Regional Capnography

  • Jihad Mallat
  • Benoit Vallet


In critically ill patients, tissue hypoperfusion is an important cause leading to multi-organ dysfunction and death, and it cannot always be detected by measuring standard global hemodynamic and oxygen-derived parameters. Gastric intramucosal PCO2 as measured by gastric tonometry has been recognized to be of clinical value as a prognostic factor, in assessing the effects of particular therapeutic interventions, and as an endpoint of resuscitation. However, this technique has several limitations that have hampered its implementation in clinical practice. The sublingual tissue bed has been shown to be damaged in models of shock, and microcirculatory changes in this area may indicate imminent changes in other important organs. The measurement of sublingual mucosal PCO2 (PslCO2) by sublingual capnography is technically simple and noninvasive and gives near instantaneous results. Clinical studies have established that high PslCO2 values and, more especially, high PslCO2 gap (PslCO2—arterial PCO2) values are correlated with impaired microcirculatory blood flow and a poor outcome in critically ill patients. Sublingual capnography seems to be the ideal noninvasive monitoring tool to evaluate the severity of shock states and the adequacy of tissue perfusion.


Tissue hypoperfusion Tissue PCO2 Tissue PCO2 gap Gastric tonometry Sublingual capnography Critical care Shock Microcirculatory alterations 


Competing Interests

None of the authors have any potential financial or nonfinancial conflict of interest related to this manuscript.


  1. 1.
    Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345(19):1368–77.CrossRefPubMedGoogle Scholar
  2. 2.
    Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2013;369(18):1726–34. Scholar
  3. 3.
    Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Intensive Care Med. 2013;39(2):165–228. Scholar
  4. 4.
    Cecconi M, De Backer D, Antonelli M, Beale R, Bakker J, Hofer C, et al. Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med. 2014;40(12):1795–815. Scholar
  5. 5.
    Sakr Y, Dubois MJ, De Backer D, Creteur J, Vincent JL. Persistent microcirculatory alterations are associated with organ failure and death in patients with septic shock. Crit Care Med. 2004;32(9):1825–31.CrossRefPubMedGoogle Scholar
  6. 6.
    Vincent JL, De Backer D. Microvascular dysfunction as a cause of organ dysfunction in severe sepsis. Crit Care. 2005;9(Suppl 4):S9–12.CrossRefPubMedPubMedCentralGoogle Scholar
  7. 7.
    Trzeciak S, Cinel I, Phillip Dellinger R, Shapiro NI, Arnold RC, Parrillo JE, et al. Resuscitating the microcirculation in sepsis: the central role of nitric oxide, emerging concepts for novel therapies, and challenges for clinical trials. Acad Emerg Med. 2008;15(5):399–413. Scholar
  8. 8.
    Mekontso-Dessap A, Castelain V, Anguel N, Bahloul M, Schauvliege F, Richard C, et al. Combination of venoarterial PCO2 difference with arteriovenous O2 content difference to detect anaerobic metabolism in patients. Intensive Care Med. 2002;28(3):272–7.CrossRefPubMedGoogle Scholar
  9. 9.
    Ince C, Sinaasappel M. Microcirculatory oxygenation and shunting in sepsis and shock. Crit Care Med. 1999;27(7):1369–77.CrossRefPubMedGoogle Scholar
  10. 10.
    De Backer D, Creteur J, Preiser JC, Dubois MJ, Vincent JL. Microvascular blood flow is altered in patients with sepsis. Am J Respir Crit Care Med. 2002;166(1):98–104.CrossRefPubMedGoogle Scholar
  11. 11.
    Fink MP. Bench-to-bedside review: cytopathic hypoxia. Crit Care. 2002;6(6):491–9.CrossRefPubMedPubMedCentralGoogle Scholar
  12. 12.
    Hotchkiss RS, Karl IE. Reevaluation of the role of cellular hypoxia and bioenergetic failure in sepsis. JAMA. 1992;267(11):1503–10.CrossRefPubMedGoogle Scholar
  13. 13.
    James JH, Luchette FA, McCarter FD, Fischer JE. Lactate is an unreliable indicator of tissue hypoxia in injury or sepsis. Lancet. 1999;354(9177):505–8.CrossRefPubMedGoogle Scholar
  14. 14.
