静脉-动脉血二氧化碳分压差

张彩虹 ,  魏小艳 ,  朱元州

巴楚医学 ›› 2026, Vol. 9 ›› Issue (2) : 10 -15.

PDF (1165KB)
巴楚医学 ›› 2026, Vol. 9 ›› Issue (2) : 10 -15. DOI: 10.3969/j.issn.2096-6113.2026.02.002

静脉-动脉血二氧化碳分压差

作者信息 +

Venous-to-Arterial Carbon Dioxide Partial Pressure Difference

Author information +
文章历史 +
PDF (1192K)

摘要

混合静脉血氧饱和度(SvO2)和中心静脉血氧饱和度(ScvO2)用于指导休克复苏,但ScvO2并不能指导改善脓毒症患者预后。静脉-动脉血二氧化碳分压差(ΔPCO2)被提出可以作为评估复苏效果的重要指标。生理状态下ΔPCO2约为5~7 mmHg,其升高提示心输出量相对不足,用于指导液体复苏、正性肌力药物滴定,进而评估治疗反应。然而,ΔPCO2存在局限性:高血流状态下其变化不敏感;脓毒症等炎症状态下微循环障碍可导致其与心输出量关系复杂化;正常ΔPCO2不能排除局部灌注不足;测量易受技术误差影响。结合其他参数综合解读ΔPCO2,能够床旁、动态地评估心输出量与代谢需求的匹配程度,有助于实现更精准的个体化复苏目标。

Abstract

Mixed venous oxygen saturation (SvO2) and central venous oxygen saturation (ScvO2) are commonly used to guide shock resuscitation. However, ScvO2 monitoring alone has not been shown to improve outcomes in patients with sepsis. The venous-to-arterial carbon dioxide partial pressure difference (ΔPCO2) has been proposed as an important indicator for evaluating the adequacy of resuscitation. Under physiological conditions, ΔPCO2 typically ranges from 5 to 7 mmHg. An increase in ΔPCO2 indicates a relatively insufficient cardiac output, which can be used to guide fluid resuscitation and titration of inotropic agents, thereby helping to assess the hemodynamic response to therapy. Nevertheless, ΔPCO2 has limitations: its sensitivity decreases under hyperdynamic circulatory states; in inflammatory conditions such as sepsis, microcirculatory dysfunction can complicate the relationship between ΔPCO2 and cardiac output; a normal ΔPCO2 does not exclude regional hypoperfusion; measurement errors may occur due to technical variability. When interpreted in conjunction with other hemodynamic and metabolic parameters, ΔPCO2 enables bedside and dynamic assessment of the balance between cardiac output and metabolic demand, thereby supporting more precise, individualized resuscitation strategies.

关键词

休克 / 静脉-动脉血二氧化碳分压差 / 组织灌注 / 心输出量 / 氧代谢

Key words

shock / venous-to-arterial carbon dioxide partial pressure difference (ΔPCO2) / tissue perfusion / cardiac output / oxygen metabolism

引用本文

引用格式 ▾
张彩虹,魏小艳,朱元州. 静脉-动脉血二氧化碳分压差[J]. 巴楚医学, 2026, 9(2): 10-15 DOI:10.3969/j.issn.2096-6113.2026.02.002

登录浏览全文

4963

注册一个新账户 忘记密码

参考文献

[1]

Miller A, Wilkinson J, Kasal J. Diagnosis of shock states[J]. Crit Care Clin, 2025, 41(3): 397-428.

[2]

朱元州. 血流动力学2024[J]. 巴楚医学, 2024, 7(1): 8-23.

[3]

Ltaief Z, Schneider A G, Liaudet L. Pathophysiology and clinical implications of the veno—arterial PCO2 gap[J]. Crit Care, 2021, 25(1): 318.

[4]

Lamia B, Monnet X, Teboul J L. Meaning of arterio—venous PCO2 difference in circulatory shock[J]. Minerva Anestesiol, 2006, 72(6): 597-604.

[5]

Cousin V L, Joye R, Wacker J, et al. Use of CO2—derived variables in cardiac intensive care unit: pathophysiology and clinical implications[J]. J Cardiovasc Dev Dis, 2023, 10(5): 208.

[6]

Said A, Rogers S, Doctor A. Red cell physiology and signaling relevant to the critical care setting[J]. Curr Opin Pediatr, 2015, 27(3): 267-276.

[7]

Suresh K, Shimoda L A. Lung circulation[J]. Compr Physiol, 2016, 6(2): 897-943.

