Respiration 2004;71:348–352

A Normal FEV1/VC Ratio Does Not Exclude Airway Obstruction

Stănescu D. · Veriter C.
Pulmonary Laboratory and Division, Cliniques Universitaires Saint-Luc, Brussels, Belgium
email Corresponding Author


 goto top of outline Key Words

  • Airway obstruction
  • Small airways
  • Forced expiratory volume in 1 s
  • Spirometry
  • Lung function

 goto top of outline Abstract

Background: A decreased forced expiratory volume in 1 s/vital capacity (FEV1/VC) ratio is the hallmark of the definition of airway obstruction. We recently suggested that a lung function pattern, we called small airways syndrome (SAOS), has a normal FEV1/VC and total lung capacity (TLC) and reflects obstruction of small airways. Objectives: To substantiate our hypothesis we measured and compared lung function tests including maximal expiratory flow rates (MEFR), sensitive indicators of airway obstruction, in SAOS subjects and in matched controls. Methods: We selected 12 subjects with the pattern of SAOS, but without chronic lung or heart disease (average age: 40.7 ± 7.8 years) and 36 age-matched subjects with normal lung function (42.8 ± 6.3 years). We measured static and dynamic lung volumes, MEFR and lung diffusing capacity (DLCO). Results: SAOS subjects were heavier smokers (p < 0.05) and body mass index was less than in control subjects (p < 0.01). Both FEV1/VC ratio and TLC were comparable in the two groups. However, FEV1, VC, DLCO, and MEFR were lower and residual volume (RV) and RV/TLC ratio were higher (p < 0.05) in the SAOS group than in the control one. Furthermore, the MEFR curve of the SAOS group was displaced to the left without any change in slope, suggesting premature airway closure. Conclusion: Our results suggest that a normal FEV1/VC ratio does not exclude airway obstruction. A decrease of FEV1, provided TLC is normal, reflects small airway obstruction.

Copyright © 2004 S. Karger AG, Basel

goto top of outline Introduction

A decreased forced expiratory volume in 1 s/vital capacity (FEV1/VC) ratio is the hallmark of the definition of airway obstruction. In the presence of a low FEV1/VC the magnitude of the decrease of FEV1 is used to characterize the degree of severity of obstruction [1, 2]. We have recently reported that a functional pattern characterized by decreased VC and FEV1 and increased residual volume (RV) and RV/total lung capacity (TLC), but normal TLC and FEV1/VC reflects an obstruction of small airways. We called it small airways obstructive syndrome (SAOS) [3]. This pattern is variously considered by some authors a ‘nonspecific ventilatory limitation’, a ‘restrictive process’, or a ‘nonspecific finding’ [1, 4].

To substantiate our previous data we performed in SAOS subjects and in matched controls lung function tests including the measurement of maximal expiratory flow rates (MEFR), sensitive indicators of airway obstruction. We concluded that provided TLC is normal a decreased FEV1 reflects airway obstruction even if the FEV1/VC ratio is still normal.


goto top of outline Methods

We evaluated lung function studies in 48 subjects referred to the lung function laboratory of the University Hospital Saint-Luc in Brussels, Belgium. Selection criteria were as follows: male subjects aged more than 30 and less than 50 years, without chronic lung or heart disease, with either SAOS (normal TLC, decreased VC and FEV1, increased RV and normal FEV1/VC) or normal lung function tests. Most subjects were sent to the laboratory for preoperative assessment. Four hundred sixty-six subjects out of 1,908 male subjects referred to the laboratory over a period of 6 months were aged between 30 and 50 years. Two hundred thirty-five subjects had been former smokers and were excluded from further analysis. The rest of them, 231 subjects, had never smoked or had smoked continuously. Twelve subjects (average age: 40.7 ± 7.8 years) out of 231 had an SAOS pattern. Thirty-six subjects (42.8 ± 6.3 years) had normal lung function. Abnormal values were those outside the mean predicted values ±1 SD. Predicted values were from this laboratory [5] or from other studies [6, 7] in close agreement with the results we obtained in a sample of normal subjects. Only male subjects were selected because spirographic reference values [6] are not reliable for females. We limited the age range to avoid the inclusion of elderly subjects with SAOS.

