Relationship between lung function, ventilation-perfusion inequality and extent of emphysema as assessed by...

The development of the high-resolution computed tomography (HRCT) has improved the ability to detect and quantify emphysema in various groups of patients with chronic airflow obstruction (COPD). Significant correlations have previously been found between indices of air flow obstruction, hyperinflation, reduced diffusing capacity for carbon monoxide (DLCO), and the extent of emphysema (emph.%) assessed by HRCT. However, the relationship between emph.% and ventilation-perfusion (V(A)/Q) inequality in COPD is unknown. Twenty COPD patients with a mean forced expiratory volume in 1 s (FEV1) of 38.2 (+/- 15.5)% in percent of predicted value (%P), a mean PaO2 value of 9.6 (+/- 1.3) kPa, and a mean diffusing capacity of 43.6 (+/- 23.0)%P, were subjected to measurements by the multiple elimination inert gas technique (MIGET). The extent of emphysema was determined by HRCT at both full inspiration, emph.I(%) and at full expiration, emph.E(%), with a cut-off limit of -910 Hounsfield Units (HU) using the "Density Mask" method. The ventilation directed towards high V(A)/Q areas was 73 (+/- 10.2)% and the mean ventilation (V-mean) was elevated about three times compared to normal. The mean emph.(I)% and emph.(E) was 45.6 (+/- 16.9) and 32.7 (+/- 190)%, respectively. Significant correlations were shown between the emphysema extent and several lung function parameters, but no correlation was found between the emphysema extent and the V(A)/Q relationships or the blood gas values. Reduced DLCO%P correlated with less high V(A)/Q ventilation (r=0.73, P < 0.05) for the subgroup of COPD patients with DLCO(%P) less than 50% (n=12).

In COPD patients, suffering from moderate to severe emphysema without severe blood gas impairment, no correlation was shown between the extent of emphysema, as assessed by HRCT, and the severity of ventilation-perfusion inequality. A substantial collateral ventilation in severe emphysema may be a mechanism that prevents a deterioration in V(A)/Q relationships and in blood gas levels.