[8]

Ospina—Tascón G A, Bautista—Rincón D F, Umaña M, et al. Persistently high venous—to—arterial carbon dioxide differences during early resuscitation are associated with poor outcomes in septic shock[J]. Crit Care, 2013, 17(6): R294.

[9]

Mahutte C K, Jaffe M B, Chen P A, et al. Oxygen Fick and modified carbon dioxide Fick cardiac outputs[J]. Crit Care Med, 1994, 22(1): 86-95.

[10]

Diaztagle Fernández J J, Rodríguez Murcia J C, Sprockel Díaz J J. Venous—to—arterial carbon dioxide difference in the resuscitation of patients with severe sepsis and septic shock: a systematic review[J]. Med Intensiva, 2017, 41(7): 401-410.

[11]

Adrogué H J, Rashad M N, Gorin A B, et al. Assessing acid—base status in circulatory failure. Differences between arterial and central venous blood[J]. N Engl J Med, 1989, 320(20): 1312-1316.

[12]

Chong W H, Saha B K, Medarov B I. Comparing central venous blood gas to arterial blood gas and determining its utility in critically ill patients: narrative review[J]. Anesth Analg, 2021, 133(2): 374-378.

[13]

Vallée F, Vallet B, Mathe O, et al. Central venous—to—arterial carbon dioxide difference: an additional target for goal—directed therapy in septic shock[J]. Intensive Care Med, 2008, 34(12): 2218-2225.

[14]

van Beest P A, Lont M C, Holman N D, et al. Central venous—arterial pCO2 difference as a tool in resuscitation of septic patients[J]. Intensive Care Med, 2013, 39(6): 1034-1039.

[15]

Dubin A, Estenssoro E. Mechanisms of tissue hypercarbia in sepsis[J]. Front Biosci, 2008, 13: 1340-1351.

[16]

Groeneveld A B, Vermeij C G, Thijs L G. Arterial and mixed venous blood acid—base balance during hypoperfusion with incremental positive end—expiratory pressure in the pig[J]. Anesth Analg, 1991, 73(5): 576-582.

[17]

Zhang H, Vincent J L. Arteriovenous differences in PCO2 and pH are good indicators of critical hypoperfusion[J]. Am Rev Respir Dis, 1993, 148(4 Pt 1): 867-871.

[18]

Van der Linden P, Rausin I, Deltell A, et al. Detection of tissue hypoxia by arteriovenous gradient for PCO2 and pH in anesthetized dogs during progressive hemorrhage[J]. Anesth Analg, 1995, 80(2): 269-275.

[19]

Rackow E C, Astiz M E, Mecher C E, et al. Increased venous—arterial carbon dioxide tension difference during severe sepsis in rats[J]. Crit Care Med, 1994, 22(1): 121-125.

[20]

Benjamin E. Venous hypercarbia: a nonspecific marker of hypoperfusion[J]. Crit Care Med, 1994, 22(1): 9-10.

[21]

Teboul J L, Mercat A, Lenique F, et al. Value of the venous—arterial PCO2 gradient to reflect the oxygen supply to demand in humans: effects of dobutamine[J]. Crit Care Med, 1998, 26(6): 1007-1010.

[22]

Bakker J, Vincent J L, Gris P, et al. Veno—arterial carbon dioxide gradient in human septic shock[J]. Chest, 1992, 101(2): 509-515.

[23]

Vallet B, Teboul J L, Cain S, et al. Venoarterial CO2 difference during regional ischemic or hypoxic hypoxia[J]. J Appl Physiol (1985), 2000, 89(4): 1317-1321.

[24]

Mecher C E, Rackow E C, Astiz M E, et al. Venous hypercarbia associated with severe sepsis and systemic hypoperfusion[J]. Crit Care Med, 1990, 18(6): 585-589.

[25]

Wasserman K, Beaver W L, Whipp B J. Gas exchange theory and the lactic acidosis (anaerobic) threshold[J]. Circulation, 1990, 81(1 Suppl): Ⅱ14-Ⅱ30.

[26]

Cohen I L, Sheikh F M, Perkins R J, et al. Effect of hemorrhagic shock and reperfusion on the respiratory quotient in swine[J]. Crit Care Med, 1995, 23(3): 545-552.

[27]

Dubin A, Murias G, Estenssoro E, et al. End—tidal CO2 pressure determinants during hemorrhagic shock[J]. Intensive Care Med, 2000, 26(11): 1619-1623.

