Jhanji Shaman, Stirling Sarah, Patel Nakul, Hinds Charles J, Pearse Rupert M
Barts and The London School of Medicine and Dentistry, Queen Mary's University of London, London, United Kingdom.
Crit Care Med. 2009 Jun;37(6):1961-6. doi: 10.1097/CCM.0b013e3181a00a1c.
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.
Single-center interventional study.
University hospital intensive care unit.
Sixteen patients with established septic shock.
The norepinephrine dose was escalated to achieve incremental increases in the MAP from 60 to 70, 80, and 90 mm Hg.
In addition to routine clinical measurements, cardiac output was determined using lithium dilution and arterial waveform analysis, cutaneous tissue Pto2 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 (sd) norepinephrine dose increased from 0.18 (0.18) microg x kg(-1) x min(-1) at 60 mm Hg to 0.41 (0.26) microg x kg(-1) x 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 x min(-1) x m(-2) (p < 0.01), cutaneous Pto2 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.
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.
探讨逐步增加去甲肾上腺素剂量以逐步提高平均动脉压（MAP）对感染性休克患者微血管血流和组织氧合的影响。
单中心干预性研究。
大学医院重症监护病房。
16例确诊的感染性休克患者。
逐步增加去甲肾上腺素剂量，使MAP从60逐步提高到70、80和90mmHg。
除常规临床测量外，采用锂稀释法和动脉波形分析法测定心输出量，用Clark电极测量皮肤组织氧分压（Pto2），用激光多普勒血流仪评估皮肤红细胞通量，用侧流暗视野成像评估舌下微血管血流。去甲肾上腺素平均（标准差）剂量从MAP为60mmHg时的0.18（0.18）μg·kg⁻¹·min⁻¹增加到MAP为90mmHg时的0.41（0.26）μg·kg⁻¹·min⁻¹（p<0.0001）。在此期间，全身氧输送从487（418 - 642）增加到662（498 - 829）mL·min⁻¹·m⁻²（p<0.01），皮肤Pto2从44（11）增加到54（13）mmHg（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）。侧流暗视野成像未发现舌下微血管血流指数、血管密度、灌注血管比例、灌注血管密度或异质性指数有变化。
在感染性休克患者中，通过增加去甲肾上腺素剂量使MAP升高，可导致全身氧输送、皮肤微血管血流和组织氧合增加。舌下微血管血流的原有异常未发生变化。需要进一步研究以明确感染性休克患者血管活性药物治疗的最佳终点。
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