al-Saedi S A, Lemke R P, Haider Z A, Cates D B, Kwiatkowski K, Rigatto H
University of Manitoba, Dept. of Pediatrics, Winnipeg, MB, Canada.
Am J Perinatol. 1997 Apr;14(4):195-200. doi: 10.1055/s-2007-994126.
We tested the hypothesis that in preterm infants, prolonged apneas (apneas > or = 20 sec) are not random events but are preceded by frequent and progressively longer respiratory pauses associated with changes in ventilatory variables. We studied 36 preterm infants with apnea [birth weight 1190 +/- 60 g (mean +/- SEM), study weight 1300 +/- 60 g, gestational age 28 +/- 1 weeks, and postnatal age 23 +/- 2 days]. A nosepiece with a flow-through system was used to measure ventilation and alveolar gases. Throughout the monitoring period for each infant we established 10-min moving "window of observation" followed by a 1-min interval examined for the detection of a prolonged apnea. Within the 10-min window, three variables were defined: the number of apneic episodes, the maximum length of a single apneic episode, and the total duration of apneic time. During the following minute (eleventh) the presence or absence of a prolonged apnea was determined. Chi-square test for a linear-trend in the rate of prolonged apnea and multiple logistic regression analysis showed that the relative risk of a prolonged apnea increases significantly from preceding periods without apnea to preceding periods containing the potential predictors of prolonged apnea. The strongest predictor was total duration of apneic time in the previous 10 min. When the 1 min before prolonged apnea was compared with the 1 min of similar sleep state not having prolonged apnea, minute ventilation decreased, primarily due to a decrease in respiratory frequency. Oxygen saturation decreased and alveolar PCO2 did not change. These findings suggest that prolonged apnea is not a random event but is preceded by a disturbance of the respiratory control system characterized by (1) frequent apneas of progressive duration, (2) decrease in respiratory minute volume and frequency, and (3) decreased O2 saturation.
在早产儿中，长时间呼吸暂停（呼吸暂停≥20秒）并非随机事件，而是在与通气变量变化相关的频繁且逐渐延长的呼吸停顿之前出现。我们研究了36例患有呼吸暂停的早产儿[出生体重1190±60克（均值±标准误），研究时体重1300±60克，胎龄28±1周，出生后年龄23±2天]。使用带有流通系统的鼻夹来测量通气和肺泡气体。在对每个婴儿的整个监测期间，我们建立了10分钟的移动“观察窗口”，随后检查1分钟以检测是否出现长时间呼吸暂停。在这10分钟的窗口内，定义了三个变量：呼吸暂停发作次数、单次呼吸暂停发作的最长时长以及呼吸暂停总时长。在接下来的1分钟（第11分钟）确定是否存在长时间呼吸暂停。对长时间呼吸暂停发生率的线性趋势进行卡方检验和多因素逻辑回归分析表明，从无呼吸暂停的前期到包含长时间呼吸暂停潜在预测因素的前期，长时间呼吸暂停的相对风险显著增加。最强的预测因素是前10分钟呼吸暂停的总时长。当将长时间呼吸暂停前的1分钟与处于类似睡眠状态但无长时间呼吸暂停的1分钟进行比较时，分钟通气量下降，主要是由于呼吸频率降低。氧饱和度下降，而肺泡二氧化碳分压未改变。这些发现表明，长时间呼吸暂停并非随机事件，而是在呼吸控制系统受到干扰之前出现，其特征为：（1）持续时间逐渐延长的频繁呼吸暂停；（2）呼吸分钟量和频率降低；（3）氧饱和度降低。
