Changes of Arterial Carbon‐dioxide Tension in Patients With Chronic Lung Disease Breathing Oxygen

SUMMARY Pulmonary ventilation and arterial carbon‐dioxide tension (Pco2) were compared in 54 patients with chronic lung disease breathing air and breathing oxygen. Changes in arterial Pco2 did not simply reflect the effects of changes in ventilation which occurred with oxygen breathing, even after allowance had been made for ventilation‐induced changes in physiological dead space. It was necessary to invoke changes in respiratory muscle work and redistribution of pulmonary blood flow to explain the data in all instances. Changes of respiratory muscle work “buffered” the anticipated changes in arterial Pco2. Reversal of “compensatory” regional pulmonary vasoconstriction by oxygen produced levels of arterial Pco2 higher than those to be expected from changes in ventilation alone.