What is diffusing capacity and why is it important?

How do clinical disorders affect lung carbon monoxide diffusion capacity (DLCO)? Click this article to find out more!
Michael A. Grippi, MD
Michael A. Grippi, MD
3m read
Editors:Shelley Jacobs, PhD
Peer reviewers:Franz Wiesbauer, MD MPH Internist
Last update24th Nov 2020

Lung carbon monoxide diffusing capacity (DLCO) is a good indicator of the physiological health of the lungs—a value below the predicted range becomes a clue to the presence of a physiological problem.

However, there are a number of normal physiological factors that can affect the measurement obtained.

Changes to DLCO? Check these physiological factors first

There are six normal physiological factors that can affect DLCO measurements:

Figure 1. Physiological factors that affect lung carbon monoxide diffusing capacity (DLCO) measurements.

When changes to DLCO indicate pathology

COPD

DLCO declines in chronic obstructive pulmonary disease (COPD), with greater changes in emphysema than chronic bronchitis because of greater loss of alveolar surface area in emphysema.

Figure 2. Lung carbon monoxide diffusing capacity (DLCO) is reduced with a loss of alveolar surface area, as seen in chronic obstructive pulmonary disease (COPD).

Restrictive disorders

Restrictive disorders that include pulmonary parenchymal disease (e.g., pulmonary fibrosis) are also accompanied by declines in DLCO.

Figure 3. In restrictive pulmonary disorders, lung carbon monoxide diffusing capacity (DLCO) is preserved unless the pulmonary parenchyma is also affected. These disorders (e.g., pulmonary fibrosis) are accompanied by reduced DLCO.
Widening of the pulmonary interstitium or flooding of the alveoli impairs gas movement across the alveolar-capillary membrane and is reflected in a decreased DLCO.
Figure 4. Lung carbon monoxide diffusing capacity (DLCO) is reduced when the pulmonary interstitium is widened or flooded.
Thrombotic or embolic occlusion of branches of the pulmonary artery reduces DLCO, as do disorders of the pulmonary capillaries (e.g., vasculitis). Severe pulmonary hypertension may be associated with obliteration of the pulmonary capillaries and a reduction in DLCO.
Figure 5. Lung carbon monoxide diffusing capacity (DLCO) is reduced with thrombotic or embolic occlusion pulmonary artery branches.

Acute alveolar hemorrhage is associated with an increase in DLCO. This is secondary to hemoglobin in the alveoli serving as a sink for carbon monoxide used during measurement. When alveolar hemorrhage is chronic or recurrent, the resulting lung fibrosis reduces DLCO.

Figure 6. Lung carbon monoxide diffusing capacity (DLCO) is increased during acute alveolar hemorrhage due to alveoli serving as a sink for carbon monoxide. DLCO is reduced in chronic or recurrent alveolar hemorrhage due to lung fibrosis.

Other disorders

Through an increase in capillary red blood cells, polycythemia results in an increase in DLCO. Anemia, with reduced red cell mass, reduces DLCO.

Figure 7. Summary of disorders that affect lung carbon monoxide diffusing capacity (DLCO).

Changes to carbon dioxide diffusion

Mild abnormalities of the pulmonary parenchyma are usually not associated with an increased arterial-alveolar gradient for carbon dioxide. With more advanced thickening of the alveolar-capillary membrane and a reduction in DLCO to about 25% of normal, an arterial-alveolar gradient for carbon dioxide may arise.

Figure 8. Mild abnormalities of the pulmonary parenchyma are not associated with an increased arterial-alveolar gradient of carbon dioxide (CO2). But, advanced thickening of the alveolar-capillary membrane and reduction in lung carbon monoxide diffusing capacity (DLCO) can increase the carbon dioxide gradient, thus reducing CO2.

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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 J. 45: 227–243. PMID: 25323225

About the author

Michael A. Grippi, MD
Michael is Vice Chairman in the Department of Medicine and Associate Professor of Medicine in the Pulmonary, Allergy, and Critical Care Division at the Perelman School of Medicine, University of Pennsylvania, USA.
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