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Marion Boyd Gillespie; Paul W. Flint, MD; Philip L. Smith, MD; David W. Eisele, MD; Alan R. Schwartz, MD

Arch Otolaryngol Head Neck Surg. 1995;121(3):335-339.

Abstract
To determine the mechanism for obstructive sleep apnea in two patients with clinical abnormalities of laryngeal function, airflow dynamics during sleep were analyzed. The site of airway obstruction was assessed by examining pressure gradients across specific airway segments. The relation between maximal inspiratory airflow and nasal pressure was analyzed to determine (1) the critical pressure, a measure of the collapsibility of the laryngeal airway, and (2) the effect of nasal continuous positive airway pressure on airflow during sleep. Large inspiratory pressure gradients developed during sleep between the supraglottic and pleural spaces, indicating that collapse had occurred in the larynx. Elevated critical pressures of —6.4 and +1.2 cm H₂O, respectively, occurred in the two patients. When the nasal pressure was raised to 10 cm H₂O, normal levels of tidal airflow occurred, and obstructive apneas were eliminated. These findings indicate that sleep apnea was caused by laryngeal airflow obstruction that resulted from elevations in the collapsibility of the larynx. The response to nasal continuous positive airway pressure suggested that laryngeal sleep apnea was similar to pharyngeal sleep apnea in pathophysiologic characteristic and response to treatment.

(Arch Otolaryngol Head Neck Surg. 1995;121:335-339)

Author Affiliations
From the Department of Otolaryngology (Mr Gillespie and Drs Flint and Eisele) and the Johns Hopkins Sleep Disorders Center, Division of Pulmonary and Critical Care Medicine, Department of Medicine (Drs Smith and Schwartz), The Johns Hopkins Medical Institutions, Baltimore, Md.

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