The role of hypoventilation and ventilation-perfusion redistribution in oxygen-induced hypercapnia during acute exacerbations of chronic obstructive pulmonary disease

The detailed mechanisms of oxygen-induced hypercapnia were examined in 22 p atients during an acute exacerbation of chronic obstructive pulmonary disea se. Ventilation, cardiac output, and the distribution of ventilation-perfus ion ((V) over dot A/(Q) over dot) ratios were measured using the multiple i nert gas elimination technique breathing air and then 100% oxygen through a nose mask. Twelve patients were classified as retainers (R) when Pa-CO2 ro se by more than 3 mm Hg (8.3 +/- 5.6; mean +/- SD) after breathing 100% oxy gen for at least 20 min. The other 10 patients showed a change in Pa-CO2 of -1.3 +/- 2.2 mm Hg breathing oxygen and were classified as nonretainers (N R). Ventilation fell significantly from 9.0 +/- 7.5 to 7.2 +/- 1.2 L/min in the R group breathing oxygen (p = 0.007), whereas there was no change in v entilation in the NR group (9.8 +/- 1.8 to 9.9 +/- 1.8 L/min). The dispersi on of (V) over dot A/(Q) over dot ratios as measured by log SD of blood flo w (log SD (Q) over dot) increased significantly in both R (0.96 +/- 0.17 to 1.13 +/- 0.17) and NR (0.77 +/- 0.20 to 1.04 +/- 0.23, p < 0.05) groups br eathing oxygen, whereas log SD of ventilation (fog SD (Q) over dot) increas ed only In the R group (0.97 +/- 0.24 to 1.20 +/- 0.46, p < 0.05). This stu dy suggests that an overall reduction in ventilation characterizes oxygen-i nduced hypercapnia, as an increased dispersion of blood flow from release o f hypoxic vasoconstriction occurred to a significant and similar degree in both groups. The significant increase in wasted ventilation (alveolar dead space) in the R group only may be secondary to the higher carbon dioxide te nsion, perhaps related to bronchodilatation.