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哮喘患儿睡眠期间的动脉血氧饱和度下降及其与气道阻塞和通气驱动的关系。

Arterial oxygen desaturation during sleep in children with asthma and its relation to airway obstruction and ventilatory drive.

作者信息

Smith T F, Hudgel D W

出版信息

Pediatrics. 1980 Nov;66(5):746-51.

PMID:7432880
Abstract

The possibility that arterial oxygen saturation (SaO2) decreases during sleep in children with chronic bronchial asthma was investigated. The relationship between decreases in sleep SaO2 and airflow obstruction and ventilatory drives, as characterized by ventilatory and inspiratory muscle activity responses to hypoxia and hypercapnia was also examined. Sixteen asthmatics on suboptimal bronchodilator therapy and ten healthy children were studied. Both maximum decrease in SaO2 and number of desaturations (decrease in SaO2 greater than or equal to 4%) per hour during sleep were greater in the asthmatics than in the control subjects. Both maximum decrease in SaO2 and number of desaturations per hour asleep were correlated with change in FEV1 and FEF25%-75% over the sleep period. Changes in SaO2 were not related to awake measurements of ventilatory drive. Eight of the asthmatics also were studied when on a more optimal medication regimen. On this program they had less airflow obstruction before and after sleep, and the number and extent of decreases in SaO2 were not different from those of the control subjects. We conclude: (1) decreases in SaO2 occurred during sleep in suboptimally treated asthmatic children; (2) SaO2 changes during sleep were related to the amount of air-flow obstruction that developed during sleep; (3) SaO2 changes during sleep were not related to ventilatory drive measured during wakefulness; and (4) a good therapeutic regimen eliminated abnormal amounts of sleep hypoxemia by improving airflow limitation. However, as the results of this study indicate, when their pulmonary status is unstable, asthmatic children may develop clinically significant hypoxemia during sleep.

摘要

我们研究了慢性支气管哮喘患儿睡眠期间动脉血氧饱和度(SaO2)降低的可能性。同时也探讨了睡眠期间SaO2降低与气流阻塞及通气驱动之间的关系,这些关系通过对低氧和高碳酸血症的通气及吸气肌活动反应来表征。我们对16名接受次优支气管扩张剂治疗的哮喘患儿和10名健康儿童进行了研究。哮喘患儿睡眠期间SaO2的最大降幅及每小时的血氧饱和度下降次数(SaO2下降≥4%)均高于对照组。睡眠期间SaO2的最大降幅及每小时的血氧饱和度下降次数均与睡眠期间第一秒用力呼气容积(FEV1)和25%-75%用力呼气流量(FEF25%-75%)的变化相关。SaO2的变化与清醒时通气驱动的测量结果无关。我们还对其中8名哮喘患儿在采用更优化药物治疗方案时进行了研究。在此方案下,他们睡眠前后的气流阻塞情况减轻,且SaO2下降的次数和程度与对照组无差异。我们得出以下结论:(1)接受次优治疗的哮喘患儿睡眠期间会出现SaO2下降;(2)睡眠期间SaO2的变化与睡眠期间出现的气流阻塞程度有关;(3)睡眠期间SaO2的变化与清醒时测量的通气驱动无关;(4)良好的治疗方案可通过改善气流受限消除异常的睡眠低氧血症。然而,正如本研究结果所示,当哮喘患儿的肺部状况不稳定时,他们在睡眠期间可能会出现具有临床意义的低氧血症。

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