摘要
目的:通过对COPD合并呼吸衰竭患者中血浆NT-proBNP水平进行检测,探讨其在COPD病情发展过程中的变化以及临床意义。方法:两组患者均于住院次日空腹抽取肘正中静脉血3 mL,以备检测血浆NT-proBNP水平,同时行动脉采血血气分析检测。采用加拿大瑞邦生物医学有限公司生产的锐普荧光干式定量分析仪严格按照说明操作进行检测血浆NT-proBNP。采用RocheOmnic血气分析仪测定动脉血氧分压(PaO2)、血二氧化碳分压(PaCO2)。结果:两组血清NT-proBNP水平比较差异有统计学意义(P<0.05),实验组明显高于正常对照组。不同程度低氧血症的NT-proBNP水平比较差异有统计学意义(P<0.05),提示:NT-proBNPs水平随着PaO2的降低而升高。实验组68例COPD患者PaO2与血清NT-proBNP水平呈负相关(一0.641,P<0.05),而PaC02与血清NT-proBNP水平无相关性(r=0.143,P>0.05)。结论:血浆NT-proBNP水平检测在COPD呼吸衰竭的诊断、病情严重程度以及发展变化的预测中均具有较好的临床价值,对指导治疗COPD呼吸衰竭患者有重要的意义,值得进一步研究。
Objective:To discuss the change and clinical significance of plasma NT-proBNP detection in the COPD patients developing process,through the plasma NT-proBNP detection for COPD patients with respiratory failure.Methods:All patients in the hospital the next day were extrated cubital vein 3mL,to prepare plasma NT-proBNP level and arterial blood gas analysis testing.Biomedical Co.,the Canadian Ruibang sharp production of dry general quantitative fluorescence analyzer in strict accordance with the instructions for plasma NT-proBNP.Blood gas analyzer were used to test RocheOmnic arterial oxygen pressure(PaO2),blood carbon dioxide partial pressure(PaCO2).Results: Serum NT-proBNP level was significantly(P〈0.05),experimental group was significantly higher than the control group.Varying degrees of hypoxemia compared NT-proBNP level was significantly(P 〈0.05),prompts: NT-proBNPs levels increased with the decrease of PaO2.Experimental group of 68 patients with COPD PaO2and serum NT-proBNP level was negatively correlated(a 0.641,P 〈0.05),while PaC02 serum NT-proBNP levels with no correlation(r = 0.143,P〉 0.05).Conclusion: Plasma NTproBNP level of detection of respiratory failure in COPD diagnosis,severity and prediction of development and change have better clinical value in guiding treatment of COPD patients with respiratory failure are important and warrant further study.
出处
《中国医药导刊》
2012年第5期758-759,共2页
Chinese Journal of Medicinal Guide
关键词
脑利钠肽N端前体肽
阻塞性肺疾病
慢性病
呼吸衰竭
N-terminal brain natriuretic peptide precursor peptide; Obstructive pulmonary disease; Chronic disease; respiratory failure