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Am. J. Respir. Crit. Care Med., Volume 161, Number 5, May 2000, 1524-1529

The Role of Hypoventilation and Ventilation-Perfusion Redistribution in Oxygen-induced Hypercapnia during Acute Exacerbations of Chronic Obstructive Pulmonary Disease

TRACEY D. ROBINSON, DAVID B. FREIBERG, JEFF A. REGNIS, and IVEN H. YOUNG

Department of Respiratory Medicine, Royal Prince Alfred Hospital, Sydney; and the University of Sydney, Sydney, Australia

The detailed mechanisms of oxygen-induced hypercapnia were examined in 22 patients during an acute exacerbation of chronic obstructive pulmonary disease. Ventilation, cardiac output, and the distribution of ventilation-perfusion (V A/Q ) ratios were measured using the multiple inert gas elimination technique breathing air and then 100% oxygen through a nose mask. Twelve patients were classified as retainers (R) when PaCO2 rose by more than 3 mm Hg (8.3 ± 5.6; mean ± SD) after breathing 100% oxygen for at least 20 min. The other 10 patients showed a change in PaCO2 of -1.3 ± 2.2 mm Hg breathing oxygen and were classified as nonretainers (NR). Ventilation fell significantly from 9.0 ± 1.5 to 7.2 ± 1.2 L/min in the R group breathing oxygen (p = 0.007), whereas there was no change in ventilation in the NR group (9.8 ± 1.8 to 9.9 ± 1.8 L/min). The dispersion of V A/Q ratios as measured by log SD of blood flow (log SD Q) 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 breathing oxygen, whereas log SD of ventilation (log SD Q ) increased only in the R group (0.97 ± 0.24 to 1.20 ± 0.46, p < 0.05). This study suggests that an overall reduction in ventilation characterizes oxygen-induced hypercapnia, as an increased dispersion of blood flow from release of 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 tension, perhaps related to bronchodilatation.




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