Effect of sleep on respiratory muscle activity during mechanical ventilation.
Effect of sleep on respiratory muscle activity during mechanical ventilation.
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睡眠对机械通气期间呼吸肌活动的影响。
DOI：
10.1164/ajrccm/147.1.32
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Skatrud,JB
中科院分区：
文献类型：
--
作者：
Simon,PM;Dempsey,JA;Landry,DM;Skatrud,JB
本研究的目的是确定在机械通气过程中意识是否对呼吸的神经机械抑制的表达至关重要。同样的机械通气模型也被用来评估睡眠状态在睡眠中引起CO2潴留的相对重要性。使用正压通气抑制呼吸肌活动;然后添加002，直到再次出现吸气努力，这定义了复张阈值（PCO 2 RT）。通过使用被动机械通气保持呼吸系统的力学恒定，使我们能够测量呼吸控制器的输出，而不依赖于这些参数。8名正常受试者在清醒和睡眠期间使用鼻罩进行机械过度通气，流速、频率和潮气量匹配。当无法检测到吸气肌活动且潮气末Pco 2（PETCO 2）低于30 mm Hg时，以阶梯式增量添加吸入002，直至再次发生吸气。与清醒状态相比，睡眠状态增加了正常呼吸PETCO 2（42±4 vs 38±3 mm Hg）和Pc 02 RT（48±3 vs 46±2 mm Hg）。机械通气期间吸气肌活动的神经机械抑制在清醒和睡眠期间均存在，如Pe 02 RT和正常呼吸PETCO 2之间的平均差异分别为8和6 mm Hg所证明的。比较清醒和睡眠时的复张阈值，以评估睡眠对呼吸运动输出的影响，而不受负荷变化的影响，即呼吸力学保持不变。Pc 0 2 RT是在睡眠期间高于在清醒的每一个主题，表明与觉醒刺激的损失在设定点的变化。还测定了清醒和睡眠（4 mm Hg）之间平均正常呼吸PETCO 2的差异，以评估呼吸力学不再保持恒定时睡眠对Pco 2的影响。平均正常呼吸PETCO 2（4 mm Hg）的差异大于平均Pc 02 RT（2 mm Hg）的差异，表明并非所有睡眠期间发生的CO2潴留都是由于设定点的变化。我们的结论是，意识是不必要的表达呼吸的神经机械抑制在机械通气。我们的研究结果进一步支持了这一概念，即设置点和呼吸负荷的变化，如上气道阻力的增加是睡眠诱导的CO，retention.The的重要性的清醒状态的非化学神经输入到呼吸中枢的处理的重要性是不清楚的。意识是气道负荷期间机械感受器反馈的即时表达所必需的（1-4），但它不是对吸气肌缩短的代偿反应所必需的（5）。在清醒的人中，在机械通气期间对吸气肌活动的实质性神经机械抑制作用已经被证明（6，7）。机械通气时呼吸肌的去负荷导致呼吸运动输出减少。Henke和同事（8）证明了在睡眠期间被动等二氧化碳通气对吸气肌活动的部分抑制，表明存在
The purpose of this study was to determine whether consciousness was critical for the expression of neuromechanical inhibition of breathing during mechanica) ventilation. This same mechanical ventilation model also was used to evaluate the relative importance of sleep state in causing CO 2 retention during sleep. Positive pressure ventilation was used to suppress respiratory muscle activity; 002 was then added until a reappearance of inspiratory effort, which defined the recruitment threshold (PCO2RT). Keeping the mechanics of the respiratory system constant through the use of passive mechanical ventilation allowed us to measure the output of the respiratory controller, independent of these parameters. Eight normai subjects were mechanically hyperventilated with a nasal mask during wakefulness and sleep with matched flow rates, frequencies, and tidal volumes. When inspiratory muscle activity was undetectable and end-tidal Pco 2 (PETCO2) fel] below 30 mm Hg, inspired 002 was added in stepped increments until inspiration reoccurred. The sleeping state increased both eupneic PETCO2 (42±4 versus 38±3 mm Hg) and Pc02 RT (48±3 versus 46±2 mm Hg) compared with that during wakefulness. Neuromechanical inhibition of inspiratory muscle activity during mechanical ventilation was present during both wakefulness and sleep, as evidenced by the mean difference between Pe02 RT and eupneic PETCO2 of 8 and 6 mm Hg, respectively. Recruitment thresholds during wakefulness and sleep were compared to evaluate the effect of sleep on respiratory motor output independent of changes in load, ie, respiratory mechanics held constant. Pc0 2 RT was higher during sleep than during wakefulness in every subject, indicating a change in set point associated with the loss of the wakefulness stimulus. The difference in mean eupneic PETCO2 between wakefulness and sleep (4 mm Hg) also was determined to evaluate the effect of sleep on Pco2 when respiratory mechanics were no longer held constant. The difference in mean eupneic PETCO2 (4 mm Hg) was greater than the difference in mean Pc02 RT (2 mm Hg), suggesting that not all the CO2 retention incurred during sleep was due to changes in set point. We conclude that consciousness is not necessary for the expression of neuromechanical inhibition of breathing during mechanical ventilation. Our findings further support the concept that both changes in set point and respiratory load such as an increase in upper airway resistance are important determinants of sleep-induced CO, retention.The importance of the wakefulness state in the processing of nonchemical neural input to the respiratory center is not clear. Consciousness is required for the immediate expression of mechanical receptor feedback during airway loading (1-4), but it is not necessary for the compensatory response to inspiratory muscle shortening (5). A substantial neuromechanical inhibitory effect on inspiratory muscle activity during mechanical ventilation in awake humans hes been shown (6, 7). Respiratory motor output decreased in response to unloading of respiratory muscles during mechanical ventilation. Henke and coworkers (8) demonstrated a partial inhibition of inspiratory muscle activity during sleep with passive isocapnic ventilation, suggesting the presence of