Pathogenesis of Obstructive and Central Sleep Apnea

Abstract

Considerable progress has been made over the last several decades in our understanding of the pathophysiology of both central and obstructive sleep apnea. Central sleep apnea, in its various forms, is generally the product of an unstable ventilatory control system (high loop gain) with increased controller gain (high hypercapnic responsiveness) generally being the cause. High plant gain can contribute under certain circumstances (hypercapnic patients). On the other hand, obstructive sleep apnea can develop as the result of a variety of physiologic characteristics. The combinations of these may vary considerably between patients. Most obstructive apnea patients have an anatomically small upper airway with augmented pharyngeal dilator muscle activation maintaining airway patency awake, but not asleep. However, individual variability in several phenotypic characteristics may ultimately determine who develops apnea and how severe the apnea will be. These include: (1) upper airway anatomy, (2) the ability of upper airway dilator muscles to respond to rising intrapharyngeal negative pressure and increasing Co(2) during sleep, (3) arousal threshold in response to respiratory stimulation, and (4) loop gain (ventilatory control instability). As a result, patients may respond to different therapeutic approaches based on the predominant abnormality leading to the sleep-disordered breathing.

Sleep Apnea and Cardiovascular Disease

“…Although deficient pharyngeal anatomy and variable upper airway dilator muscle control awake and asleep are likely the predominant causes of pharyngeal collapse in most patients with OSA, other mechanisms also likely contribute. [25][26][27][28] Loss of lung volume during sleep reduces longitudinal traction on the upper airway, rendering it more collapsible. In addition, ventilatory control system instability is associated with cycling respiratory output to ventilatory pump muscles and upper airway dilator muscles.…”

Clinical analysis of pharyngeal musculature and genioglossus exercising to treat obstructive sleep apnea and hypopnea syndrome

“…Also, the degree of dilatation of the upper airway muscles correlates closely with OSAHS. There are over twenty muscles that contribute to the upper airway, among which the genioglossus, levator veli palati muscle, and tensor veli palatini are the most important dilators (White, 2005).…”

Circulating Endothelial Cells and Endothelial Progenitor Cells in Obstructive Sleep Apnea

“…The subjects in this study had moderate degrees of desaturation, as assessed by nadir SaO 2 . If hypoxia is critical to changes in either CECs or circulating EPCs, then it is possible that subjects with more profound nocturnal desaturation, such as those with lower resting lung volumes [26,27] or longer apnea duration [28], might demonstrate altered numbers of CECs and circulating EPCs. In addition, we chose to express the degree of hypoxemia as nadir SaO 2 , which may not be as sensitive as other noninvasive markers such as percentage of time during sleep spent with an SaO 2 < 90%.…”