[28]

Ferrara G, Kanoore Edul V S, Martins E, et al. Intestinal and sublingual microcirculation are more severely compromised in hemodilution than in hemorrhage[J]. J Appl Physiol (1985), 2016, 120(10): 1132-1140.

[29]

Martikainen T J, Tenhunen J J, Giovannini I, et al. Epinephrine induces tissue perfusion deficit in porcine endotoxin shock: evaluation by regional CO2 content gradients and lactate—to—pyruvate ratios[J]. Am J Physiol Gastrointest Liver Physiol, 2005, 288 (3): G586-G592.

[30]

Ultman J S, Bursztein S. Analysis of error in the determination of respiratory gas exchange at varying FIO2 [J]. J Appl Physiol Respir Environ Exerc Physiol, 1981, 50(1): 210-216.

[31]

Mekontso—Dessap A, Castelain V, Anguel N, et al. Combination of venoarterial PCO2 difference with arteriovenous O2 content difference to detect anaerobic metabolism in patients[J]. Intensive Care Med, 2002, 28(3): 272-277.

[32]

West J B, Luks A M, Nitin A J. West's Respiratory Physiology: The Essentials, 11th edition[M ]. Netherlands: Wolters Kluwer Health, 2020: 109-111.

[33]

Hall J E, Hall M E. Guyton and Hall Textbook of Medical Physiology, 14th edition[M]. USA: Elsevier, 2020: 245-258.

[34]

Gattinoni L, Brazzi L, Pelosi P, et al. A trial of goal—oriented hemodynamic therapy in critically ill patients. SvO2 Collaborative Group[J]. N Engl J Med, 1995, 333(16): 1025-1032.

[35]

Hayes M A, Timmins A C, Yau E H, et al. Elevation of systemic oxygen delivery in the treatment of critically ill patients[J]. N Engl J Med, 1994, 330(24): 1717-1722.

[36]

Nassar B, Badr M, Van Grunderbeeck N, et al. Central venous—to—arterial PCO(2) difference as a marker to identify fluid responsiveness in septic shock[J]. Sci Rep, 2021, 11(1): 17256.

[37]

Zante B, Reichenspurner H, Kubik M, et al. Increased admission central venous—arterial CO2 difference predicts ICU—mortality in adult cardiac surgery patients[J]. Heart Lung, 2019, 48(5): 421-427.

[38]

Nassar B, Mallat J. Usefulness of venous—to—arterial partial pressure of CO2 difference to assess oxygen supply to demand adequacy: effects of dobutamine[J]. J Thorac Dis, 2019, 11(Suppl 11): S1574-S1578.

[39]

Mari A, Nougue H, Mateo J, et al. Transcutaneous PCO(2) monitoring in critically ill patients: update and perspectives[J]. J Thorac Dis, 2019, 11(Suppl 11): S1558-S1567.

[40]

Yuriditsky E, Zhang R S, Bakker J, et al. Relationship between the mixed venous—to—arterial carbon dioxide gradient and the cardiac index in acute pulmonary embolism[J]. Eur Heart J Acute Cardiovasc Care, 2024, 13(6): 493-500.

[41]

Denault A, Bélisle S, Babin D, et al. Difficult separation from cardiopulmonary bypass and deltaPCO2 [J]. Can J Anaesth, 2001, 48(2): 196-199.

[42]

Montalti A, Belliato M, Gelsomino S, et al. Continuous monitoring of membrane lung carbon dioxide removal during ECMO: experimental testing of a new volumetric capnometer[J]. Perfusion, 2019, 34(7): 538-543.

[43]

Akamatsu T, Inata Y, Tachibana K, et al. Elevated central venous to arterial CO2 difference is not associated with poor clinical outcomes after cardiac surgery with cardiopulmonary bypass in children[J]. Pediatr Crit Care Med, 2017, 18(9): 859-862.

[44]

Felice V B, Araujo D T, Meregalli A F. Value of central venous to arterial CO2 difference after early goal—directed therapy in septic shock patients[J]. Indian J Crit Care Med, 2019, 23(10): 449-453.

[45]

Heino A, Hartikainen J, Merasto M E, et al. Systemic and regional pCO2 gradients as markers of intestinal ischaemia[J]. Intensive Care Med, 1998, 24(6): 599-604.

基金资助

华中科技大学同济医学院护理学院2024年度自主创新基金项目(ZZCX2024L001)

AI Summary AI Mindmap
PDF (1165KB)

0

访问

0

被引

详细

导航
相关文章

AI思维导图

/