ABSTRACT
Several different definitions have been proposed by the various guidelines and several of these are shown in Table 34.2. No specific ATS definition is given here, as until recently this was based on the non-proportional Venn diagram developed by Snider to cope with the differential contributions of the underlying pathology to the individual COPD patient. The problems of defining COPD are dealt with in Chapter 1 but one further aspect should be stressed here. The definition selected by all guidelines leans towards terms that can be applied practically. Hence the emphasis on airflow obstruction (reduced FEV1/FVC or, in the ERS version, slow forced emptying of the lungs) and lack of spontaneous variability (largely fixed in the BTS definition, not fully reversible in GOLD). Most definitions stress the progressive nature of the symptoms and physiological change and GOLD emphasizes the key role of inhaled insults as a pathogenic mechanism. Based on these approaches clinicians should be able to identify a patient with COPD and apply an appropriate management strategy. However, these definitions focus on the clinicophysiological outcomes of the processes that are occurring within the lower respiratory tract of the COPD patient. They are not the ideal way of identifying patients when a specific mechanism is to be studied, for example regulation of vascular endothelial growth factor (VEGF) in the pulmonary endothelium as a mechanism promoting apoptosis in emphysema.6 They also do not account for the heterogeneity of the disease. Clearly, not all patients who meet the clinical definitions have a significant degree of emphysema. Thus studies of this mechanism or indeed of agents to promote alveolar regeneration would not necessarily be appropriate in a clinically defined COPD population. We are still ignorant of the role of individual pathologic phenotypes in the natural history of COPD, but the development of these mechanistic studies, together with the availability of quantitative CT scanning (see Chapter 21), may provide the necessary stimulus to initiate these longer-term investigations. Until such data are available, the definition of COPD will remain a compromise equivalent to that of ‘cardiac failure’ but without the specificity that allows us to subclassify cardiac dysfunction into systolic and diastolic or determine even more basic causes of
the problem such as valvular abnormalities. Clearly, there is much work to be done in this area of COPD research.
