Nygren Andreas, Thorén Anders, Ricksten Sven-Erik
Department of Cardiothoracic Anesthesia and Intensive Care, Sahlgrenska University Hospital, Göteborg, Sweden.
Shock. 2007 Nov;28(5):536-43. doi: 10.1097/shk.0b013e318063e71f.
Patients with norepinephrine-dependent vasodilatory shock after cardiac surgery (n = 10) were compared with uncomplicated postcardiac surgery patients (n = 10) with respect to jejunal mucosal perfusion, gastric-arterial PCO2 gradient, and splanchnic oxygen demand/supply relationship. Furthermore, the effects of norepinephrine-induced variations in MAP on these variables were evaluated in vasodilatory shock. Norepinephrine infusion rate was randomly and sequentially titrated to target MAPs of 60, 75, and 90 mmHg (0.25 +/- 0.24, 0.37 +/- 0.21, and 0.55 +/- 0.39 microg/kg per minute, respectively). Data on jejunal mucosal perfusion, jejunal mucosal hematocrit, and red blood cell (RBC) velocity (laser Doppler flowmetry) as well as gastric-arterial PCO2 gradient (gastric tonometry) and splanchnic oxygen and lactate extraction (hepatic vein catheter) were obtained. Splanchnic oxygen extraction was 71 +/- 16% in the vasodilatory shock group and 41 +/- 9% in the control group (P < 0.001), whereas splanchnic lactate extraction did not differ between the two groups. Jejunal mucosal perfusion (61%; P < 0.001), RBC velocity (35%; P < 0.01), and gastric-arterial mucosal PCO2 gradient (150%; P < 0.001) were higher in the vasodilatory shock group compared with those of the control group. Jejunal mucosal perfusion, jejunal mucosal hematocrit, RBC velocity, gastric-arterial mucosal PCO2 gradient, splanchnic oxygen extraction, and splanchnic lactate extraction were not affected by increasing infusion rates of norepinephrine. In patients with norepinephrine-dependent vasodilatory shock after cardiac surgery, intestinal mucosal perfusion was higher, whereas splanchnic and gastric oxygen demand/supply relationships were impaired compared with postoperative controls, suggesting that intestinal mucosal perfusion is prioritized in vasodilatory shock. Increasing MAP from 60 to 90 mmHg with norepinephrine in clinical vasodilatory shock does not affect intestinal mucosal perfusion and gastric or global splanchnic oxygen demand/supply relationships.
将心脏手术后去甲肾上腺素依赖型血管舒张性休克患者（n = 10）与心脏手术后无并发症患者（n = 10）在空肠黏膜灌注、胃 - 动脉二氧化碳分压差以及内脏氧供需关系方面进行比较。此外，在血管舒张性休克中评估了去甲肾上腺素诱导的平均动脉压（MAP）变化对这些变量的影响。去甲肾上腺素输注速率随机且依次滴定至目标MAP为60、75和90 mmHg（分别为0.25±0.24、0.37±0.21和0.55±0.39微克/千克每分钟）。获取了空肠黏膜灌注、空肠黏膜血细胞比容和红细胞（RBC）速度（激光多普勒血流仪）以及胃 - 动脉二氧化碳分压差（胃张力测定法）和内脏氧及乳酸摄取（肝静脉导管）的数据。血管舒张性休克组的内脏氧摄取为71±16%，对照组为41±9%（P < 0.001），而两组之间的内脏乳酸摄取无差异。与对照组相比，血管舒张性休克组的空肠黏膜灌注（61%；P < 0.001）、RBC速度（35%；P < 0.01）和胃 - 动脉黏膜二氧化碳分压差（150%；P < 0.001）更高。空肠黏膜灌注、空肠黏膜血细胞比容、RBC速度、胃 - 动脉黏膜二氧化碳分压差、内脏氧摄取和内脏乳酸摄取不受去甲肾上腺素输注速率增加的影响。在心脏手术后去甲肾上腺素依赖型血管舒张性休克患者中，与术后对照组相比，肠黏膜灌注更高，而内脏和胃的氧供需关系受损，这表明在血管舒张性休克中肠黏膜灌注被优先考虑。在临床血管舒张性休克中，用去甲肾上腺素将MAP从60 mmHg提高到90 mmHg并不影响肠黏膜灌注以及胃或整体内脏的氧供需关系。
