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气管内气体吹入对油酸诱导的犬肺损伤的吸气潮气量保留作用。

Inspiratory tidal volume sparing effects of tracheal gas insufflation in dogs with oleic acid-induced lung injury.

作者信息

Nahum A, Ravenscraft S A, Adams A B, Marini J J

机构信息

Department of Pulmonary and Critical Care, St Paul-Ramsey Medical Center, University of Minnesota 55101-2595, USA.

出版信息

J Crit Care. 1995 Sep;10(3):115-21. doi: 10.1016/0883-9441(95)90002-0.

Abstract

PURPOSE

Tracheal gas insufflation (TGI) improves the efficiency of conventional mechanical ventilation (CMV) by reducing the series dead space of the airways. Consequently, application of TGI as an adjunct to CMV may permit reducing tidal volume (VT) while limiting CO2 retention. We tested the extent to which panexpiratory TGI allows reduction of VT while maintaining PaCO2 constant in an oleic acid-induced lung injury model.

METHODS

We studied six anesthetized, paralyzed, and mechanically ventilated dogs. Oleic acid injury was induced by injecting 0.09 mL/kg of oleic acid into the right atrium. After stabilization of lung injury the VT-sparing effect of TGI was tested by progressively increasing catheter flow rate (Vc) from 2 to 5, 10, and 15 L/min while decreasing VT by an amount that maintained PaCO2 constant (approximately 47 mm Hg) with respect to baseline (Vc = 0 L/min).

RESULTS

Tidal volume was decreased from a baseline value of 0.360 +/- 0.030 L to 0.238 +/- 0.054 L at Vc of 15 L/min. The reduction in VT was associated with a decrement in peak and end-inspiratory plateau airway opening pressure from 32 +/- 3 to 28 +/- 6 cm H2O and from 25 +/- 2 to 21 +/- 3 cm H2O, respectively. Total physiological dead space fraction decreased from a baseline value of 0.60 +/- 0.08 to 0.31 +/- 0.20 during TGI at 15 L/min. TGI did not affect cardiac output, PaO2, or pulmonary venous admixture.

CONCLUSION

We conclude that TGI can be a useful adjunct to CMV during acute lung injury to limit VT while avoiding CO2 retention.

摘要

目的

气管内气体吹入(TGI)通过减少气道串联死腔来提高传统机械通气(CMV)的效率。因此,将TGI作为CMV的辅助手段可能允许减少潮气量(VT),同时限制二氧化碳潴留。我们在油酸诱导的肺损伤模型中测试了全呼气期TGI在维持动脉血二氧化碳分压(PaCO2)恒定的情况下允许减少VT的程度。

方法

我们研究了6只麻醉、麻痹并接受机械通气的犬。通过向右心房注射0.09 mL/kg油酸诱导油酸损伤。在肺损伤稳定后,通过将导管流速(Vc)从2 L/min逐步增加到5、10和15 L/min,同时将VT降低一定量以维持相对于基线(Vc = 0 L/min)的PaCO2恒定(约47 mmHg),来测试TGI的减少VT的效果。

结果

在Vc为15 L/min时,潮气量从基线值0.360±0.030 L降至0.238±0.054 L。VT的减少分别与吸气峰压和吸气末平台气道开口压力从32±3 cmH2O降至28±6 cmH2O以及从25±2 cmH2O降至21±3 cmH2O相关。在15 L/min的TGI期间,总生理死腔分数从基线值0.60±0.08降至0.31±0.20。TGI不影响心输出量、PaO2或肺静脉混合血。

结论

我们得出结论,在急性肺损伤期间,TGI可作为CMV的有用辅助手段,以限制VT同时避免二氧化碳潴留。

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