CONSTANT-FLOW INSUFFLATION PREVENTS ARTERIAL OXYGEN DESATURATION DURING ENDOTRACHEAL SUCTIONING

CONSTANT-FLOW INSUFFLATION PREVENTS ARTERIAL OXYGEN DESATURATION DURING ENDOTRACHEAL SUCTIONING
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DOI:
10.1164/ajrccm/144.2.395
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发表时间:
1991-08-01
期刊:
AMERICAN REVIEW OF RESPIRATORY DISEASE
影响因子:
--
通讯作者:
HARF, A
HARF, A
中科院分区:
其他
文献类型:
--
作者:
BROCHARD, L;MION, G;HARF, A

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在机械通气患者中,与呼吸机断开连接和气管内吸痰可诱导呼吸暂停导致的主要动脉血氧饱和度下降、吸入氧分数变化和肺容量减少。 本研究的目的是测试在此过程中输送氧气和维持肺容量的简单方法的有效性。 我们的研究分两部分进行。 在第一部分中,在7名因急性呼吸衰竭(Pa(O2)/FI(O2)= 347 +/- 33 mm Hg)接受通气的患者中使用了恒流吹入氧气(CFI),作为在呼吸暂停和与呼吸机断开连接期间维持动脉氧合的一种手段。 CFI通过改良的气管内导管给药,其中小毛细血管允许在与呼吸机断开连接期间在导管的气管末端附近输送高速射流。 与单纯呼吸暂停相比,CFI可防止动脉氧分压下降(在两种情况下,断开90 s后,CFI期间为16 +/- 7 mm Hg,呼吸暂停期间为117 +/- 27 mm Hg,p < 0.001),但不能减少高碳酸血症的发生。 CFI的有效性来自于向气管内注入氧气和维持空气夹带诱导的肺泡正压(平均10.4 +/- 1.1 cm H2O),防止了通常在断开连接后发生的肺容量下降(CFI期间+338 +/- 88 ml vs呼吸暂停期间-344 +/- 64 ml,p < 0.01)。 在研究的第二部分,CFI用于预防气管内吸痰引起的动脉血氧饱和度下降。 在其他7名镇静但未瘫痪的患者中(Pa(O2)/FI(O2)= 199 +/- 34 mm Hg),在给予或不给予CFI的情况下进行气管内吸痰。当使用CFI时,7名患者中有5名患者的氧饱和度下降被完全阻止,但在所有患者中均观察到氧饱和度下降,在标准抽吸期间达到-15.6 +/- 2.6%。 在剩下的两名患者中,使用CFI时,去饱和度低得多,恢复时间短得多。 在这些期间的跨肺压和肺顺应性的测量表明,CFI能够防止吸痰引起的肺容量减少。通过CT扫描对5例患者的肺容量进行评估,结果表明,CFI可防止气管内吸痰引起的肺容量下降27%。 我们建议使用这种简单的方法作为一种手段,以避免或最大限度地减少因急性呼吸衰竭而接受通气的严重低氧血症患者在与呼吸机断开连接或气管内吸痰期间的动脉血氧饱和度下降。
In mechanically ventilated patients, disconnection from the ventilator and endotracheal suctioning can induce major arterial oxygen desaturation resulting from apnea, changes in inspired oxygen fraction, and decrease in lung volume. The aim of this study was to test the efficacy of a simple method of delivering oxygen and maintaining lung volume during this process. Our study was conducted in two parts. In the first part, constant-flow insufflation of oxygen (CFI) was used in seven patients ventilated for acute respiratory failure (Pa(O2)/FI(O2) = 347 +/- 33 mm Hg) as a means of maintaining arterial oxygenation during apnea and disconnection from the ventilator. CFI was administered via a modified endotracheal tube in which small capillaries allowed delivery of a high-velocity jet flow near te tracheal end of the tube during disconnection from the ventilator. In comparison to apnea alone, CFI prevented a fall in arterial oxygen tension (16 +/- 7 mm Hg during CFI versus 117 +/- 27 during apnea, after 90 s of disconnection in the two situations, p < 0.001), whereas it did not reduce the development of hypercapnia. The efficacy of CFI resulted both from the injection of oxygen into the trachea and from the maintenance of positive alveolar pressure induced by air entrainment (mean 10.4 +/- 1.1 cm H2O), preventing a fall in lung volume usually occurring after disconnection (+338 +/- 88 ml during CFI versus -344 +/- 64 ml during apnea, p < 0.01). In the second part of the study CFI was used to prevent arterial oxygen desaturation induced by endotracheal suctioning. In seven other patients who were sedated but not paralyzed (Pa(O2)/FI(O2) = 199 +/- 34 mm Hg), endotracheal suctioning was performed with or without administration of CFI. In five of the seven patients oxygen desaturation was fully prevented when CFI was used, but it was observed in all patients and reached -15.6 +/- 2.6% during standard suctioning. In the two remaining patients, desaturation was much lower and recovery time was much shorter when CFI was used. Measurements of transpulmonary pressure and lung compliance during these periods suggested that CFI was able to prevent a decrease in lung volume induced by suctioning. Assessment of lung volume by CT scanning in five patients demonstrated that CFI prevented the 27% fall in lung volume induced by endotracheal suctioning. We propose to use this simple method as a means to avoid or minimize arterial oxygen desaturation during disconnection from the ventilator or during endotracheal suctioning in severely hypoxemic patients ventilated for acute respiratory failure.