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间歇正压通气加低流量间歇给氧(呼气末至吸气开始)并不能改善二氧化碳清除。

IPPV plus low-flow intermittent oxygen insufflation (end-exhalation to beginning inhalation) does not improve CO2 elimination.

作者信息

Burk N, Benumof J L, Ozaki G T, Miller L, Howell H B

机构信息

Department of Anesthesia, University of California, San Diego School of Medicine, La Jolla 92093.

出版信息

J Cardiothorac Vasc Anesth. 1991 Feb;5(1):46-50. doi: 10.1016/1053-0770(91)90092-8.

DOI:10.1016/1053-0770(91)90092-8
PMID:1907868
Abstract

It has been previously reported that continuous insufflation of low-flow O2 (0.05 to 0.20 L/kg/min), both supracarinally and subcarinally, in addition to intermittent positive-pressure ventilation (IPPV) (IPPV + O2 at a specific flow rate) caused progressive hemodynamic deterioration in patients. As demonstrated in a subsequent mechanical lung model, the hemodynamic deterioration was most probably due to lung hyperexpansion. The purpose of this study was to test the hypothesis that the O2 retarded the outflow of gas from the lung during exhalation and that if the insufflation were limited to the period of time from the end of tidal exhalation (EE) to the beginning of the next IPPV tidal inspiration (BI), lung hyperexpansion would not occur. The use of intermittent O2 in addition to IPPV was studied in both a mechanical lung model and in patients under general anesthesia; the mechanical lung model permitted direct examination of lung volume, and the patient study allowed determination of gas exchange effects. In the mechanical lung model and in the patients, a wide range of EE-BI O2 flow rates were used; respectively, 1 to 40 L/min and 0.05 to 0.20 L/kg/min. In the mechanical lung model, lung pressure and volume at EE and end-inspiration did not increase as long as the O2 flow was kept at or below 10 L/min. In the patients, airway pressure and hemodynamics did not change appreciably, but there was also no increase in CO2 elimination.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

此前有报道称,在患者中,除间歇性正压通气(IPPV)(特定流速下的IPPV + O₂)外,经隆突上和隆突下持续吹入低流量O₂(0.05至0.20 L/kg/min)会导致渐进性血流动力学恶化。如后续机械肺模型所示,血流动力学恶化很可能是由于肺过度膨胀。本研究的目的是检验以下假设:O₂在呼气时阻碍气体从肺流出,并且如果吹入仅限于从潮气末呼气(EE)结束到下一次IPPV潮气吸气(BI)开始的时间段,则不会发生肺过度膨胀。在机械肺模型和全身麻醉患者中研究了除IPPV外使用间歇性O₂的情况;机械肺模型允许直接检查肺容积,患者研究则可确定气体交换效果。在机械肺模型和患者中,使用了广泛的EE - BI O₂流速范围;分别为1至40 L/min和0.05至0.20 L/kg/min。在机械肺模型中,只要O₂流速保持在10 L/min或以下,EE和吸气末的肺压力和容积就不会增加。在患者中,气道压力和血流动力学没有明显变化,但CO₂清除也没有增加。(摘要截断于250字)

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