AP-HP, Hôpitaux Universitaires Paris-Sud, Hôpital de Bicêtre, Service de Réanimation Médicale, Le Kremlin-Bicêtre, France.
Crit Care Med. 2013 Jun;41(6):1412-20. doi: 10.1097/CCM.0b013e318275cece.
During circulatory failure, the ultimate goal of treatments that increase cardiac output is to reduce tissue hypoxia. This can only occur if oxygen consumption depends on oxygen delivery. We compared the ability of central venous oxygen saturation and markers of anaerobic metabolism to predict whether a fluid-induced increase in oxygen delivery results in an increase in oxygen consumption.
Prospective study.
ICU.
Fifty-one patients with an acute circulatory failure (78% of septic origin).
Before and after a volume expansion (500 mL of saline), we measured cardiac index, o2- and Co2-derived variables and lactate.
Volume expansion increased cardiac index ≥ 15% in 49% of patients ("volume-responders"). Oxygen delivery significantly increased in these 25 patients (+32% ± 16%, p < 0.0001). An increase in oxygen consumption ≥ 15% concomitantly occurred in 56% of these 25 volume-responders (+38% ± 28%). Compared with the volume-responders in whom oxygen consumption did not increase, the volume-responders in whom oxygen consumption increased ≥ 15% were characterized by a higher lactate (2.3 ± 1.1 mmol/L vs. 5.5 ± 4.0 mmol/L, respectively) and a higher ratio of the veno-arterial carbon dioxide tension difference (P(v - a)Co2) over the arteriovenous oxygen content difference (C(a - v)o2). A fluid-induced increase in oxygen consumption greater than or equal to 15% was not predicted by baseline central venous oxygen saturation but by high baseline lactate and (P(v - a)Co2/C(a - v)o2 ratio (areas under the receiving operating characteristics curves: 0.68 ± 0.11, 0.94 ± 0.05, and 0.91 ± 0.06). In volume-nonresponders, volume expansion did not significantly change cardiac index, but the oxygen delivery decreased due to a hemodilution-induced decrease in hematocrit.
In volume-responders, unlike markers of anaerobic metabolism, central venous oxygen saturation did not allow the prediction of whether a fluid-induced increase in oxygen delivery would result in an increase in oxygen consumption. This suggests that along with indicators of volume-responsiveness, the indicators of anaerobic metabolism should be considered instead of central venous oxygen saturation for starting hemodynamic resuscitation.
在循环衰竭期间，增加心输出量的治疗的最终目标是减少组织缺氧。只有当氧耗取决于氧输送时，这才能实现。我们比较了中心静脉血氧饱和度和无氧代谢标志物预测液体诱导的氧输送增加是否会导致氧耗增加的能力。
前瞻性研究。
重症监护病房。
51 例急性循环衰竭患者（78%为感染性起源）。
在容量扩张（500 毫升生理盐水）前后，我们测量了心指数、氧和二氧化碳衍生变量以及乳酸。
在 49%的患者（“容量反应者”）中，容量扩张使心指数增加≥15%。在这 25 名患者中，氧输送显著增加（增加 32%±16%，p<0.0001）。同时，这 25 名容量反应者中有 56%的氧耗增加≥15%。与氧耗未增加的容量反应者相比，氧耗增加≥15%的容量反应者的乳酸水平更高（分别为 2.3±1.1mmol/L 和 5.5±4.0mmol/L），静脉-动脉二氧化碳分压差（P（v-a）Co2）与动静脉氧含量差（C（a-v）o2）的比值更高。氧耗增加≥15%不是通过基线中心静脉血氧饱和度预测的，而是通过高基线乳酸和（P（v-a）Co2/C（a-v）o2）比值预测的（接受者操作特征曲线下面积：0.68±0.11、0.94±0.05 和 0.91±0.06）。在容量无反应者中，容量扩张没有显著改变心指数，但由于血细胞比容降低引起的血液稀释导致氧输送减少。
与无氧代谢标志物不同，在容量反应者中，中心静脉血氧饱和度不能预测液体诱导的氧输送增加是否会导致氧耗增加。这表明，除了容量反应性指标外，还应考虑无氧代谢指标，而不是中心静脉血氧饱和度，以开始血流动力学复苏。
