Before the scientific medical community became aware that obstructive sleep apnoea was an extremely prevalent disorder, SULLIVAN et al. [1] described what is still the best treatment available for this disorder: continuous positive airway pressure (CPAP) applied through the nose during sleep. The common endpoint of obstructive sleep apnoea, obstructive sleep hypopnoea and upper airway resistance syndrome is an increase in pharyngeal resistance occurring during sleep, leading to increased efficient or inefficient respiratory efforts that usually terminate with an arousal reaction [2]. When respiratory efforts are inefficient, hypoxia and hypercapnia develop during the period of increased pharyngeal resistance until sleep is interrupted, whereas, when respiratory efforts are efficient, hypoxia and hypercapnia are avoided. Nevertheless, the extraordinary effort necessary to sustain ventilation also leads to an arousal reaction [3]. Nasal CPAP acts essentially as a pneumatic splint pushing apart the walls of the pharynx and allowing normal spontaneous ventilation by the patients. In spite of its cumbersome nature, the treatment is so efficient that up to 80% of patients to whom it is proposed accept and comply with treatment for many years [4]. However, side-effects are not uncommon, and some patients discontinue therapy as time goes by. The continuous positive pressure necessary to ensure a good nights sleep varies from patient to patient in an individual and poorly predictable way. This makes the individual titration of pressure necessary. Usually this is done during a full or split polysomnographic night, using a trial and error process in which the pressure is slowly increased until apnoeas, hypopnoeas, snoring, episodes of flow limitation and/or arousals are abolished. Drops in saturation may persist when they are due to obesity in addition to sleep apnoea. In such cases, correction of apnoeas does not completely normalize oxygen saturation during the night. The means of titrating the pressure varies from centre to centre and there is no unique well-accepted way of performing titration. In the early years of CPAP, suppression of apnoeas was the main end-point of titration; hypopnoeas came later, and snoring, flow limitation and arousals were incorporated as targets for abolition in later years [5].
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Daniel Rodenstein (2000) studied this question.
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