    Garcia-Alvarez M, Marik P, Bellomo R. Sepsis-associated hyperlactatemia. Crit Care. 2014;18(5):503. CrossRefPubMedPubMedCentralGoogle Scholar
  15. 15.
    Marik PE. Gastric intramucosal pH. A better predictor of multiorgan dysfunction syndrome and death than oxygen-derived variables in patients with sepsis. Chest. 1993;104(1):225–9.CrossRefPubMedGoogle Scholar
  16. 16.
    De Backer D. Lactic acidosis. Intensive Care Med. 2003;29(5):699–702.CrossRefPubMedGoogle Scholar
  17. 17.
    Marik PE. Regional carbon dioxide monitoring to assess the adequacy of tissue perfusion. Curr Opin Crit Care. 2005;11(3):245–51.CrossRefPubMedGoogle Scholar
  18. 18.
    Rimachi R, Bruzzi de Carvahlo F, Orellano-Jimenez C, Cotton F, Vincent JL, De Backer D. Lactate/pyruvate ratio as a marker of tissue hypoxia in circulatory and septic shock. Anaesth Intensive Care. 2012;40(3):427–32.PubMedGoogle Scholar
  19. 19.
    Gore DC, Jahoor F, Hibbert JM, DeMaria EJ. Lactic acidosis during sepsis is related to increased pyruvate production, not deficits in tissue oxygen availability. Ann Surg. 1996;224(1):97–102.CrossRefPubMedPubMedCentralGoogle Scholar
  20. 20.
    Vary TC, Siegel JH, Nakatani T, Sato T, Aoyama H. Effect of sepsis on activity of pyruvate dehydrogenase complex in skeletal muscle and liver. Am J Phys. 1986;250(6 Pt 1):E634–40.Google Scholar
  21. 21.
    Levraut J, Ciebiera JP, Chave S, Rabary O, Jambou P, Carles M, et al. Mild hyperlactatemia in stable septic patients is due to impaired lactate clearance rather than overproduction. Am J Respir Crit Care Med. 1998;157(4 Pt 1):1021–6.CrossRefPubMedGoogle Scholar
  22. 22.
    Curtis SE, Cain SM. Regional and systemic oxygen delivery/uptake relations and lactate flux in hyperdynamic, endotoxin-treated dogs. Am Rev Respir Dis. 1992;145(2 Pt 1):348–54.CrossRefPubMedGoogle Scholar
  23. 23.
    Grundler W, Weil MH, Rackow EC. Arteriovenous carbon dioxide and pH gradients during cardiac arrest. Circulation. 1986;74(5):1071–4.CrossRefPubMedGoogle Scholar
  24. 24.
    Weil MH, Rackow EC, Trevino R, Grundler W, Falk JL, Griffel MI. Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation. N Engl J Med. 1986;315(3):153–6.CrossRefPubMedGoogle Scholar
  25. 25.
    Kette F, Weil MH, Gazmuri RJ, Bisera J, Rackow EC. Intramyocardial hypercarbic acidosis during cardiac arrest and resuscitation. Crit Care Med. 1993;21(6):901–6.CrossRefPubMedGoogle Scholar
  26. 26.
    Gudipati CV, Weil MH, Gazmuri RJ, Deshmukh HG, Bisera J, Rackow EC. Increases in coronary vein CO2 during cardiac resuscitation. J Appl Physiol (1985). 1990;68(4):1405–8.CrossRefGoogle Scholar
  27. 27.
    Desai VS, Weil MH, Tang W, Gazmuri R, Bisera J. Hepatic, renal, and cerebral tissue hypercarbia during sepsis and shock in rats. J Lab Clin Med. 1995;125(4):456–61.PubMedGoogle Scholar
  28. 28.
    Gutierrez G, Palizas F, Doglio G, Wainsztein N, Gallesio A, Pacin J, et al. Gastric intramucosal pH as a therapeutic index of tissue oxygenation in critically ill patients. Lancet. 1992;339(8787):195–9.CrossRefPubMedGoogle Scholar
  29. 29.
    Marik PE, Bankov A. Sublingual capnometry versus traditional markers of tissue oxygenation in critically ill patients. Crit Care Med. 2003;31(3):818–22.CrossRefPubMedGoogle Scholar
  30. 30.
    Levy B, Gawalkiewicz P, Vallet B, Briancon S, Nace L, Bollaert PE. Gastric capnometry with air-automated tonometry predicts outcome in critically ill patients. Crit Care Med. 2003;31(2):474–80.CrossRefPubMedGoogle Scholar
  31. 31.