Subjects refrained from smoking for at least 3 h preceding measurement of lung function indices. Spirometry was performed according to the recommendations of the American Thoracic Society [8]. Spirographic tests were done on a rolling-sealed spirometer (Morgan, Rainham, UK). Slow VC was recorded instead of forced VC. Residual volume was measured with the He-closed circuit method (Morgan, Rainham, UK). It was calculated as TLC-VC. The lung volume used to construct maximal expiratory flow volume (MEFV) curves was obtained by electrical integration of the flow rate. The latter was recorded with a linearized Lilly-type pneumotachograph. The frequency of the sampling of the analog/digital converter was 250 Hz (Medisoft, Dinant, Belgium).The spirometer and the pneumotachograph were checked every day with a 3-liter syringe. Subjects performed a minimum of 3 forced expiratory maneuvers. Reported values are the maximal ones. To take into account differences in MEFR secondary to differences in VC from one subject to another, the flow rate was plotted against the lung volume expressed as the percentage of actual TLC (fig. 1). MEFR were measured at 70, 60 and 50% actual TLC. Lung diffusing capacity (DLCO), corrected for the hemoglobin content, was measured in duplicate by the single-breath method [5].The reported figure is the mean of two values. Spirography and DLCO measurements preceded the recording of MEFR.


Fig. 1. Average MEFV curves in control (healthy) and SAOS subjects. Lung volume was expressed as percentage of actual TLC. Note the parallel shift to the left of the MEFV curve of SAOS subjects, decrease in MEFR and VC and increase in RV. ■ = Average values of MEFR at different lung volumes. Vertical bars indicate standard error of the mean (SEM). *** p < 0.001.

goto top of outline Data Analysis

All data are given as mean ± SD. Student’s test for unrelated samples was used to compare group means. A p value lower than 0.05 was regarded as statistically significant.


goto top of outline Results

Physical and lung function data in both groups of subjects are presented in table 1. Age and height were comparable in the two groups. However, SAOS subjects had a lower (p < 0.01) body mass index than control subjects. There were 6 smokers (36 ± 6 pack years) out of 12 subjects in the SAOS group and 7 smokers (19.5 ± 5 pack years) out of 36 in the control group. The smoking history was longer (p < 0.05) in the former group than in the latter one. Average TLC and FEV1/VC were comparable and within predicted limits in both groups (91% for TLC and 104% for FEV1/VC in the control group; 103% for both indices in the SAOS group). The residual volume and RV/TLC were increased and VC and FEV1 were decreased in the latter compared with the former group (p < 0.001), as well with respect to predicted values. The average MEFV curves in the two groups are presented in figure 1. In the SAOS subjects there was a parallel displacement to the left of the MEFV curve with respect to that of the control subjects. The slope of the MEFV curves was similar in the two groups. MEFR at 70, 60 and 50% TLC were all lower in SAOS than in control subjects (p < 0.001). DLCO was 23.3 ± 3.9 ml/min/mm Hg in the SAOS group (n = 6) and 31.9 ± 5.2 ml/min/mm Hg in the control group (n = 17; p < 0.01).


Table 1. Physical, functional data and smoking habits (mean ± SD) in control and SAOS subjects


goto top of outline Discussion

In a group of middle-aged male subjects selected because of an increased RV and RV/TLC, but normal TLC and FEV1/VC, we found significantly lower MEFR than in a matched control group. Since MEFR are sensitive indicators of airway obstruction the present results suggest that this functional pattern is an obstructive one. Indeed, a restrictive syndrome can be excluded since TLC was within normal limits and comparable in the two groups. Furthermore, MEFR are either normal or even increased in a restrictive syndrome and not decreased as they were in the SAOS subjects.

The SAOS subjects we studied represented a nonhomogeneous group with various pathologies but no evident chronic lung or heart disease. Their smoking history was longer, they were leaner and their DLco was lower than in control subjects suggesting the presence of subclinical pulmonary emphysema.

We also observed a parallel displacement to the left of the MEFV curve in SAOS subjects with respect to control subjects without any change in the slope (fig. 1). This pattern is similar to that reported by Olive and Hyatt [9] in asthmatic patients during the inhalation of allergens. Since ‘the slope of the MEFV curve reflects the time constant of lung emptying, i.e. the product of resistance and compliance’ a parallel shift means that in SAOS subjects this product was the same as that recorded in control subjects. This can be explained by a parallel bialveolar model (fig. 2). The upper alveolus and its airway have a normal size and behave normally. The lower one has a narrowed airway and closes at the start of expiration trapping gas and thus increasing RV and decreasing VC. Since the trapped areas are excluded from the system in terms of their contribution to the compliance and resistance of the remaining lung the MEFV curve has a normal shape and slope because it is produced by the upper alveolus and its airway, which are normal. The pattern recorded by Olive and Hyatt [9] at maximum allergen dose in asthmatic subjects is similar to that observed by us in SAOS subjects: no change in TLC, a decrease in VC, FEV1 and MEFR and an increase in RV. Obesity, a tentative explanation for premature airway closure in the SAOS subjects, can be excluded since they were in fact leaner than the control subjects. Mitral valve disease may somewhat mimic the SAOS pattern [10]. However, the absence of any decrease in TLC and FEV1/VC ratio as well as the selection criteria exclude this possibility.


