Journal of Applied Physiology AJP: Gastrointestinal and Liver Physiology
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J Appl Physiol 106: 1902-1908, 2009. First published April 16, 2009; doi:10.1152/japplphysiol.00085.2009
8750-7587/09 $8.00
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Ventilation-perfusion imbalance and chronic obstructive pulmonary disease staging severity

Roberto Rodríguez-Roisin,1,3 Mitra Drakulovic,2 Diego A. Rodríguez,2 Josep Roca,1,3 Joan Albert Barberà,1,3 and Peter D. Wagner4

1Servei de Pneumologia (Institut del Tòrax), Hospital Clinic, Institut d'Investigacions Biomédiques August Pi i Sunyer, 2Fundació Clinic de Recerca Biomèdica, and 3Ciber Enfermedades Respiratorias, Universitat de Barcelona, Barcelona, Spain; and 4Division of Physiology, University of California, San Diego, California

Submitted 28 January 2009 ; accepted in final form 9 April 2009

Chronic obstructive pulmonary disease (COPD) is characterized by a decline in forced expiratory volume in 1 s (FEV1) and, in many advanced patients, by arterial hypoxemia with or without hypercapnia. Spirometric and gas exchange abnormalities have not been found to relate closely, but this may reflect a narrow range of severity in patients studied. Therefore, we assessed the relationship between pulmonary gas exchange and airflow limitation in patients with COPD across the severity spectrum. Ventilation-perfusion (VA/Q) mismatch was measured using the multiple inert gas elimination technique in 150 patients from previous studies. The distribution of patients according to the GOLD stage of COPD was: 15 with stage 1; 40 with stage 2; 32 with stage 3; and 63 with stage 4. In GOLD stage 1, AaPO2 and VA/Q mismatch were clearly abnormal; thereafter, hypoxemia, AaPO2, and VA/Q imbalance increased, but the changes from GOLD stages 1–4 were modest. Postbronchodilator FEV1 was related to PaO2 (r = 0.62) and PaCO2 (r = –0.59) and to overall VA/Q heterogeneity (r = –0.48) (P < 0.001 each). Pulmonary gas exchange abnormalities in COPD are related to FEV1 across the spectrum of severity. VA/Q imbalance, predominantly perfusion heterogeneity, is disproportionately greater than airflow limitation in GOLD stage 1, suggesting that COPD initially involves the smallest airways, parenchyma, and pulmonary vessels with minimal spirometric disturbances. That progression of VA/Q inequality with spirometric severity is modest may reflect pathogenic processes that reduce both local ventilation and blood flow in the same regions through airway and alveolar disease and capillary involvement.

airflow limitation; arterial blood gases; chronic respiratory failure; global initiative for COPD; pulmonary gas exchange



Address for reprint requests and other correspondence: R. Rodríguez-Roisin, Servei de Pneumologia, Hospital Clínic, Villarroel, 170. 08036 Barcelona, Spain (e-mail: rororo{at}clinic.ub.es)







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