ABSTRACT
Sleep onset portends alterations in ventilatory control and the mechanics of upper airway and thoracoabdominal structures. Decreased ventilatory drive or increased upper airway resistance can cause respiratory events—discrete periods of reduced (hypopnea) or absent (apnea) airflow—that define the diagnosis of sleep-disordered breathing (SDB). This chapter summarizes the multiple pathophysiologic mechanisms contributing to decreased ventilatory drive (central apnea/hypopnea) or increased upper airway resistance (obstructive apnea/hypopnea). The chemoreflex control system maintains blood gas partial pressures through changes in ventilation by altering drive to respiratory pump muscles as well as muscles maintaining patency of the collapsible upper airway. Ventilatory control instability—brought about by changes in chemoreflex sensitivity (loop gain), circulatory delay, or the apneic threshold—may contribute to both central and obstructive apneas and hypopneas. Sleep-wake transitions and arousals may further contribute to ventilatory control instability, promoting respiratory events. Contributions to upper airway resistance include local factors (the intrinsic “collapsibility” of the upper airway, the pressure of surrounding tissues) and more distant factors (lung mechanics, the negative intraluminal airway pressure developed by the respiratory pump). Whether respiratory events are predominantly central or obstructive depends on the complex interaction of these multiple pathophysiologic mechanisms.
