM sleep (23) (Figure 7). Consequently, PaCO2 measured shortly after waking is more likely to be elevated than values obtained later in the day. Symptoms of nocturnal hypoventilation include morning headaches, daytime sleepiness, and lack of energy. Similar symptoms can also result from sleep disruption associated with frequent apneas and hy-popneas, even in the absence of persistent hypercapnia. Daytime somnolence is particularly common in patients with myotonic dystrophy. However, even though sleep hypopnea and apnea are frequently found in this condition, they appear not to explain the sleepiness of most patients with myotonic dystrophy (27).
The timescale of progression from nocturnal to persistent diurnal hypercapnia in patients with chronic respiratory muscle weakness is not known.
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