期刊文献+

左西孟旦对脓毒性休克患者血流动力学及心肌损伤标志物的影响 被引量:21

Effects of levosimendan on hemodynamics and markers of myocardial damage in patients with septic shock
原文传递
导出
摘要 目的探讨左西孟旦对脓毒性休克患者血流动力学及心肌损伤标志物的影响。方法将38例液体复苏后左室射血分数(LVEF)<45%的脓毒性休克患者分为多巴酚丁胺组及左西孟旦组,每组均为19例。多巴酚丁胺组予以5μg·kg^(-1)·min^(-1)多巴酚丁胺微泵连续24 h静脉维持;左西孟旦组予以0.2μg·kg^(-1)·min^(-1)微泵连续24 h静脉维持。采用脉搏指示连续心排血量(Pi CCO)监测血流动力学指标包括心率、中心静脉压(CVP)、平均动脉压(MAP)、每搏指数、心脏指数、左心室每搏工作指数(LVSWI)、外周血管阻力指数(SVRI)、胸腔内血容积指数(ITBVI)、全心舒张末容积指数(GEDI)、血管外肺水指数(EVLWI)、氧输送量指数(DO2I)、氧耗量指数(VO2I)变化;,并记录治疗前后人心型脂肪酸结合蛋白(h-FABP)、肌钙蛋白I(TNI)、脑钠肽、LVEF以及血乳酸水平。同时对两组患者机械通气时间、住ICU时间、住院时间以及28 d病死率进行比较。结果两组患者治疗前心率(t=0.984,P=0.332)、CVP(t=0.979,P=0.334)、MAP(t=0.301,P=0.765)、每搏指数(t=0.320,P=0.750)、心脏指数(t=1.209,P=0.235)、LVSWI(t=1.306,P=0.200)、SVRI(t=1.365,P=0.181)、ITBVI(t=0841,P=0.406)、GEDI(t=0.706,P=0.484)、EVLWI(t=0.167,P=0.869)、DO2I(t=0.467,P=0.644)、VO2I(t=0.485,P=0.631)、hFABP(t=1.462,P=0.152)、TNI(t=0.397,P=0.693)、脑钠肽(t=0.302,P=0.764)、LVEF(t=0.494,P=0.624)以及血乳酸水平(t=1.071,P=0.291)、比较,差异均无统计学意义。与多巴酚丁胺组相比较,左西孟旦治疗后SVI[(34±10)ml/m2 vs.(40±9)ml/m2,t=2.261,P=0.030]、心脏指数[(3.1±0.4)L·min^(-1)·m^(-2) vs.(3.5±0.3)L·min^(-1)·m^(-2),t=3.487,P=0.001]、LVSWI[(33.8±2.9)kg·min^(-1)·m^(-2) vs.(36.9±2.7)kg·min^(-1)·m^(-2),t=3.410,P=0.002]、DO2I[(720±50)kg·min^(-1)·m^(-2) vs.(755±52)kg·min^(-1)·m^(-2),t=2.133,P=0.040]及VO2I[(127±15)kg·min^(-1)·m^(-2) vs.(140±18)kg·min^(-1)·m^(-2),t=2.241,P=0.031]、LVEF[(39±8)%vs.(46±8)%,t=2.485,P=0.018)]均明显增加,EVLWI[(8.9±3.0)ml/kg vs.(6.4±2.8)ml/kg,t=2.665,P=0.012]、h-FABP[(13.1±3.8)μg/L vs.(8.5±2.6)μg/L,t=4.355,P<0.001]、TNI[(0.28±0.10)μg/L vs.(0.20±0.11)μg/L,t=2.346,P=0.025]、脑钠肽[(381±49)ng/L vs.(233±39)ng/L,t=10.380,P<0.001]及血乳酸水平[(4.3±1.0)mmol/L vs.(3.6±0.8)mmol/L,t=2.383,P=0.022]均明显下降。但是两组患者机械通气时间、ICU时间、住院时间以及28 d病死率比较,差异均无统计学意义(t=0.171、0.209、0.290、0.117,P均>0.05)。结论与多巴酚丁胺相比,左西孟旦可减轻脓毒性休克患者心肌损伤、增强心脏收缩功能、改善血流动力学及组织灌注。 Objective To investigate the effects of levosimendan on hemodynamics and markers of myocardial damage in patients with septic shock. Methods Thirty-eight patients with left ventricular ejective fraction less than 45% related to septic shock after 48 h of fluid resuscitation were randomly divided into the dobutamine group(19 cases) and levosimendan group(19 cases). Patients in the dobutamine group received dobutamine(5 μg·kg^(-1)·min^(-1)) for 24 h after fluid resuscitation, and patients in the levosimendan group were given levosimendan(0.2 μg·kg^(-1)·min^(-1)) for 24 h at the same time. The hemodynamics including heart rate, central venous pressure(CVP), mean arterial pressure(MAP), stroke volume index, cardiac index, left ventricular stroke work index(LVSWI), systemic vascular resistance(SVRI), intrathoracic blood volume index(ITBVI), global end diastolic volume index(GEDI), extravascular lung water index(EVLWI), oxygen delivery index(DO2I), oxygen consumption index(VO2I) were detected by pulse indicator continuous cardiac output(Pi CCO), and the levels of human heart-type fatty acid binding protein(h-FABP), troponin I(TNI), brain natriuretic peptide, LVEF and blood lactic acid were recorded before and 24 h after treatment in the two groups. Meanwhile, mechanical ventilation time, length of stay in ICU and hospital, 28-day mortality were also compared between the two groups. Results The heart rate(t = 0.984, P = 0.332), CVP(t = 0.979, P = 0.334), MAP(t =0.301, P = 0.765), stroke volume index(t = 0.320, P = 0.750), cardiac index(t = 1.209, P = 0.235),LVSWI(t = 1.306, P = 0.200), SVRI(t = 1.365, P = 0.181), ITBVI(t = 0841, P = 0.406), GEDI(t =0.706, P = 0.484), EVLWI(t = 0.167, P = 0.869), DO2I(t = 0.467, P = 0.644), VO2I(t = 0.485, P =0.631), h-FABP(t = 1.462, P = 0.152), TNI(t = 0.397, P = 0.693), brain natriuretic peptide(t =0.302, P = 0.764), LVEF(t = 0.494, P = 0.624) and blood lactic acid(t = 1.071, P = 0.291) all showed no significant differences before and after the treatment. Compared with the dobutamine group, the levels of SVI [(34 ± 10) ml / m2 vs.(40 ± 9) ml / m2, t = 2.261, P = 0.030], cardiac index[(3.1 ± 0.4) L·min^(-1)·m^(-2)vs.(3.5 ± 0.3) L·min^(-1)·m^(-2), t = 3.487, P = 0.001], LVSWI [(33.8 ± 2.9) kg·min^(-1)·m^(-2)vs.(36.9 ± 2.7) kg·min^(-1)·m^(-2), t = 3.410, P = 0.002], DO2 I [(720 ± 50) kg·min^(-1)·m^(-2)vs.(755 ± 52) kg·min^(-1)·m^(-2),t = 2.133, P = 0.040], VO2 I [(127 ± 15) kg·min^(-1)·m^(-2)vs.(140 ± 18) kg·min^(-1)·m^(-2), t = 2.241, P =0.031], LVEF [(39 ± 8)% vs.(46 ± 8)%, t = 2.485, P = 0.018] increased obviously, and the EVLWI[(8.9 ± 3.0) ml / kg vs.(6.4 ± 2.8) ml / kg, t = 2.665, P = 0.012], h-FABP[(13.1 ± 3.8) μg / L vs.(8.5 ±2.6) μg / L, t = 4.355, P〈0.001], TNI [(0.28 ± 0.10) μg / L vs.(0.20 ± 0.11) μg / L, t = 2.346, P =0.025], brain natriuretic peptide [(381 ± 49) ng / L vs.(233 ± 39) ng / L, t = 10.380, P〈0.001] and blood lactic acid [(4.3 ± 1.0) mmol / L vs.(3.6 ± 0.8) mmol / L, t = 2.383, P = 0.022] decreased markedly after the treatment. However, there were no significant differences in the mechanical ventilation time, length of stay in ICU and hospital, 28-day mortality between the two groups(t =0.171, 0.209, 0.290, 0.117, all P〉0.05). Conclusion Compared with dobutamine, levosimendan can alleviate myocardial damage, strengthen myocardial systolic function, and improve hemodynamics and tissue perfusion in patients with septic shock.
出处 《中华危重症医学杂志(电子版)》 CAS 2016年第3期163-168,共6页 Chinese Journal of Critical Care Medicine:Electronic Edition
基金 浙江省科技厅公益性技术应用研究基金项目(2013C33G5260034)
关键词 左西孟旦 休克 脓毒性 血流动力学 心肌损伤 Levosimendan Shock septic Hemodynamics Myocardial damage
  • 相关文献