Fig. 2. Schematically, a bialveolar model of a normal subject is shown (a). In a subject with SAOS (b) the upper alveolus and its airway have a normal size and empty normally producing a normal MEFV (continuous line, c). The lower alveolus also has a normal size but its airway is narrowed and closes during emptying (interrupted line, c) trapping gas and thus increasing RV. The slope of both MEFV curves is parallel.

The central feature of the SAOS pattern is the increase in RV and RV/TLC. Small airway closure sets the limit of expiration in elderly subjects and in pathologic conditions associated with the loss of lung elastic recoil (extrinsic obstruction) or narrowing and obliteration of these airways (intrinsic obstruction) [2, 11, 12, 13], suggesting the involvement of small airways in the pathogenesis of SAOS. The SAOS pattern was observed in old subjects, in asymptomatic asthmatics and as an early change in chronic obstructive pulmonary disease [14, 15, 16] but its individuality was not previously recognized. The European Respiratory Society had emphasized 10 years ago that the decrease of VC (and consequently of FEV1) without change in TLC may be the consequence of an increase in RV due to premature small airway closure (gas trapping) [17]. Some authors consider a decrease of VC an indicator, though a nonspecific one, of small airway involvement [18]. Mathematically, FEV1 can be partitioned as follows: FEV1 = FEV1/forced vital capacity (FVC) × FVC [19]. A decrease of FEV1 can thus be the direct consequence of the decrease of FVC (or VC) without any change in the FEV1/VC ratio. In a recent study on lung volume reduction surgery, changes in FEV1 were predominantly determined by changes in FVC rather than by changes in the FEV1/VC ratio [19]. Some asthmatic patients improve their FEV1 following bronchodilation without any change in the FEV1/VC ratio (unpubl. observations).

Our explanation is based on indirect evidence. Although airway closure was demonstrated in healthy subjects [20], this method is difficult to apply in the clinical setting. Imaging techniques (CT scan) may provide indirect evidence of gas trapping. However, we were reluctant to submit healthy as well as SAOS subjects to the risk of radiation. Although indirectly, in the absence of obesity or cardiac disease and in the presence of a normal TLC, there is no other evident explanation for our findings. The paradox lies in a reduced VC, which may be interpreted as ‘restriction’ that is responsible for the decrease of FEV1 and MEFR. In fact, the former is the consequence of the obstruction of small airways, which is the primum movens.

Certain possible limitations of this study need to be considered. By excluding subjects older than 50 as well as those with chronic lung disease, such as asthma, we probably underestimated the actual frequency of the SAOS pattern, which in our study was about 5%. Since only male subjects were selected our results cannot be automatically extrapolated to females. Because we measured TLC with the He-dilution method the lung volume may have been underestimated in the SAOS group. However, the RV/TLC ratio will be much less different than RV or TLC. Since the MEFV curves were recorded at the mouth and not by plethysmography we did not take into account the effect of gas compression. However, since in SAOS subjects trapped gas was excluded from the system, lung emptying will not be different between the two groups. An increase in RV and consequently a decrease in VC can also be produced by dynamic airflow obstruction [21, 22, 23, 24]. This is the reason why we measured slow VC instead of FVC.

In conclusion, our results suggest that a normal FEV1/VC does not exclude airway obstruction. A decrease of FEV1, provided TLC is within normal limits, reflects small airway obstruction. Although the SAOS syndrome affects only a minority of subjects, to call this pattern a ‘nonspecific finding’ or a restrictive ‘process’ is to overlook an obstructive pathology.


goto top of outline Acknowledgments

We thank Prof. K.P. Van de Woestjine for careful reading and criticism of the manuscript and Mr. C. Pahulycz for technical help.

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 goto top of outline Author Contacts

Dan Stănescu, MD, PhD
Av de la Chapelle 132
BE–1950 Kraainem (Belgium)
Tel./Fax +32 2 7207387

 goto top of outline Article Information

Received: January 29, 2004
Accepted: March 5, 2004
Number of Print Pages : 5
Number of Figures : 2, Number of Tables : 1, Number of References : 24

 goto top of outline Publication Details

Respiration (International Review of Thoracic Diseases)
Founded 1944 as ‘Schweizerische Zeitschrift für Tuberkulose und Pneumonologie’ by E. Bachmann, M. Gilbert, F. Häberlin, W. Löffler, P. Steiner and E. Uehlinger, continued 1962–1967 as ‘Medicina Thoracalis’ as of 1968 as ‘Respiration’, H. Herzog (1962–1997)
Official Journal of the European Association for Bronchology and Interventional Pulmonology

Vol. 71, No. 4, Year 2004 (Cover Date: July-August 2004)

Journal Editor: C.T. Bolliger, Cape Town
ISSN: 0025–7931 (print), 1423–0356 (Online)

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