Ospina-Tascón Gustavo A, De Backer Daniel, Aldana José L, Marín Alberto F García, Calderón Luis E, Chica Julián, García-Gallardo Gustavo, Orozco Nicolás, Mallat Jihad
Department of Intensive Care, Fundación Valle del Lili, Cali, Colombia.
Translational Research Laboratory in Critical Care Medicine (TransLab-CCM), Universidad Icesi, Cali, Colombia.
Intensive Care Med Exp. 2025 Sep 8;13(1):93. doi: 10.1186/s40635-025-00805-0.
The relationship between carbon dioxide pressures (PCO) and contents (CCO) is linked to the Haldane effect. Nevertheless, under shock conditions, hydrogen ion accumulation might strongly influence the discrepancies between PCO and CCO. This study aims to evaluate the impact of hydrogen ion accumulation and hemoglobin oxygen saturation (Haldane effect) on PCO:CCO relationships during induction and resuscitation of endotoxemic shock.
Shock was induced by an escalating dose of lipopolysaccharide in 12 female Landrace pigs. Norepinephrine was then started to maintain mean arterial pressure ≥ 75 mmHg, while successive fluid boluses were administered targeting arterial lactate < 2.0 mmol·L or decreases > 10% per 30 min. Mesenteric venous and arterial PCO were measured at baseline, time of shock, and then, every hour for 6 h, while their respective CCO were computed using the Douglas equation. Mesenteric venous-to-arterial PCO and CCO differences (i.e., ΔPCO and ΔCCO), and then, their absolute arithmetic differences (i.e., [|ΔPCO - ΔCCO|]) were calculated. Discrepancies in [|ΔPCO - ΔCCO|] between adjacent measurement time points (i.e., ∆-[|ΔPCO - ΔCCO|]) were compared with the variations in mesenteric venous O saturation (∆-SO) and arterial-to-mesenteric venous pH (∆-pH). In addition, arterial and venous CCO values were recalculated, maintaining baseline pH (Def) or SO values (Def) to then quantify the impact of pH and SO on the PCO:CCO relationship.
Variations in ∆-[|∆PCO - ∆CCO|]) were paralleled by ∆-pH (R = 0.56, p < 0.001), while poorly correlated with ∆-SO (R = 0.15, p < 0.001). When variations in pH were not included in CCO calculations (i.e., Def-CCO), both arterial and mesenteric venous CCO disagreed in ranges from 21.8 to 50.4% and 15.3 to 47.6%, respectively. Conversely, overestimation of CCO was almost null when variations in SvmesO were not assumed (Def). Calculations under Def-CCO conditions revealed an almost linear relationship between PCO and CCO, contrasting with a non-linear relationship when pH variations were acknowledged.
Regional splanchnic PCO:CCO relationship was mostly influenced by hydrogen ion accumulation rather than the Haldane effect during development and resuscitation of endotoxemic shock. Predominant influence of hydrogen ion accumulation on PCO:CCO dissociation curve during endotoxemic shock could have important implications when interpreting ΔPCO and its combination with arterial-to-venous oxygen differences in vasodilated shock conditions.
二氧化碳分压（PCO）与含量（CCO）之间的关系与哈代效应相关。然而，在休克状态下，氢离子蓄积可能会强烈影响PCO与CCO之间的差异。本研究旨在评估氢离子蓄积和血红蛋白氧饱和度（哈代效应）对内毒素性休克诱导和复苏过程中PCO:CCO关系的影响。
对12头雌性长白猪逐步增加脂多糖剂量以诱导休克。然后开始使用去甲肾上腺素维持平均动脉压≥75 mmHg，同时连续给予液体冲击，目标是使动脉血乳酸<2.0 mmol·L或每30分钟降低>10%。在基线、休克时以及随后的6小时内每小时测量肠系膜静脉和动脉的PCO，同时使用道格拉斯方程计算它们各自的CCO。计算肠系膜静脉与动脉的PCO和CCO差值（即ΔPCO和ΔCCO），然后计算它们的绝对算术差值（即[|ΔPCO - ΔCCO|]）。比较相邻测量时间点[|ΔPCO - ΔCCO|]的差异（即∆-[|ΔPCO - ΔCCO|]）与肠系膜静脉血氧饱和度变化（∆-SO）和动脉血与肠系膜静脉血pH值变化（∆-pH）。此外，重新计算动脉和静脉CCO值，保持基线pH值（Def）或血氧饱和度值（Def），然后量化pH值和血氧饱和度对PCO:CCO关系的影响。
∆-[|∆PCO - ∆CCO|]的变化与∆-pH平行（R = 0.56，p < 0.001），而与∆-SO相关性较差（R = 0.15，p < 0.001）。当CCO计算中不包括pH值变化时（即Def-CCO），动脉和肠系膜静脉CCO的差异范围分别为21.8%至50.4%和15.3%至47.6%。相反，当不考虑SvmesO变化时（Def），CCO的高估几乎为零。在Def-CCO条件下的计算显示PCO与CCO之间几乎呈线性关系，这与考虑pH值变化时的非线性关系形成对比。
在内毒素性休克的发生和复苏过程中，局部内脏PCO:CCO关系主要受氢离子蓄积影响，而非哈代效应。在内毒素性休克期间，氢离子蓄积对PCO:CCO解离曲线的主要影响在解释ΔPCO及其与血管扩张性休克状态下动静脉氧差的组合时可能具有重要意义。
