Obstructive ventilatory defect with normal forced expiratory volume in one second/vital capacity ratio

To the Editors:

Pellegrino et al. 1 now define obstructive ventilatory defect not only on the basis of a low forced expiratory volume in one second (FEV₁)/vital capacity (VC) ratio but also as a particular pattern with a normal FEV₁/VC ratio. Although they write that “the definition of an obstructive pulmonary defect given in the present document is consistent with the 1991 American Thoracic Society 2 statement of interpretation,” a definition of an obstructive defect characterised by a normal FEV₁/VC ratio cannot be found in this latter document.

Incidentally, this pattern was described several years ago and called “small airways obstructive syndrome”. It is characterised by a normal total lung capacity (TLC) and FEV₁/VC ratio, but high residual volume (RV) and low VC and FEV₁ due to premature airways closure 3. It was emphasised that a decrease in FEV₁, provided FEV₁/VC is normal, calls for measurement of lung volumes. In the absence of such measurements, this pattern would be ignored and called a restrictive or a “nonspecific defect” 4.

Subsequently, lung function was compared in healthy subjects and those with small airways obstructive syndrome 5, 6. The pattern is characterised by a parallel displacement to the left of the flow–volume curve with respect to that of the healthy subjects, resulting in significant decreases of maximal flows.

None of these cited papers can be found in the reference section of the article by Pellegrino et al. 1. Curiously enough, recently, two authors of this report felt it appropriate to write an editorial on these data, emphasising their interest 7.

Some authors have reported physiological abnormalities compatible with this pattern or mimicking some of its particularities 8, 9. However, its individuality as an obstructive defect has not been previously recognised. For example, in patients with acute induced asthma, Olive and Hyatt 10 reported a parallel displacement to the left of the flow–volume curve with respect to the control curve, resulting in a decrease of maximal flows and airway conductance and an increase in RV. There was a slight increase in TLC. No comments were made on the FEV₁/VC ratio. On calculating this ratio, it appeared that about half of the subjects did not change their FEV₁/VC following induced bronchoconstriction.

Pellegrino et al. 1 write that this pattern is “observed” or “caused by failure of the patient to inhale or exhale completely or when the flow is so slow that the subject cannot exhale long enough to empty the lungs to RV […] Measurement of slow VC (inspiratory or expiratory) may then give a more correct estimate of the FEV/VC ratio.”

Failure to inhale completely would result not only in a reduced VC but also, necessarily, in a reduced TLC, and therefore the defect should be called restrictive not obstructive.

Failure to exhale completely, or when the flow is so slow that the subject cannot exhale long enough to empty the lungs, would reduce vital capacity and increase residual volume but would not influence forced expiratory volume in one second, therefore not complying with the definition of this pattern, see figure 1b in 1, also see 7. Indeed, forced expiratory volume in one second, which reflects maximal flow at high lung volumes and mid-vital capacity, is not decreased as a result of a slow expiration or incomplete emptying of the lung. Therefore, this physiological abnormality cannot be called obstructive. Only premature small airways closure may explain this pattern.