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© 2008 The American Thoracic Society
doi: 10.1513/pats.200707-111MG
Pathophysiology of Pediatric Obstructive Sleep Apnea
1 Division of Respiratory Diseases, Department of Medicine, Children's Hospital, and Harvard Medical School, Boston, Massachusetts; and 2 Division of Pulmonary Diseases, Department of Medicine, Tufts–New England Medical Center, and Tufts Medical School, Boston, Massachusetts
Correspondence and requests for reprints should be addressed to Eliot S. Katz, M.D., Division of Respiratory Diseases, Mailstop 208, Children's Hospital, Boston, 300 Longwood Avenue, Boston, MA 02115. E-mail: eliot.katz{at}childrens.harvard.edu
ABSTRACT
Sleep-disordered breathing is a common and serious cause of metabolic, cardiovascular, and neurocognitive morbidity in children. The spectrum of obstructive sleep-disordered breathing ranges from habitual snoring to partial or complete airway obstruction, termed obstructive sleep apnea (OSA). Breathing patterns due to airway narrowing are highly variable, including obstructive cycling, increased respiratory effort, flow limitation, tachypnea, and/or gas exchange abnormalities. As a consequence, sleep homeostasis may be disturbed. Increased upper airway resistance is an essential component of OSA, including any combination of narrowing/retropositioning of the maxilla/mandible and/or adenotonsillar hypertrophy. However, in addition to anatomic factors, the stability of the upper airway is predicated on neuromuscular activation, ventilatory control, and arousal threshold. During sleep, most children with OSA intermittently attain a stable breathing pattern, indicating successful neuromuscular activation. At sleep onset, airway muscle activity is reduced, ventilatory variability increases, and an apneic threshold slightly below eupneic levels is observed in non-REM sleep. Airway collapse is offset by pharyngeal dilator activity in response to hypercapnia and negative lumenal pressure. Ventilatory overshoot results in sudden reduction in airway muscle activation, contributing to obstruction during non-REM sleep. Arousal from sleep exacerbates ventilatory instability and, thus, obstructive cycling. Paroxysmal reductions in pharyngeal dilator activity related to central REM sleep processes likely account for the disproportionate severity of OSA observed during REM sleep. Understanding the pathophysiology of pediatric OSA may permit more precise clinical phenotyping, and therefore improve or target therapies related to anatomy, neuromuscular compensation, ventilatory control, and/or arousal threshold.
Key Words: children • sleep-disordered breathing
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