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Pathophysiology and Treatment of Central sleep Apnea

1986; Elsevier BV; Volume: 90; Issue: 2 Linguagem: Inglês

10.1378/chest.90.2.154

1931-3543

Leslie G. Olson, Kingman P. Strohl,

Tracheal and airway disorders

Apneas occurring during sleep are divided into those in which inspiratory efforts are absent (central sleep apnea, CSA) and those in which inspiratory efforts are present, and airflow is absent because the upper airway is occluded (obstructive sleep apnea, OSA). Obstructive sleep apnea is much more common in adult patients, but a few have predominantly central apneas. Patients with CSA tend to be older than the average patient with sleep apnea, often have associated neurologic disease, and are less likely to display the typical clinical picture of sleep apnea. The article by Issa and Sullivan in this issue (see page 165) reports the significant therapeutic observation that nasal CPAP is effective in the treatment of CSA, and uses this observation to propose a new theory of the pathogenesis of CSA. From an immediately practical point of view, the present article has three points to make: (1) as a diagnostic consideration, the distribution of CSA and OSA in an individual can depend on posture; in all eight patients of Issa and Sullivan, CSA was confined to the supine posture. (2) CSA can be effectively treated with nasal CPAP, and this treatment is effective long-term. (3) Higher nasal pressures are required to treat CSA than to treat OSA, so that CSA can occur in patients in whom OSA has been abolished. Others have reported studies in which nasal CPAP was relatively ineffective for CSA,1Sanders MH Nasal CPAP effect on patterns of sleep apnea.Chest. 1985; 86: 839-844Abstract Full Text Full Text PDF Scopus (54) Google Scholar but this may have occurred because they did not use high enough pressures. These results underscore the fact that the effective use of nasal CPAP requires meticulous evaluation of each patient and individualized therapy. Nasal CPAP may not be a complete answer to the therapeutic problems of CSA, because difficulty in managing the apparatus at home may be a major problem for neurologically impaired patients. Tracheostomy, however, is not likely to be any better in this regard, and will usually be much worse; low flow oxygen may be the best approach in the very infirm CSA patient. It has been generally believed for some time that OSA and CSA are alternative manifestations of a single underlying pathology. Obstructive apneas are thought to occur when there is inadequate motor drive to upper airway muscles in the presence of effective diaphragmatic contraction, and central apnea is easily conceptualized as a closely related but more severe phenomenon, with inadequate drive to both the upper airways muscles and the diaphragm.2Longobardo GS Gothe B Goldman MD Cherniack NS Sleep apnea considered as a control system instability.Respir Physiol. 1982; 50: 311-333Crossref PubMed Scopus (148) Google Scholar However, the exact etiology of CSA and its relationship to OSA have been elusive. Issa and Sullivan now suggest that central apnea is secondary to passive upper airway closure, which causes stimulation of mucosal sensory receptors and reflex apnea. The argument presented by Issa and Sullivan to support their suggestion is that: (1) central apneas occurred when the patients were supine, and passive airway closure is more likely in supine subjects; (2) in two patients, airway anesthesia abolished apneas; and (3) in one patient, airway occlusion produced by nasal obstruction was followed by brief expiratory pauses. Some aspects of this argument require careful consideration. It is, of course, true that snoring and OSA are worse in subjects sleeping supine than in those sleeping prone or in the lateral posture. However, there is no evidence that passive airway closure actually occurs commonly in sleeping subjects in the supine posture. Issa and Sullivan have previously reported that airway closure is easier to induce in supine than in lateral posture,3Issa FG Sullivan CE Upper airway closing pressures in obstructive sleep apnea.J Appl Physiol. 1984; 57: 520-527Crossref PubMed Scopus (180) Google Scholar but still in all cases some negative pressure was required to close the airway. Equally, there is no reason to believe that passive airway closure does not occur in these patients, but demonstration of the fact would lend support to Issa and Sullivan's hypothesis. The physiology of upper airway sensory receptors is complex and poorly understood, and although there is evidence of receptors that could mediate the reflex, the authors propose there is also evidence inconsistent with the hypothesis. For instance, there are in humans upper airway flow receptors whose stimulation depresses inspiratory efforts4McBride D Whitelaw WA A physiological stimulus to upper airway receptors in humans.J Appl Physiol. 1981; 51: 1189-1197Crossref PubMed Scopus (94) Google Scholar and whose inactivation by airways closure would presumably increase the likelihood of breathing. In OSA, there is a progressive increase in breathing efforts in the presence of a closed airway, so some explanation is needed of the absence of the mucosal apnea reflex in this situation. Even more puzzling is the fact that when Issa and Sullivan's CSA patients have OSA they also exhibit progressive increases of inspiratory effort. Why would they respond differently to airway occlusion when they were supine than when in the lateral posture? The response to airway anesthesia is persuasive evidence in the authors' favor, and it is to be hoped that more patients will be studied in this way. Clarification of this point is especially important since it is reported that in animals upper airway anesthesia causes airway obstruction.5Abu-Osba YK Mathew OP Thach BT An animal model for airway sensory deprivation producing obstructive apnea with post-mortem findings of sudden infant death syndrome.Pediatrics. 1981; 68: 796-801PubMed Google Scholar The demonstration that both CSA and OSA respond to nasal CPAP seems strong evidence that the same pathophysiologic processes cause both disorders. How these processes lead to one or another dominant form of apnea is unclear. Issa and Sullivan's hypothesis raises two possibilities: airway mucosal sensation could be abnormal and cause the disorder, or normal mucosal inputs could be mishandled by malfunctioning central neural pathways. The frequency of clinically apparent neurologic disease in CSA patients suggests the latter, but this is speculation. Exploration of these possibilities should significantly advance understanding of the role of upper airway sensation in normal and abnormal respiratory function. Reversal of Central Sleep Apnea Using Nasal CPAPCHESTVol. 90Issue 2PreviewBased on the theory that obstructive (OSA) and central (CSA) sleep apneas share common pathophysiologic mechanisms, we attempted to treat eight patients with predominantly CSA by continuous positive airway pressure (CPAP). All patients exhibited repetitive episodes of CSA and mixed sleep apneas (MSA) in the supine position with a mean duration of 23.7±0.7 s and 34.5±1.3 s, respectively. The pattern of apnea changed when the subject lay in the lateral position. Five patients were observed to develop OSA in the lateral position with a mean duration of 27.2 ±1.5 s, while the other three patients snored continuously. Full-Text PDF