Saludes P, Proença L, Gruartmoner G, Enseñat L, Pérez-Madrigal A, Espinal C, Mesquida J
Critical Care Department, Hospital de Sabadell, Corporació Sanitària Universitària Parc Taulí, Universitat Autònoma de Barcelona, Parc Tauli, 1, 08208, Sabadell, Spain.
Serviço de Medicina Interna, Hospital Prof. Dr. Fernando Fonseca, Amadora, Portugal.
J Clin Monit Comput. 2017 Dec;31(6):1203-1211. doi: 10.1007/s10877-016-9954-1. Epub 2016 Nov 10.
Central venous-to-arterial carbon dioxide difference (PCO) has demonstrated its prognostic value in critically ill patients suffering from shock, and current expert recommendations advocate for further resuscitation interventions when PCO is elevated. PCO combination with arterial-venous oxygen content difference (PCO/CO) seems to enhance its performance when assessing anaerobic metabolism. However, the fact that PCO values might be altered by changes in blood O content (the Haldane effect), has been presented as a limitation of PCO-derived variables. The present study aimed at exploring the impact of hyperoxia on PCO and PCO/CO during the early phase of shock. Prospective interventional study. Ventilated patients suffering from shock within the first 24 h of ICU admission. Patients requiring FiO ≥ 0.5 were excluded. At inclusion, simultaneous arterial and central venous blood samples were collected. Patients underwent a hyperoxygenation test (5 min of FiO 100%), and arterial and central venous blood samples were repeated. Oxygenation and CO variables were calculated at both time points. Twenty patients were studied. The main cause of shock was septic shock (70%). The hyperoxygenation trial increased oxygenation parameters in arterial and venous blood, whereas PCO only changed at the venous site. Resulting PCO and PCO/CO significantly increased [6.8 (4.9, 8.1) vs. 7.6 (6.7, 8.5) mmHg, p 0.001; and 1.9 (1.4, 2.2) vs. 2.3 (1.8, 3), p < 0.001, respectively]. Baseline PCO, PCO/CO and SO correlated with the magnitude of PO augmentation at the venous site within the trial (ρ -0.46, p 0.04; ρ 0.6, p < 0.01; and ρ 0.7, p < 0.001, respectively). Increased PCO/CO values were associated with higher mortality in our sample [1.46 (1.21, 1.89) survivors vs. 2.23 (1.86, 2.8) non-survivors, p < 0.01]. PCO and PCO/CO are influenced by oxygenation changes not related to flow. Elevated PCO and PCO/CO values might not only derive from cardiac output inadequacy, but also from venous hyperoxia. Elevated PCO/CO values were associated with higher PO transmission to the venous compartment, suggesting higher shunting phenomena.
中心静脉 - 动脉二氧化碳分压差（PCO）已在休克重症患者中显示出其预后价值，目前专家建议当PCO升高时应采取进一步的复苏干预措施。在评估无氧代谢时，PCO与动静脉氧含量差（PCO/CO）相结合似乎能提高其评估效能。然而，PCO值可能会因血液氧含量变化（哈氏效应）而改变，这一事实被认为是PCO衍生变量的一个局限性。本研究旨在探讨高氧对休克早期PCO和PCO/CO的影响。前瞻性干预研究。入住重症监护病房（ICU）首24小时内发生休克的通气患者。排除需要吸入氧分数（FiO）≥0.5的患者。纳入研究时，同时采集动脉血和中心静脉血样本。患者接受高氧试验（FiO 100%持续5分钟），之后重复采集动脉血和中心静脉血样本。在两个时间点计算氧合和二氧化碳变量。共研究了20例患者。休克的主要原因是脓毒性休克（70%）。高氧试验增加了动脉血和静脉血中的氧合参数，而PCO仅在静脉部位发生变化。最终PCO和PCO/CO显著升高[分别为6.8（4.9，8.1）mmHg对7.6（6.7，8.5）mmHg，p<0.001；以及1.9（1.4，2.2）对2.3（1.8，3），p<0.001]。基线PCO、PCO/CO和血氧饱和度（SO）与试验中静脉部位氧分压（PO）升高幅度相关（相关系数分别为 -0.46，p = 0.04；0.6，p<0.01；以及0.7，p<0.001）。在我们的样本中，PCO/CO值升高与较高的死亡率相关[存活者为1.46（1.21，1.89），非存活者为2.23（1.86，2.8），p<0.01]。PCO和PCO/CO受与血流无关的氧合变化影响。PCO和PCO/CO值升高可能不仅源于心输出量不足，还源于静脉高氧。PCO/CO值升高与较高的PO向静脉腔的传递相关，提示存在较高的分流现象。
