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Contrary to Dr Pearson's assertion in his reply in the May 1999 issue of Thorax, spirometry and forced expiratory volume in one second (FEV1) are not yet here to stay in general practice.1 The evidence is just not good enough.
We were concerned by the inaccuracies in his letter which simply serve to underline our unease with the chronic obstructive pulmonary disease (COPD) guidelines. We will come to these later but, firstly, how is FEV1 related to peak expiratory flow rate (PEFR) in patients with COPD? Is FEV1 really essential in the day to day management of COPD?
Spirometry is central to the accurate diagnosis of COPD in many patients. The ratio of FEV1 to FVC is indispensable in differentiating restrictive from obstructive patterns of respiratory breathlessness. But does FEV1 on its own offer additional information about COPD which is not available with PEFR? FEV1 represents the volume of air expired during the first second of forced expiration whereas PEFR represents the maximal flow rate (usually attained in the first 100 milliseconds). Both are derived from the flow rate, but the nub of the argument is what happens after peak flow is reached. Pearson suggests that one needs to go, not to epidemiology, but to physiology to understand this issue. He suggests that, in patients with COPD, flow rate falls dramatically after peak expiratory flow is reached which is certainly the case in the diagram (albeit mislabelled) which he presents. However, his flow-volume trace differs considerably from the flow-volume curves produced by many other researchers and it is precisely the lack of sound epidemiological evidence to support his argument which makes his conclusions seem unsafe.2 3 Patients with obstructive airway disease demonstrate some degree of airway collapse during forced expiration which is partly explained by the loss of elastic support of alveoli and respiratory bronchioles. In fact, the pattern of the flow-volume curve can be almost identical for asthma and COPD and this supports the close correlation observed between FEV1 and PEFR.4When the absolute values of FEV1 and PEFR are compared, the correlation is high (r = 0.78–0.95).5 Little work has been done on the correlation between PEFR and FEV1 for FEV1 values of less than one litre. It is conceivable that the strength of correlation will be reduced at low levels of FEV1 or PEFR. But what is the significance of this possibility? Symptoms and signs rather than FEV1 guide the management of COPD in the majority of cases. We have little treatment to offer at present to patients with advanced COPD.
While spirometry offers a significant advantage to primary care physicians and nurses in the diagnosis of COPD, it is unlikely to have a role in the day to day management of this disease. The provision of spirometry in primary care would have significant financial and organisational implications which cannot be justified on current evidence. On this basis, open access to lung function laboratories seems preferable to a primary care based service. Spirometry in primary care risks inaccuracy from unsound operator techniques due to infrequent use and potential failure to calibrate an electronic spirometer regularly.
Finally, a brief word about Dr Pearson's reply to our letter. We were disappointed that he accused us of misquoting from Kelly and Gibson.6 Dr Pearson is simply wrong in stating that there were 10 subjects with COPD. Kelly and Gibson mentioned eight patients (with a positive steroid trial and therefore presumably not COPD), and in these the correlation coefficient between individual FEV1 and PEFR values remained between 0.68 and 0.98. We were also surprised that he criticised the quotation of the paper by Richie from the Lancet on the basis of the date of publication.7 This has surely nothing to do with the validity of the data. Furthermore, Lebowitz's observation that the FEV1 and PEFR show close correlation in healthy individuals emphasises the reliability and reproducibility of PEFR.8
There is no evidence that FEV1 is more reproducible on a single occasion than PEFR. The papers by Maloet al and Verschelden et al relate to home recordings and hardly seem relevant to this issue. We refer Dr Pearson to another paper by Malo in which he showed that FEV1 is similar to PEFR in terms of non-valid recordings.9 Finally, FEV1 has not been shown to be superior to PEFR as a prognostic tool and, in fact, the evidence suggests that PEFR may be useful in this respect.10 11
The basis for using spirometry rather than peak flow in the day to day management of COPD demands a more rigorous approach than is evident from either the COPD guidelines or Dr Pearson's reply to our letter. The issue is far from resolved and current evidence is an inadequate basis on which to recommend the widespread practice of spirometric testing in primary care.
author's reply Drs White and Nolan agree that spirometry is essential for the diagnosis of COPD and, on this basis alone, I would stand by the recommendation of the guidelines that GPs need to have access to spirometry. The COPD guidelines1-1 set out three options: GP owned spirometers, a mobile service visiting practices intermittently, or open access services at hospital. Whichever option is preferred locally, the spirometric tests must be performed by trained staff to ensure adequate quality control. Single measures of peak expiratory flow (PEF) are not adequate. It is colleagues in primary care who have encouraged those involved in guidelines to believe that most GPs would prefer to have access to a spirometer in their practice. The BTS COPD consortium has been promoting spirometry for the diagnosis of COPD since, without a correct diagnosis, the chance of accurate treatment is low.1-2 How the service is provided is a matter of local choice, not for national dictat.
With regard to the day to day management of COPD after the diagnosis has been objectively made, Drs White and Nolan are concerned that spirometry may be unnecessary. In fact, no-one is recommending frequent regular spirometric testing. Serial measurements of FEV1can and do provide evidence of progression over the years, but cannot detect changes over periods of less than a few years with any degree of confidence because the rate of decline is small relative to the coefficient of variability for the measurement. Since PEF is even more variable, it is of even less value as a short term outcome measure, except in those with an asthmatic element where large changes may be apparent within days. The assessments of bronchodilator drug outcome in clinical COPD practice are therefore based on subjective responses. Research studies employ more objective health status measures.
I do not wish to get into an argument about the relative merits of PEF and FEV1 which could fill many pages. We will continue to disagree on many of their points. I will confine myself to two issues.
Anyone who measures PEF and spirometry on a regular basis will recognise that PEF is a much more limited and more variable measure.1-3 The issue has probably been considered too obvious to justify formal studies. It is important to be careful, when looking at such comparator data as do exist, to ensure the correct method of statistical analysis has been performed. Bland and Altman set out the reasoning clearly,1-4 and their arguments are particularly relevant to the use of correlation coefficients to relate PEF and FEV1. For two measures that are dependent on the same predictors (age, sex and height), there will always be a linear regression correlation present as long as patients of different age, sex, and height are included.
Secondly, the use of PEF in asthma is of greatest value when recorded as serial measurements several times per day. The repeated measures compensate for the high variability of individual readings and provide data on symptomatic episodes outwith the clinic and on large changes of airway size that are typical of asthma. Serial PEF is less helpful in COPD with its reduced natural variability of airway dimensions. The second paper by Malo compared home spirometry with home PEF and noted poor compliance for both. The comparison that would be relevant is with supervised spirometry recorded by trained staff, which is why the guidelines emphasise the need for staff training.
Finally, I am heartened by data presented at the recent British Thoracic Society meeting in which spirometry was used in primary care as a screening tool in a research project.1-5 It offered spirometry to all adults over 45 attending the surgery (smokers and non-smokers) and detected 6% of those studied as having undiagnosed but symptomatic COPD, a high yield of treatable disease from an inexpensive programme. Other primary care studies are in progress. I remain of the view that, in time, all GPs will have easy access to spirometry and be able to interpret the results as efficiently as they presently measure and manage blood pressure or blood sugar.
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