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先天性心脏病重度肺动脉高压对腺苷的急性反应
引用本文:张端珍,朱鲜阳,崔春生,张坡,盛晓棠,王琦光. 先天性心脏病重度肺动脉高压对腺苷的急性反应[J]. 心脏杂志, 2011, 23(2): 241-244
作者姓名:张端珍  朱鲜阳  崔春生  张坡  盛晓棠  王琦光
作者单位:沈阳军区总医院先心病内科,辽宁 沈阳 110016
摘    要:目的: 探讨先天性心脏病(CHD)并发重度肺动脉高压(PAH)患者对腺苷的急性血流动力学反应。方法: 对25例CHD并发严重PAH患者采用腺苷进行急性肺血管扩张试验,检测其血流动力学指标变化。结果: 25例患者中,仅7例患者达到最大剂量无不良反应。给予腺苷后,肺动脉压力和主动脉压力均显著降低(P<0.05),股动脉血氧饱和度,肺血管阻力,肺循环/体循环血流量比值,肺动脉/主动脉平均压比值,肺血管阻力/体循环阻力比值(Rp/Rs)均无明显变化。没有患者肺动脉平均压降至40 mmHg以下。12例患者肺血管阻力和Rp/Rs降低10%以上,与另外13例患者比较,二者在年龄,肺动脉压力,肺动脉/主动脉平均压比值,肺循环/体循环血流量比值,肺血管阻力和Rp/Rs等方面均无明显差异。结论: 在CHD并发重度PAH患者中,采用腺苷进行急性肺血管扩张试验可引起肺动脉和体循环压力同步降低,而对肺血管阻力无明显影响。

关 键 词:心脏病,先天性   肺动脉高压   腺苷   血流动力学   急性肺血管扩张试验
收稿时间:2010-03-16

Acute hemodynamic responses to adenosine in patients with congenital heart disease and severe pulmonary hypertension
ZHANG Duan-zhen,ZHU Xian-yang,CUI Chun-Sheng,ZHANG Po,SHENG Xiao-tang,WANG Qi-guang. Acute hemodynamic responses to adenosine in patients with congenital heart disease and severe pulmonary hypertension[J]. Chinese Heart Journal, 2011, 23(2): 241-244
Authors:ZHANG Duan-zhen  ZHU Xian-yang  CUI Chun-Sheng  ZHANG Po  SHENG Xiao-tang  WANG Qi-guang
Affiliation:ZHANG Duan-zhen,ZHU Xian-yang,CUI Chun-Sheng,ZHANG Po,SHENG Xiao-tang,WANG Qi-guang(Department of Congenital Heart Disease,General Hospital,Shenyang Military Area Command,Shenyang 110016,Liaoning,China)
Abstract:AIM: To investigate the acute hemodynamic responses to adenosine in patients with congenital heart disease (CHD) and severe pulmonary arterial hypertension (PAH). METHODS: Twenty-five patients with severe PAH secondary to left-to-right shunt CHDs underwent acute vasodilator test using IV adenosine infusion. Hemodynamic parameters were detected and analyzed. RESULTS: Only seven patients received the maximal dose 200 μg/(kg·min) of adenosine infusion without adverse effects. The tolerance dose of adenosine was (145±27) μg/(kg·min) in the other 18 patients. Both pulmonary artery pressure and systemic arterial pressure significantly decreased (P<0.05) after administration of adenosine, whereas the oxygen saturation of femoral artery blood, pulmonary vascular resistance, pulmonary-to-systemic flow ratio, mean pulmonary-to-aortic pressure and pulmonary-to-systemic vascular resistance ratio showed no significant changes. Mean pulmonary arterial pressure was >40 mmHg in all study patients. No significant difference was observed in the age and baseline hemodynamics between the patients with decreasing pulmonary vascular resistance and mean pulmonary-to-aortic pressure ratio >10% and the patients without these changes. CONCLUSION: Administration of adenosine induces synchronous decreases in pulmonary artery pressure and systemic arterial pressure but exerts no effect on pulmonary vascular resistance in patients with CHD and severe PAH.
Keywords:congenital heart defect  pulmonary arterial hypertension  adenosine  hemodynamics  acute vasodilator test  
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