How are PaCO2 and minute ventilation related?

Unsure how to determine arterial carbon dioxide tension in your patients? In this article, learn how to calculate PaCO2 with minute ventilation.
Last update4th Dec 2020

The arterial carbon dioxide tension (partial pressure of carbon dioxide in the arteries, PaCO2) is determined by the rate of carbon dioxide production (VCO2) and the level of minute alveolar ventilation (VA).

Figure 1. Calculation for arterial carbon dioxide tension (PaCO2) is determined from the rate of carbon dioxide production (VCO2) and minute alveolar ventilation (VA).

Hence, at a constant rate of carbon dioxide production, the arterial carbon dioxide tension remains constant as long as alveolar ventilation remains constant.

Clinically, however, we don’t measure minute alveolar ventilation; rather, we measure the overall level of a patient’s ventilation, or minute ventilation (VE), which is the alveolar ventilation plus the dead space ventilation (VD). So, we can use this to calculate the partial pressure of carbon dioxide in the arteries by reworking the above equation as follows.

Figure 2. Expanded calculation for arterial carbon dioxide tension (PaCO2) which is determined from the rate of carbon dioxide production (VCO2) and the difference between minute ventilation (VE) and dead space ventilation (VD).

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Pathological changes to PaCO2

At a constant rate of carbon dioxide production, the arterial partial pressure of carbon dioxide falls with increasing minute ventilation and rises with declines in minute ventilation.

Figure 3. Arterial carbon dioxide tension (PaCO2) shifts with changes in minute ventilation. At a constant rate of CO2 production, PaCO2 falls with increasing minute ventilation (VE) and PaCO2 rises with declines in VE.

Furthermore, PaCO2 rises with increasing dead space, as seen in various disease states like chronic obstructive pulmonary disease (COPD) and acute respiratory distress syndrome (ARDS), and falls with declines in the proportion of dead space—as seen with large volume breaths during which VD stays constant but the difference between VD and VT increases.

Figure 4. Arterial carbon dioxide tension (PaCO2) shifts with changes in dead space ventilation (VD). PaCO2 rises with increasing dead space and falls with increases in the difference between minute ventilation (VE) and dead space.

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Recommended reading

  • Grippi, MA. 1995. “Gas exchange in the lung”. In: Lippincott's Pathophysiology Series: Pulmonary Pathophysiology. 1st edition. Philadelphia: Lippincott Williams & Wilkins. (Grippi 1995, 137–149)
  • Grippi, MA. 1995. “Clinical presentations: gas exchange and transport”. In: Lippincott's Pathophysiology Series: Pulmonary Pathophysiology. 1st edition. Philadelphia: Lippincott Williams & Wilkins. (Grippi 1995, 171–176)
  • Grippi, MA and Tino, G. 2015. “Pulmonary function testing”. In: Fishman's Pulmonary Diseases and Disorders, edited by MA, Grippi (editor-in-chief), JA, Elias, JA, Fishman, RM, Kotloff, AI, Pack, RM, Senior (editors). 5th edition. New York: McGraw-Hill Education. (Grippi and Tino 2015, 502–536)
  • Tino, G and Grippi, MA. 1995. “Gas transport to and from peripheral tissues”. In: Lippincott's Pathophysiology Series: Pulmonary Pathophysiology. 1st edition. Philadelphia: Lippincott Williams & Wilkins. (Tino and Grippi 1995, 151–170)
  • Wagner, PD. 2015. The physiologic basis of pulmonary gas exchange: implications for clinical interpretation of arterial blood gases. Eur Respir J45: 227–243. PMID: 25323225

About the author

Michael A. Grippi, MD
Vice Chairman, Department of Medicine | Pulmonary, Allergy, and Critical Care Division, Perelman School of Medicine, University of Pennsylvania, USA.
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