ABG Interpretation
 

Assessing the PaCO₂

 
 
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Overview

  • The PaCO₂ is the arterial partial pressure of carbon dioxide, as measured on an arterial blood gas.
  • An increase or decrease in the PaCO₂ level suggests the presence of a respiratory process causing an acid-base imbalance. This can either be primary (the derangement is due to a respiratory issue) or secondary (there is respiratory compensation for a metabolic issue).
      • Normal Range

      • 36 - 44 mmHg

Hypercapnia

  • An increased PaCO₂ of greater than 44 mmHg on an arterial blood gas suggests the presence of a respiratory process - either primary (respiratory acidosis) or secondary (respiratory compensation of metabolic alkalosis).
    • Interpretation

    • Reduced pH with elevated PCO - suggests respiratory acidosis
    • Elevated pH with elevated PCO and elevated HCO₃ - suggests respiratory compensation for metabolic alkalosis
    • Normal pH with elevated PCO and elevated HCO₃ - suggests mixed respiratory acidosis-metabolic alkalosis

Hypocapnia

  • A reduced PaCO₂ of less than 36 mmHg on an arterial blood gas suggests the presence of a respiratory process - either primary (respiratory alkalosis) or secondary (respiratory compensation of metabolic acidosis).
    • Interpretation

    • Elevated pH with reduced PCO - suggests respiratory alkalosis
    • Reduced pH with reduced PCO and reduced HCO₃ - suggests respiratory compensation for metabolic acidosis
    • Normal pH with reduced PCO and reduced HCO₃ - suggests mixed respiratory alkalosis-metabolic acidosis
Last updated on February 7th, 2020
 
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 Andersen L, Mackenhauer J, Roberts J, Berg K, Cocchi M, Donnino M. Etiology and Therapeutic Approach to Elevated Lactate Levels. Mayo Clin Proc. 2013;88:1127-1140.
Beasley R, McNaughton A, Robinson G. New look at the oxyhaemoglobin dissociation curve. The Lancet. 2006;367:1124-1126.
 Bellomo R. Bench-to-bedside review: lactate and the kidney. Critical Care 2002;6(4):1. Berend K, de Vries A, Gans R. Physiological Approach to Assessment of Acid-Base Disturbances. N Engl J Med. 2014;371:1434-1445. Brenner BE. Alveolar-arterial oxygen gradients. Ann Emerg Med. 1980;9:648-648. Brindley PG, Butler MS, Cembrowski G, Brindley DN. Falsely elevated point-of-care lactate measurement after ingestion of ethylene glycol. Canadian Medical Association Journal 2007;176(8):1097-9. Donnino MW, Carney E, Cocchi MN, Barbash I, et al. Thiamine deficiency in critically ill patients with sepsis. Journal of critical care 2010;25(4):576-81. Gore DC, Jahoor F, Hibbert JM, DeMaria EJ. Lactic acidosis during sepsis is related to increased pyruvate production, not deficits in tissue oxygen availability. Annals of surgery 1996;224(1):97. Kraut JA, Madias NE. Lactic acidosis. N Engl J Med. 2014; 371: 2309-2319. Levraut J, Ciebiera JP, Chave S, Rabary O, et al. Mild hyperlactatemia in stable septic patients is due to impaired lactate clearance rather than overproduction. Am J RespirCrit Care Med. 1998; 157(4 Pt 1):1021-6. Levy B, Gibot S, Franck P, Cravoisy A, et al. Relation between muscle Na+ K+ ATPase activity and raised lactate concentrations in septic shock: a prospective study. The Lancet 2005;365(9462):871-5. Marino PL. Marino's the ICU Book. Fourthition. ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2014. McCarter FD, Nierman SR, James JH, Wang L, et al. Role of skeletal muscle Na+–K+ ATPase activity in increased lactate production in sub–acute sepsis. Life sciences 2002;70(16):1875-88. Moreau R, Hadengue A, Soupison T, Kirstetter P, et al. Septic shock in patients with cirrhosis: hemodynamic and metabolic characteristics and intensive care unit outcome. Critical care medicine 1992;20(6):746. Perriello G, Jorde R, Nurjhan N, Stumvoll M, et al. Estimation of glucose-alanine-lactate-glutamine cycles in postabsorptive humans: role of skeletal muscle. American Journal of Physiology-Endocrinology and Metabolism 1995;269(3):E443-50. Phypers B, Pierce JT. Lactate physiology in health and disease. Continuing education in Anaesthesia, critical care & pain. 2006 Jun 1;6(3):128-32. Stacpoole PW. Lactic acidosis. Endocrinol Metab Clin North Am 1993 Jun; 22(2) 221-45.
Tunney P, Chinnan NK. Serum Lactate in Intensive Care: Practical Points and Pitfalls. inflammation. 2016;6:7.
 Vary TC. Sepsis-induced alterations in pyruvate dehydrogenase complex activity in rat skeletal muscle: effects on plasma lactate. Shock 1996;6(2):89-94. Venkatesh B, Morgan T, Garrett P. Measuring the lactate gap. The Lancet 2001;358(9295):1806.
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