    Connett RJ, Honig CR, Gayeski TE, Brooks GA. Defining hypoxia: a systems view of VO2, glycolysis, energetics, and intracellular PO2. J Appl Physiol (1985). 1990;68(3):833–42.CrossRefGoogle Scholar
  32. 32.
    Schlichtig R, Bowles SA. Distinguishing between aerobic and anaerobic appearance of dissolved CO2 in intestine during low flow. J Appl Physiol (1985). 1994;76(6):2443–51.CrossRefGoogle Scholar
  33. 33.
    Teboul JL, Michard F, Richard C. Critical analysis of venoarterial CO2 gradient as a marker of tissue hypoxia. In: Vincent JL, editor. Yearbook of intensive care and emergency medicine. Heidelberg: Springer; 1996. p. 296–307.CrossRefGoogle Scholar
  34. 34.
    Randall HM Jr, Cohen JJ. Anaerobic CO2 production by dog kidney in vitro. Am J Phys. 1966;211(2):493–505.Google Scholar
  35. 35.
    Dubin A, Estenssoro E, Murias G, Canales H, Sottile P, Badie J, et al. Effects of hemorrhage on gastrointestinal oxygenation. Intensive Care Med. 2001;27(12):1931–6.CrossRefPubMedGoogle Scholar
  36. 36.
    Vallet B, Teboul JL, Cain S, Curtis S. Venoarterial CO(2) difference during regional ischemic or hypoxic hypoxia. J Appl Physiol (1985). 2000;89(4):1317–21.CrossRefGoogle Scholar
  37. 37.
    Nevière R, Chagnon JL, Teboul JL, Vallet B, Wattel F. Small intestine intramucosal PCO(2) and microvascular blood flow during hypoxic and ischemic hypoxia. Crit Care Med. 2002;30(2):379–84.CrossRefPubMedGoogle Scholar
  38. 38.
    Dubin A, Estenssoro E, Murias G, Pozo MO, Sottile JP, Barán M, et al. Intramucosal-arterial Pco2 gradient does not reflect intestinal dysoxia in anemic hypoxia. J Trauma. 2004;57(6):1211–7.CrossRefPubMedGoogle Scholar
  39. 39.
    Dubin A, Murias G, Estenssoro E, Canales H, Badie J, Pozo M, et al. Intramucosal-arterial PCO2 gap fails to reflect intestinal dysoxia in hypoxic hypoxia. Crit Care. 2002;6(6):514–20.CrossRefPubMedPubMedCentralGoogle Scholar
  40. 40.
    Creteur J, De Backer D, Sakr Y, Koch M, Vincent JL. Sublingual capnometry tracks microcirculatory changes in septic patients. Intensive Care Med. 2006;32(4):516–23.CrossRefPubMedGoogle Scholar
  41. 41.
    Gutierrez G. A mathematical model of tissue-blood carbon dioxide exchange during hypoxia. Am J Respir Crit Care Med. 2004;169(4):525–33.CrossRefPubMedGoogle Scholar
  42. 42.
    Nelson DP, Beyer C, Samsel RW, Wood LD, Schumacker PT. Pathological supply dependence of O2 uptake during bacteremia in dogs. J Appl Physiol (1985). 1987;63(4):1487–92.CrossRefGoogle Scholar
  43. 43.
    Pastores SM, Katz DP, Kvetan V. Splanchnic ischemia and gut mucosal injury in sepsis and the multiple organ dysfunction syndrome. Am J Gastroenterol. 1996;91(9):1697–710.PubMedGoogle Scholar
  44. 44.
    Doig CJ, Sutherland LR, Sandham JD, Fick GH, Verhoef M, Meddings JB. Increased intestinal permeability is associated with the development of multiple organ dysfunction syndrome in critically ill ICU patients. Am J Respir Crit Care Med. 1998;158(2):444–51.CrossRefPubMedGoogle Scholar
  45. 45.
    Meakins JL, Marshall JC. The gastrointestinal tract: the motor of MOF. Arch Surg. 1986;121:197–201.Google Scholar
  46. 46.
    Dantzker DR. The gastrointestinal tract. The canary of the body? JAMA. 1993;270(10):1247–8.CrossRefPubMedGoogle Scholar
  47. 47.
