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Updated: May 10, 2026

A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
Causes of and compensations for hypoxemia and hypercapnia
1Department of Medicine, University of California, San Diego, La Jolla, CA, USA. jwest@ucsd.edu
Abstract:
By far the commonest cause of impaired gas exchange in patients with lung disease is ventilation-perfusion inequality. This is a complicated topic and much can be learned from computer models. Ventilation-perfusion inequality always causes hypoxemia, that is, an abnormally low PO2 in arterial blood. However, it is also the commonest cause of an increased arterial PCO2, or hypercapnia, in patients with chronic obstructive pulmonary disease (COPD). There is often confusion in this area with some people attributing the CO2 retention to "hypoventilation" when in fact these patients are usually moving much more air into their lungs than normal subjects. A patient with COPD can often return the arterial PCO2 to normal by increasing the ventilation. However, this does not return the arterial PO2 to normal because of the different shapes of the oxygen and carbon dioxide dissociation curves. Increasing pulmonary blood flow in the presence of ventilation-perfusion inequality usually raises the arterial PO2 but much less than increasing ventilation. Raising the inspired oxygen concentration is typically very effective in increasing the arterial PO2. Ventilation-perfusion inequality interferes with the transfer of all gases by the lung including the anesthetic gases. The gas exchange behavior of a lung depends greatly on the pattern of ventilation-perfusion inequality. It is theoretically possible to find a distribution that improves the transfer of some gases but this requires bizarre conditions that can never occur in practice.
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