The effect of increasing doses of norepinephrine on tissue oxygenation and microvascular flow in patients with septic shock
The effect of increasing doses of norepinephrine on tissue oxygenation and microvascular flow in patients with septic shock
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DOI：
10.1097/ccm.0b013e3181a00a1c
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发表时间：
2009-06-01
影响因子：
8.8
通讯作者：
Pearse, Rupert M.
中科院分区：
文献类型：
--
作者：
Jhanji, Shaman;Stirling, Sarah;Pearse, Rupert M.
客观的。旨在研究逐渐增加去甲肾上腺素剂量（旨在逐步增加平均动脉压（MAP））对感染性休克患者微血管血流和组织氧合的影响。设计：单中心介入研究。设置。大学医院重症监护病房。患者：十六名已确诊感染性休克的患者。干预措施。去甲肾上腺素剂量逐步增加，以实现 MAP 从 60 毫米汞柱增加到 70 毫米汞柱、80 毫米汞柱和 90 毫米汞柱。 测量和主要结果：除了常规临床测量外，还使用锂稀释和动脉波形分析确定心输出量，使用克拉克电极测量皮肤组织 Pt0(2)，使用激光多普勒血流测定法评估皮肤红细胞流量，并使用侧流暗视野成像评估舌下微血管血流。平均 (So) 去甲肾上腺素剂量从 0.18 (0.18) μg 增加。千克（-1）。 min(-1) 在 60 mm Hg 至 0.41 (0.26) mu g 。千克（-1）。 90 毫米汞柱下的分钟 (-1) (p < 0.0001)。在此期间，全球氧气输送量从 487 (418-642) mL 增加到 662 (498-829) mL。分钟(-1) 。 m(-2) (p < 0.01)，皮肤 Pt0(2) 从 44 (11) 增加到 54 (13) mm Hg (p < 0.0001)，皮肤微血管红细胞通量从 26.1 (16.2-41.9) 增加到 33.3 (20.3-46.7) 灌注单位 (p < 0.05)。侧流暗场成像未发现舌下微血管流量指数、血管密度、灌注血管比例、灌注血管密度或异质性指数发生变化。结论：在感染性休克患者中，通过增加去甲肾上腺素剂量来提高平均动脉压，导致整体氧输送、皮肤微血管流量和组织氧合增加。先前存在的舌下微血管血流异常没有变化。需要进一步研究来明确脓毒症休克患者升压药治疗的最佳终点。 （重症监护医学 2009 年；37：1961-1966）
Objective. To investigate the effect of escalating doses of norepinephrine, aimed at achieving incremental increases in mean arterial pressure (MAP), on microvascular flow and tissue oxygenation in patients with septic shock.Design: Single-center interventional study.Setting. University hospital intensive care unit.Patients: Sixteen patients with established septic shock.Interventions. The norepinephrine dose was escalated to achieve incremental increases in the MAP from 60 to 70, 80, and 90 mm Hg.Measurements and Main Results: In addition to routine clinical measurements, cardiac output was determined using lithium dilution and arterial waveform analysis, cutaneous tissue Pt0(2) was measured using a Clark electrode, cutaneous red blood cell flux was assessed using laser Doppler flowmetry, and sublingual microvascular flow was evaluated using sidestream darkfield imaging. The mean (So) norepinephrine dose increased from 0.18 (0.18) mu g . kg(-1) . min(-1) at 60 mm Hg to 0.41 (0.26) mu g . kg(-1) . min(-1) at 90 mm Hg (p < 0.0001). During this period, global oxygen delivery increased from 487 (418-642) to 662 (498-829) mL . min(-1) . m(-2) (p < 0.01), cutaneous Pt0(2) increased from 44 (11) to 54 (13) mm Hg (p < 0.0001) and cutaneous microvascular red blood cell flux increased from 26.1 (16.2-41.9) to 33.3 (20.3-46.7) perfusion units (p < 0.05). No changes in sublingual microvascular flow index, vessel density, the proportion of perfused vessels, perfused vessel density, or heterogeneity index were identified by sidestream darkfield imaging.Conclusions: In patients with septic shock, targeting higher MAP by increasing the dose of norepinephrine resulted in an increase in global oxygen delivery, cutaneous microvascular flow, and tissue oxygenation. There were no changes in preexisting abnormalities of sublingual microvascular flow. Further research is required to clarify the optimal end points for vasopressor therapy in patients with septic shock. (Crit Care Med 2009; 37: 1961-1966)