Sleep disordered breathing (SDB) is characterized by abnormalities of respiratory pattern (pauses in breathing) or the quantity of ventilation during sleep. Obstructive sleep apnea (OSA), the most common such disorder, is characterized by the repetitive collapse or partial collapse of the upper airway during sleep and the need to arouse to resume ventilation. Sleep is thus disrupted, yielding waking somnolence and diminished neurocognitive performance. The recurrent sleep arousal in association with intermittent hypoxia and hypercapnia has been implicated in the occurrence of adverse cardiovascular outcomes. In addition, there is evolving evidence that SDB may contribute to insulin resistance and other components of the metabolic syndrome. Despite considerable progress, most patients remain undiagnosed and the principal therapeutic approach, continuous positive airway pressure (CPAP), remains somewhat cumbersome and hence not associated with optimal compliance rates.
SDB is exacerbated by alcohol intake. We continue to have a very incomplete understanding of the neurobiologic mechanisms responsible for the sleep-induced changes in upper airway motor control that lead to pharyngeal collapse. The reversibility with therapy of apnea-induced hypertension and other presumed adverse cardiovascular outcomes is largely untested. The explanation for reduced prevalence of SDB in women compared to men and why women present for therapy even less often than the prevalence numbers would suggest remain unresolved. It is unclear to what extent SDB in the elderly represents the same disorder as is encountered in younger populations and thus deserves similar therapy.
Cheyne-Stokes respiration, another type of SDB, is characterized by a crescendo – decrescendo pattern of respiration and is commonly seen during sleep in patients with congestive heart failure. The presence of this respiratory pattern appears to be an important risk factor for the progression of heart failure. More data are needed, however, to clarify the mechanisms leading to Cheyne-Stokes respiration, the impact of this abnormal ventilatory pattern on cardiac function, and the effect of treatment on survival.
– Reversibility with CPAP therapy of many of the neurocognitive and quality of life detriments associated with SDB is suggested by relatively small, short-term trials.
– The strength of the association between SDB and systemic hypertension in animal models and large, prospective epidemiologic studies is becoming more evident. Cross-sectional data also suggest an important association between SDB and stroke, myocardial infarction, and congestive heart failure.
– Studies addressing control of the pharyngeal musculature awake and asleep have demonstrated the ability of these muscles to respond to local stimuli awake, thereby compensating for deficient anatomy/collapsibility and maintaining airway patency. The loss of these reflex mechanisms during sleep is an important factor in the pathogenesis of SDB.
– Increasing evidence suggests a familial/genetic influence on predisposition to SDB independent of obesity. This genetic influence may be mediated differently in different racial and ethnic groups.
– The efficacy of oral appliances (primarily mandibular advancing devices) in patients with mild to moderate SDB and of upper airway surgical procedures over a range of apnea severity has been evaluated. However, more information is needed before their roles can be clearly delineated.
– Data suggest that positive airway pressure therapy can, over several weeks, eliminate Cheyne-Stokes respiration in heart failure patients and lead to improved transplant-free survival.