    Edouard AR, Degrémont AC, Duranteau J, Pussard E, Berdeaux A, Samii K. Heterogeneous regional vascular responses to simulated transient hypovolemia in man. Intensive Care Med. 1994;20(6):414–20.CrossRefPubMedGoogle Scholar
  48. 48.
    Hamilton-Davies C, Mythen MG, Salmon JB, Jacobson D, Shukla A, Webb AR. Comparison of commonly used clinical indicators of hypovolaemia with gastrointestinal tonometry. Intensive Care Med. 1997;23(3):276–81.CrossRefPubMedGoogle Scholar
  49. 49.
    Friedman G, Berlot G, Kahn RJ, Vincent JL. Combined measurements of blood lactate concentrations and gastric intramucosal pH in patients with severe sepsis. Crit Care Med. 1995;23(7):1184–93.CrossRefPubMedGoogle Scholar
  50. 50.
    Oud L, Haupt MT. Persistent gastric intramucosal ischemia in patients with sepsis following resuscitation from shock. Chest. 1999;115(5):1390–6.CrossRefPubMedGoogle Scholar
  51. 51.
    Morgan TJ, Venkatesh B, Endre ZH. Accuracy of intramucosal pH calculated from arterial bicarbonate and the Henderson-Hasselbalch equation: assessment using simulated ischemia. Crit Care Med. 1999;27(11):2495–9.CrossRefPubMedGoogle Scholar
  52. 52.
    Pernat A, Weil MH, Tang W, Yamaguchi H, Pernat AM, Sun S, et al. Effects of hyper- and hypoventilation on gastric and sublingual PCO(2). J Appl Physiol (1985). 1999;87(3):933–7.CrossRefGoogle Scholar
  53. 53.
    Vincent JL, Creteur J. Gastric mucosal pH is definitely obsolete—please tell us more about gastric mucosal PCO2. Crit Care Med. 1998;26(9):1479–81.CrossRefPubMedGoogle Scholar
  54. 54.
    Schlichtig R, Mehta N, Gayowski TJ. Tissue-arterial PCO2 difference is a better marker of ischemia than intramural pH (pHi) or arterial pH-pHi difference. J Crit Care. 1996;11(2):51–6.CrossRefPubMedGoogle Scholar
  55. 55.
    Bennett-Guerrero E, Panah MH, Bodian CA, Methikalam BJ, Alfarone JR, DePerio M, et al. Automated detection of gastric luminal partial pressure of carbon dioxide during cardiovascular surgery using the Tonocap. Anesthesiology. 2000;92(1):38–45.CrossRefPubMedGoogle Scholar
  56. 56.
    Lebuffe G, Decoene C, Pol A, Prat A, Vallet B. Regional capnometry with air-automated tonometry detects circulatory failure earlier than conventional hemodynamics after cardiac surgery. Anesth Analg. 1999;89(5):1084–90.CrossRefPubMedGoogle Scholar
  57. 57.
    Holland J, Carey M, Hughes N, Sweeney K, Byrne PJ, Healy M, et al. Intraoperative splanchnic hypoperfusion, increased intestinal permeability, down-regulation of monocyte class II major histocompatibility complex expression, exaggerated acute phase response, and sepsis. Am J Surg. 2005;190(3):393–400.CrossRefPubMedGoogle Scholar
  58. 58.
    Lebuffe G, Vallet B, Takala J, Hartstein G, Lamy M, Mythen M, et al. A european, multicenter, observational study to assess the value of gastric-to-end tidal PCO2 difference in predicting postoperative complications. Anesth Analg. 2004;99(1):166–72.CrossRefPubMedGoogle Scholar
  59. 59.
    Kirton OC, Windsor J, Wedderburn R, Hudson-Civetta J, Shatz DV, Mataragas NR, et al. Failure of splanchnic resuscitation in the acutely injured trauma patient correlates with multiple organ system failure and length of stay in the ICU. Chest. 1998;113(4):1064–9.CrossRefPubMedGoogle Scholar
  60. 60.
    Ivatury RR, Simon RJ, Islam S, Fueg A, Rohman M, Stahl WM. A prospective randomized study of end points of resuscitation after major trauma: global oxygen transport indices versus organ-specific gastric mucosal pH. J Am Coll Surg. 1996;183(2):145–54.PubMedGoogle Scholar
  61. 61.
