the middle-aged working population, and can occur in 35-50% of some groups, such as diabetics, the morbidly obese, or the elderly (>65 years of age). Snoring is a mild form of upper airway obstruction, where the soft palate vibrates during inspiration at 40-60 Hz and impedes airflow. Obstructive apneas can occur during all sleep stages, however, often they are longer and result in more severe hypoxemia during REM (rapid eye movement) sleep. REM sleep is also called active sleep and is the sleep stage during which dreaming occurs. During REM, there is atonia (lack of muscle tone) and a general inhibition of sensory input, which inhibits afferent information from the lungs and ventilatory muscles, causing breathing to be more irregular.
Obstructive apnea can occur when reflexes do not respond to the normal negative pressure in the upper airways during inspiratory flow and induce the normal contractions of upper airway muscles to support the airways in an open position. Increased inspiratory effort, for example, in response to chemoreceptor stimulation, makes the tendency for airway collapse worse if the upper airways do not respond also. Therefore, the fundamental problem in obstructive apnea is a lack of coordination between the inspiratory and upper airway muscles and this is worst in REM sleep. The most effective treatment for obstructive apneas is nasal continuous positive airway pressure
(nasal CPAP). This treatment applies a positive pressure to the upper airways by a mask fitted over the nose of the sleeping patient, to counteract the decrease in airway pressure during inspiration and support the airways in an open position.
Sleep apnea also occurs in other conditions also. High-altitude sleep apnea may occur in normal subjects when sleeping on the mountains because of instabilities in the ventilatory control system. The ventilatory drive from Pao2 is increased at high altitude, but the ventilatory drive from Paco2 is decreased (because hypoxia stimulates hyperventilation). These changes can lead to periodic central apneas when other ventilatory drives are decreased during sleep. Abnormal interactions in ventilatory control may also be involved in sudden infant death syndrome (SIDS). SIDS, or crib death, refers to the unexplained death of an infant during sleep. SIDS probably results from multiple causes, but an immature ventilatory control system that fails to arouse an infant during sleep apnea is certainly one cause. The risk for SIDS decreases with age, as breathing becomes more regular. Periodic breathing (recurrent apneas) occurs in 40-50% of premature infants, and in 90% of babies delivered at 28-29 weeks of gestational age. There is currently no way to predict SIDS, and treatment consists of carefully monitoring infants who have shown signs of sleep apnea.
physiologists for more than a century. The seminal studies of Bert, a French physiologist and contemporary of Claude Bernard in the late 1800s, established that the respiratory response to altitude is a response to hypoxia, or decreased inspired Po2. Barometric pressure decreases with altitude, but the body does not respond to hypobaric conditions per se. Rather, physiologic control systems monitor the decrease in partial pressure of o2, which decreases with barometric pressure: Pio2 = Fio2 (Pb — Ph2o), where Pb = barometric pressure and Fio2 = 0.21 in air at any altitude.
Acclimatization occurs during prolonged exposures to altitude and is a physiologic response in an individual, as opposed to evolutionary or genetic adaptation occurring over generations. Acclimatization to hypoxia involves multiple systems, including changes in hemoglobin (Hb-o2 affinity, Hb concentration, and erythropoiesis; see Chapter 20), the microcirculation, and cellular metabolism. This section focuses on changes in the ventilatory control system with chronic hypoxia.
Ventilatory acclimatization is a time-dependent increase in ventilation occurring over hours to weeks of continuous hypoxic exposure. Figure 10 shows how ventilation and Paco2 change during 8 hr of continuous exposure to Pio2 = 88 mm Hg, corresponding to an altitude of 13,500 ft (4115 m) above sea level. Initially, Pao2 decreases and stimulates arterial chemoreceptors, which cause a rapid reflex increase in ventilation. Metabolic rate is unchanged in humans resting at such altitudes, so increased ventilation causes a decrease in PaCo2. This decrease in PaCo2 inhibits ventilatory drive, which limits the hypoxic ventilatory response (see Fig. 7). Hence, the acute response to altitude is a compromise
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