Background The relationship between carbon dioxide pressures (PCO2) and contents (CCO2) is linked to the Haldane effect. Nevertheless, under shock conditions, hydrogen ion accumulation might strongly influence the discrepancies between PCO2 and CCO2. This study aims to evaluate the impact of hydrogen ion accumulation and hemoglobin oxygen saturation (Haldane effect) on PCO2:CCO2 relationships during induction and resuscitation of endotoxemic shock. Methods 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−1 or decreases > 10% per 30 min. Mesenteric venous and arterial PCO2 were measured at baseline, time of shock, and then, every hour for 6 h, while their respective CCO2 were computed using the Douglas equation. Mesenteric venous-to-arterial PCO2 and CCO2 differences (i.e., ΔPCO2 and ΔCCO2), and then, their absolute arithmetic differences (i.e., [|ΔPCO2 – ΔCCO2|]) were calculated. Discrepancies in [|ΔPCO2 – ΔCCO2|] between adjacent measurement time points (i.e., ∆–[|ΔPCO2 – ΔCCO2|]) were compared with the variations in mesenteric venous O2 saturation (∆–SvmesO2) and arterial-to-mesenteric venous pH (∆–pHa-vmes). In addition, arterial and venous CCO2 values were recalculated, maintaining baseline pH (DefpH) or SO2 values (DefSO2) to then quantify the impact of pH and SvmesO2 on the PCO2:CCO2 relationship. Results Variations in ∆–[|∆PCO2 – ∆CCO2|]) were paralleled by ∆–pHa-vmes (R2 = 0.56, p < 0.001), while poorly correlated with ∆–SvmesO2 (R2 = 0.15, p < 0.001). When variations in pH were not included in CCO2 calculations (i.e., DefpH–CCO2), both arterial and mesenteric venous CCO2 disagreed in ranges from 21.8 to 50.4% and 15.3 to 47.6%, respectively. Conversely, overestimation of CCO2 was almost null when variations in SvmesO2 were not assumed (DefSvmesO2). Calculations under DefpH–CCO2 conditions revealed an almost linear relationship between PCO2 and CCO2, contrasting with a non-linear relationship when pH variations were acknowledged. Conclusions Regional splanchnic PCO2:CCO2 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 PCO2:CCO2 dissociation curve during endotoxemic shock could have important implications when interpreting ΔPCO2 and its combination with arterial-to-venous oxygen differences in vasodilated shock conditions.

Regional venous-to-arterial carbon dioxide pressure and content differences during endotoxemic shock: influence of hydrogen ion accumulation vs. Haldane effect

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2025年9月8日

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Gustavo A. Ospina-Tascón,
Daniel De Backer,
José L. Aldana,
Alberto F. García Marín,
Luis E. Calderón,
Julián Chica,
Gustavo García-Gallardo,
Nicolás Orozco,
Jihad Mallat

摘要

Background

The relationship between carbon dioxide pressures (PCO₂) and contents (CCO₂) is linked to the Haldane effect. Nevertheless, under shock conditions, hydrogen ion accumulation might strongly influence the discrepancies between PCO₂ and CCO₂. This study aims to evaluate the impact of hydrogen ion accumulation and hemoglobin oxygen saturation (Haldane effect) on PCO₂:CCO₂ relationships during induction and resuscitation of endotoxemic shock.

Methods

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⁻¹ or decreases > 10% per 30 min. Mesenteric venous and arterial PCO₂ were measured at baseline, time of shock, and then, every hour for 6 h, while their respective CCO₂ were computed using the Douglas equation. Mesenteric venous-to-arterial PCO₂ and CCO₂ differences (i.e., ΔPCO₂ and ΔCCO₂), and then, their absolute arithmetic differences (i.e., [|ΔPCO₂ – ΔCCO₂|]) were calculated. Discrepancies in [|ΔPCO₂ – ΔCCO₂|] between adjacent measurement time points (i.e., ∆–[|ΔPCO₂ – ΔCCO₂|]) were compared with the variations in mesenteric venous O₂ saturation (∆–S_vmesO₂) and arterial-to-mesenteric venous pH (∆–pH_a-vmes). In addition, arterial and venous CCO₂ values were recalculated, maintaining baseline pH (Def_pH) or SO₂ values (Def_SO2) to then quantify the impact of pH and S_vmesO₂ on the PCO₂:CCO₂ relationship.

Results

Variations in ∆–[|∆PCO₂ – ∆CCO₂|]) were paralleled by ∆–pH_a-vmes (R² = 0.56, p < 0.001), while poorly correlated with ∆–S_vmesO₂ (R² = 0.15, p < 0.001). When variations in pH were not included in CCO₂ calculations (i.e., Def_pH–CCO₂), both arterial and mesenteric venous CCO₂ disagreed in ranges from 21.8 to 50.4% and 15.3 to 47.6%, respectively. Conversely, overestimation of CCO₂ was almost null when variations in SvmesO₂ were not assumed (Def_SvmesO2). Calculations under Def_pH–CCO₂ conditions revealed an almost linear relationship between PCO₂ and CCO₂, contrasting with a non-linear relationship when pH variations were acknowledged.

Conclusions

Regional splanchnic PCO₂:CCO₂ 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 PCO₂:CCO₂ dissociation curve during endotoxemic shock could have important implications when interpreting ΔPCO₂ and its combination with arterial-to-venous oxygen differences in vasodilated shock conditions.