    Pargger H, Hampl KF, Christen P, Staender S, Scheidegger D. Gastric intramucosal pH-guided therapy in patients after elective repair of infrarenal abdominal aneurysms: is it beneficial? Intensive Care Med. 1998;24(8):769–76.CrossRefPubMedGoogle Scholar
  62. 62.
    Gomersall CD, Joynt GM, Freebairn RC, Hung V, Buckley TA, Oh TE. Resuscitation of critically ill patients based on the results of gastric tonometry: a prospective, randomized, controlled trial. Crit Care Med. 2000;28(3):607–14.CrossRefPubMedGoogle Scholar
  63. 63.
    Miami Trauma Clinical Trials Group. Splanchnic hypoperfusion-directed therapies in trauma: a prospective, randomized trial. Am Surg. 2005;71(3):252–60.Google Scholar
  64. 64.
    Palizas F, Dubin A, Regueira T, Bruhn A, Knobel E, Lazzeri S, et al. Gastric tonometry versus cardiac index as resuscitation goals in septic shock: a multicenter, randomized, controlled trial. Crit Care. 2009;13(2):R44. Scholar
  65. 65.
    Zhang X, Xuan W, Yin P, Wang L, Wu X, Wu Q. Gastric tonometry guided therapy in critical care patients: a systematic review and meta-analysis. Crit Care. 2015;19:22. Scholar
  66. 66.
    Silva E, De Backer D, Creteur J, Vincent JL. Effects of fluid challenge on gastric mucosal PCO2 in septic patients. Intensive Care Med. 2004;30(3):423–9.CrossRefPubMedGoogle Scholar
  67. 67.
    Creteur J. Gastric and sublingual capnometry. Curr Opin Crit Care. 2006 Jun;12(3):272–7.CrossRefPubMedGoogle Scholar
  68. 68.
    Jin X, Weil MH, Sun S, Tang W, Bisera J, Mason EJ. Decreases in organ blood flows associated with increases in sublingual PCO2 during hemorrhagic shock. J Appl Physiol (1985). 1998;85(6):2360–4.CrossRefGoogle Scholar
  69. 69.
    Nakagawa Y, Weil MH, Tang W, Sun S, Yamaguchi H, Jin X, et al. Sublingual capnometry for diagnosis and quantitation of circulatory shock. Am J Respir Crit Care Med. 1998;157(6 Pt 1):1838–43.CrossRefPubMedGoogle Scholar
  70. 70.
    Povoas HP, Weil MH, Tang W, Moran B, Kamohara T, Bisera J. Comparisons between sublingual and gastric tonometry during hemorrhagic shock. Chest. 2000;118(4):1127–32.CrossRefPubMedGoogle Scholar
  71. 71.
    Marik PE. Sublingual capnography: a clinical validation study. Chest. 2001;120(3):923–7.CrossRefPubMedGoogle Scholar
  72. 72.
    Rackow EC, O'Neil P, Astiz ME, Carpati CM. Sublingual capnometry and indexes of tissue perfusion in patients with circulatory failure. Chest. 2001;120(5):1633–8.CrossRefPubMedGoogle Scholar
  73. 73.
    Maciel AT, Creteur J, Vincent JL. Tissue capnometry: does the answer lie under the tongue? Intensive Care Med. 2004;30(12):2157–65.CrossRefPubMedGoogle Scholar
  74. 74.
    Weil MH, Nakagawa Y, Tang W, Sato Y, Ercoli F, Finegan R, et al. Sublingual capnometry: a new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock. Crit Care Med. 1999;27(7):1225–9.CrossRefPubMedGoogle Scholar
  75. 75.
    Palágyi P, Kaszaki J, Rostás A, Érces D, Németh M, Boros M, et al. Monitoring microcirculatory blood flow with a new sublingual tonometer in a porcine model of hemorrhagic shock. Biomed Res Int. 2015;2015:847152. CrossRefPubMedPubMedCentralGoogle Scholar

Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  • Jihad Mallat
    • 1
  • Benoit Vallet
    • 2
  1. 1.Department of Anesthesiology and Critical Care Medicine, Service de Réanimation polyvalenteCentre Hospitalier du Dr. Schaffner de LensLensFrance
  2. 2.Department of Anesthesiology and Critical Care MedicineCentre Hospitalier Universitaire de LilleLilleFrance

Personalised recommendations