Hudgel D W
Case Western Reserve University, Cleveland.
Chest. 1992 Feb;101(2):541-9. doi: 10.1378/chest.101.2.541.
This article has reviewed the anatomic, compliance, reflex, and respiratory muscle variables that affect upper airway caliber and abnormalities which may precipitate upper airway collapse during sleep. One or more of these variables may be important in the mechanism of OSA in any given patient. First, anyone with anatomic narrowing of the upper airway is susceptible to OSA. However, we do know if anatomic narrowing of the upper airway is necessary for the development of OSA. Surely, heavy snoring produces pharyngeal trauma and possibly edema or inflammation, which in turn may narrow the upper airway. Submucosal adipose tissue or cervical adipose tissue may compress the airway when the tonic electrical activity of the pharyngeal muscles decreases with sleep onset. Data reviewed support the idea that the upper airway of OSA patients may be more collapsible than the upper airway of nonapneic subjects. Intrinsic tissue abnormalities have not been demonstrated that might be responsible for this collapsibility. Changes in collapsibility found are consistent with, and may be due to, changes in tonic and phasic contraction of upper airway muscles. Abnormalities in reflexes affecting upper airway size surely might exist in OSA. Edema or inflammation of pharyngeal tissues might not only narrow the upper airway but might also impair normal function of the receptors responsible for initiating protective reflexes. We propose the fluctuation between a low- and a high-drive state contributes to upper airway collapse in OSA. With this fluctuation the balance of forces and critical pressure concepts discussed above come into play (Fig 6). By stimulating upper airway inspiratory muscles, CO2 eliminates the hypoapneic, low-drive, high-resistance periods and thereby reduces the number of apneas. In addition, preferential stimulation of upper airway muscle activity dilates the upper airway per se. If the relative value of each of these factors can be determined diagnostically, perhaps therapy can be made more specific. By being more specific, therapy should be more successful than the present practice of prescribing a particular therapy, regardless of the specific mechanism responsible for the OSA in a given patient.
本文回顾了影响上气道口径的解剖学、顺应性、反射和呼吸肌变量，以及可能在睡眠期间促使上气道塌陷的异常情况。在任何特定患者中，这些变量中的一个或多个可能在阻塞性睡眠呼吸暂停（OSA）的发病机制中起重要作用。首先，任何上气道存在解剖学狭窄的人都易患OSA。然而，我们并不清楚上气道的解剖学狭窄对于OSA的发生是否必要。当然，严重打鼾会导致咽部创伤，并可能引发水肿或炎症，进而可能使上气道变窄。当咽部肌肉的强直性电活动随着睡眠开始而降低时，黏膜下脂肪组织或颈部脂肪组织可能会压迫气道。所回顾的数据支持这样一种观点，即OSA患者的上气道可能比无呼吸暂停受试者的上气道更易塌陷。尚未证实存在可能导致这种易塌陷性的内在组织异常。所发现的易塌陷性变化与上气道肌肉的强直性和相位性收缩变化一致，并且可能是由这些变化引起的。影响上气道大小的反射异常在OSA中肯定可能存在。咽部组织的水肿或炎症不仅可能使上气道变窄，还可能损害负责启动保护性反射的感受器的正常功能。我们提出，低驱动状态和高驱动状态之间的波动导致了OSA中的上气道塌陷。随着这种波动，上述的力平衡和临界压力概念开始起作用（图6）。通过刺激上气道吸气肌，二氧化碳消除了呼吸浅慢、低驱动、高阻力期，从而减少了呼吸暂停的次数。此外，对上气道肌肉活动的优先刺激本身会扩张上气道。如果能够通过诊断确定这些因素中每一个的相对值，或许治疗可以更具针对性。通过更具针对性，治疗应该比目前无论特定患者中OSA的具体机制而开具特定治疗方法的做法更成功。
