The Heart, Sleep, and Respiration

Sleep apnea-hypopnea syndrome (SAHS) consists of recurrent episodes in which the airflow becomes limited during sleep, a consequence of anatomo-functional abnormalities of the upper airway (UA) that lead to its collapse. This leads to a reduction in oxyhemoglobin saturation (SaO2) and causes arousals from sleep. The symptoms of this syndrome include the sensation of not having been refreshed by sleep, excessive daytime sleepiness (EDS), and neuropsychiatric, respiratory and heart problems. Epidemiological studies performed in the USA and Europe have shown that SAHS is a very prevalent disorder affecting 4%-6% of men and 2%-4% of women in the general, middle-aged adult population.1,2 This prevalence, however, increases with age. It has been shown that SAHS is associated with a deterioration in quality of life, high blood pressure,3,4 the development of cardiovascular and cerebrovascular disease,5 and even with traffic accidents.6,7 SAHS is therefore associated with excess mortality.8,9 The pathophysiology of SAHS is complex and still poorly understood. The stability of the bore of the UA depends on the action of dilatory, abductor and oropharyngeal muscles that are normally activated (in a rhythmic fashion) during inspiration. The UA collapses when, for a particular cross sectional area, the force produced by these muscles is overcome by the negative pressure generated by the inspiratory action of the diaphragm and the intercostal muscles.10 The tissue pressure that leads to the collapse of the airway is known as the critical closing pressure (Pcrit). Normally, the Pcrit of the UA is negative, and is lower in normal subjects than in those who snore, and even lower in snorers with SAHS. An increase in the Pcrit The Heart, Sleep, and Respiration