Mechanisms of gas exchange response to lung volume reduction surgery in severe emphysema

Author:

Cremona George1,Barbara Joan A.2,Melgosa Teresa2,Appendini Lorenzo3,Roca Josep2,Casadio Caterina4,Donner Claudio F.5,Rodriguez-Roisin Roberto2,Wagner Peter D.6

Affiliation:

1. Unit of Respiratory Medicine, Istituto Scientifico San Raffaele, Milan, Italy;

2. Servie de Pneumologia (Thoracic Institute), Hospital Clínic-Institut d'Investigacions Biomediques August Pi Sunyer (IDIBAPS), Centro de Investigacion Biomedica en Red de Enfermedades Respiratorias (CIBERES), Universitat de Barcelona, Barcelona, Spain;

3. Divisione di Pneumologia, Fondazione Salvatore Maugeri, IRCCS, Istituto Scientifico di Veruno, Veruno, Italy;

4. Department of Thoracic Surgery, University of Eastern Piedmont, Novara, Italy;

5. Mondomedico, Multidisciplinary and Outpatient Rehabilitation Clinic, Borgomanero, Novara, Italy; and

6. Department of Medicine, University of California, San Diego, La Jolla, California

Abstract

Lung volume reduction surgery (LVRS) improves lung function, respiratory symptoms, and exercise tolerance in selected patients with chronic obstructive pulmonary disease, who have heterogeneous emphysema. However, the reported effects of LVRS on gas exchange are variable, even when lung function is improved. To clarify how LVRS affects gas exchange in chronic obstructive pulmonary disease, 23 patients were studied before LVRS, 14 of whom were again studied afterwards. We performed measurements of lung mechanics, pulmonary hemodynamics, and ventilation-perfusion (V̇a/Q̇) inequality using the multiple inert-gas elimination technique. LVRS improved arterial Po2 (PaO2) by a mean of 6 Torr ( P = 0.04), with no significant effect on arterial Pco2 (PaCO2), but with great variability in both. Lung mechanical properties improved considerably more than did gas exchange. Post-LVRS PaO2 depended mostly on its pre-LVRS value, whereas improvement in PaO2 was explained mostly by improved V̇a/Q̇ inequality, with lesser contributions from both increased ventilation and higher mixed venous Po2. However, no index of lung mechanical properties correlated with PaO2. Conversely, post-LVRS PaCO2 bore no relationship to its pre-LVRS value, whereas changes in PaCO2 were tightly related ( r2 = 0.96) to variables, reflecting decrease in static lung hyperinflation (intrinsic positive end-expiratory pressure and residual volume/total lung capacity) and increase in airflow potential (tidal volume and maximal inspiratory pressure), but not to V̇a/Q̇ distribution changes. Individual gas exchange responses to LVRS vary greatly, but can be explained by changes in combinations of determining variables that are different for oxygen and carbon dioxide.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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