参考文献15

  • 1Femandes CJ Jr, Akamine N, Knobel E. Myocardial depression in sepsis[J]. Shock, 2008 (30 suppl 1): 14- 17.
  • 2Antila S, Sundberg S, Lehtonen LA. Clinical pharma- cology oflevosimendan [J]. Clin Pharmacokinet, 2007, 46 (7): 535-552.
  • 3Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsisand septic shock: 2012[J].Crit Care Med, 2013, 41 (2): 580-637.
  • 4Givertz MM, Andreou C, Conrad CH, et al. Direct m- yocardial effects of levosimendan in humans with left ventricular dysfunction: alteration of force-frequency and relaxation-frequency relationships [J]. Circulation, 2007, 115 (10): 1218-1224.
  • 5Deschodt-Arsac V, Calmettes G, Raffard G, et al. Ab- sence of mitochondrial activation during levosimendan inotropic action in perfused paced guinea pig hearts as demonstrated by modular control analysis [J]. Am J Physiol Regul Integr Comp Physiol, 2010, 299 (3): R786-R792.
  • 6Haikala H, Nissinen E, Etemadzadeh E, et al. Tro- ponin C-mediated calcium sensitization induced by levosimendan does not impair relaxation [J]. J Cardiovasc Pharmacol, 1995, 25 (5): 794-801.
  • 7Ikonomidis I, Parissis JT, Paraskevaidis I, et al. Effe- cts of levosimendanon coronary artery flow and cardiac performancein patients with advanced heart failure[J]. Eur J Heart Fail, 2007, 9 (12): 1172-1177.
  • 8Michaels AD, McKeown B, Kostal M, et al. Effects of intravenous levosimendan on human coronary vasomotor regulation, left ventricular wall stress, and myocardial- oxygen uptake [J]. Circulation, 2005, 111 (12): 1504- 1509.
  • 9Zausig YA, Geilfus D, Missler G, et al. Direct cardiac effects of dobutamine, dopamine, epinephrine, and levosimendan in isolated septic rat hearts [J]. Shock, 2010, 34 (3): 269-274.
  • 10Morelli A, Donati A, Ertmer C, et al. Levosimendan for resuscitating the microcircuiation in patients with septic shock: a randomized controlled study [J]. Crit Care, 2010, 14 (6): R232.

二级参考文献7

共引文献854

同被引文献155

引证文献21

二级引证文献102

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部