Gillespie M B, Flint P W, Smith P L, Eisele D W, Schwartz A R
Department of Otolaryngology, Johns Hopkins Medical Institutions, Baltimore, Md.
Arch Otolaryngol Head Neck Surg. 1995 Mar;121(3):335-9. doi: 10.1001/archotol.1995.01890030063010.
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.
为确定两名喉功能存在临床异常患者的阻塞性睡眠呼吸暂停机制，对睡眠期间的气流动力学进行了分析。通过检查特定气道节段的压力梯度来评估气道阻塞部位。分析最大吸气气流与鼻压力之间的关系，以确定（1）临界压力，这是衡量喉气道可塌陷性的指标，以及（2）鼻持续气道正压对睡眠期间气流的影响。睡眠期间，声门上与胸膜腔之间出现了较大的吸气压力梯度，表明喉部发生了塌陷。两名患者的临界压力分别升高至-6.4和+1.2 cm H₂O。当鼻压力升至10 cm H₂O时，出现了正常水平的潮气量气流，阻塞性呼吸暂停得以消除。这些发现表明，睡眠呼吸暂停是由喉部气流阻塞引起的，而喉部气流阻塞是由喉部可塌陷性增加所致。对鼻持续气道正压的反应表明，喉部睡眠呼吸暂停在病理生理特征和对治疗的反应方面与咽部睡眠呼吸暂停相似。
