右美托咪定在抢救脓毒症休克患者中的临床研究

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目的探讨右美托咪定在抢救脓毒症休克患者中的临床应用。方法选择2015年6月—2016年10月亳州市人民医院重症医学科收治的脓毒症休克患者20例纳入研究,随机分为右美托咪定组10例和对照组10例,全部患者均按治疗指南积极行EGDT液体复苏,右美托咪定组经静脉泵入右美托咪定[0.2~0.7μg/(kg·h)],心率(HR)控制在60~100次/min,对照组对心率不进行特别干预,观察目标:治疗前及治疗后24、48、72 h HR、平均动脉压(MAP)、每搏量指数(SVI)、中心静脉血氧饱和度(ScvO_2)、血乳酸(Lac)的变化。结果右美托咪定组治疗后心率减慢,与治疗前比较差异有统计学意义(P<0.05),与对照组同期比较,差异亦有统计学意义(P<0.05);右美托咪定组治疗前后平均动脉压变化不明显,差异无统计学意义,与对照组同期比较,差异亦无统计学意义;右美托咪定组治疗24 h后ScvO_2上升,48 h后SVI增加,与治疗前比较差异均有统计学意义(P<0.05),与对照组同期比较,差异亦均有统计学意义(P<0.05);右美托咪定组治疗48 h后乳酸与治疗前比较,差异有统计学意义(P<0.05),与对照组同期比较,差异亦有统计学意义(P<0.05)。结论右美托咪定组治疗后HR逐渐开始减慢,SVI、ScvO_2逐渐升高,Lac逐渐降低,而MAP无明显改变。与对照组比较,右美托咪定组治疗24 h后HR明显减慢,ScvO_2开始升高,48 h起SVI升高明显,Lac降低明显。右美托咪定通过抑制脓毒症休克患者交感神经活性,稳定血流动力学,可以改善机体组织氧代谢。 Objective To investigate the clinical application of dexmedetomidine in rescue of patients with septic shock. Methods Twenty patients with septic shock admitted to the Department of Critical Care Medicine of Bozhou People’s Hospital from June 2015 to October 2016 were enrolled and randomly divided into 10 patients in the dexmedetomidine group and 10 patients in the control group. All patients The EGDT liquid resuscitation was actively performed according to the treatment guideline. The dexmedetomidine group was intravenously dripped with dexmedetomidine [0.2-0.7 μg / (kg · h)] and the heart rate (HR) was controlled at 60-100 times / min. The control group did not make any special intervention on heart rate, and observed the target HR, mean arterial pressure (MAP), stroke volume index (SVI), central venous oxygen saturation (ScvO 2) Changes in blood lactic acid (Lac). Results Dexmedetomidine decreased heart rate after treatment, with statistical significance (P <0.05), compared with the control group at the same period, the difference was also statistically significant (P <0.05); dexmedetomidine The change of mean arterial pressure was not significant before and after treatment in group A, with no significant difference between the two groups. There was no significant difference between the two groups in the same period of treatment. ScvO 2 increased 24 h after dexmedetomidine treatment and SVI increased 48 h after treatment The differences were statistically significant before treatment (P <0.05), compared with the control group over the same period, the differences were also statistically significant (P <0.05); dexmedetomidine group 48 h after treatment lactic acid compared with before treatment, The difference was statistically significant (P <0.05), compared with the control group over the same period, the difference was also statistically significant (P <0.05). Conclusion HR decreased gradually after dexmedetomidine treatment, SVI, ScvO_2 gradually increased, Lac gradually decreased, while MAP did not change significantly. Compared with the control group, the HR of dexmedetomidine group decreased significantly after 24 h of treatment, ScvO 2 began to increase, SVI increased significantly after 48 h, Lac decreased significantly. Dexmedetomidine stabilizes hemodynamics by inhibiting sympathetic activity in patients with septic shock and can improve oxygen metabolism in the body tissue.
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