容许性高碳酸血症对急性肺损伤动物心肺功能影响的观察  

Effects of permissive hypercapnia on cardiopulmonary function in acute lung injury model

作　　者：黄建安[1] 王光杰[1] 马家用[1] 蒋文平[1] 朱晔涵[1] 凌春华[1] 黄小怡 陶岳多[1] 

机构地区：[1]苏州医学院附属第一医院呼吸科所

出　　处：《中华结核和呼吸杂志》1997年第2期76-79,共4页Chinese Journal of Tuberculosis and Respiratory Diseases

摘　　要：观察不同水平的容许性高碳酸血症（ＰＨＣ）对油酸型急性肺损伤（ＡＬＩ）模型的心肺功能影响。方法复制猪ＡＬＩ模型，四腔热稀释漂浮导管监测血液动力学及不同潮气量致不同程度的ＰＨＣ。结果ＡＬＩ导致明显的心肺功能恶化。呼气末正压可改善部分病理生理指标，但吸气末平台压（Ｐｅｅ）明显升高。潮气量（ＶＴ）降至７．７±０．３ｍｌ／ｋｇ、动脉血二氧化碳分压（ＰａＣＯ２）升至９．４４±１．２７ｋＰａ（１ｋＰａ＝７．５ｍｍＨｇ）时，心输出量明显改善而其它心肺功能无明显改变。ＶＴ降至６．１±０．６ｍｌ／ｋｇ、Ｐａ－ＣＯ２为１２．１±１．０５ｋＰａ时，虽气道峰压下降，但Ｐｅｅ未见降低且其它心肺指标恶化。结论合适的低潮气量致一定程度的ＰＨＣ是较为安全的通气方式。Objective TO observe the effects of permissive hypercapnia on cardiopulmonary func tion in oleic acid induced acute lung injury(ALI)models.MethodALL models of pigs were induced successfully by infusing oleic acid,Swan Ganz cathether was used for monitoring hemodynamics and dif ferent low tidal volumes were set for variable hypercapnia.Results ALI was characterized by an in crease in airway pressure and a decrease in static compliance(Cst)、artery oxygen tension(PaO 2)、oxy genation index and cardiac output.There was also an increase in mean pulmonary artery pressure(mPAP)、pulmonary vascular resistance(PVR)、systemic vascular resistance(SVR)and shunt fraction.Afterusing 0.98 kPa(1kPa=10.2cmH 2O)PEEP,some of cardiopulmonary functions were im proved.While reduced tidal volume to 7.7±0.3ml/kg and PaCO 2 increased to 9.44±1.27kPa(1kPa=7.5mmHg),which caused neither a change in PaO 2/FiO 2、PaO 2、Cst nor in SVR、PVR but an increase in cardiac output.Though ventilation setting did not change except for the reducing tidal vol ume to 6.1±0.6ml/kg and PaCO 2 reached 12.1±1.05kPa,then various adverse effects on cardiopul monary system were observed..Conclusion It seems that mechanical ventilation with permissive hyper capnia was safe at certain level.

关 键 词：急性 肺损伤 呼吸功能 高碳酸血症 容许性 

分 类 号：R589.6[医药卫生—内分泌] R563.02[医药卫生—内科学]