• Spirometry records both FEV1 and FVC and thus FEV1/FVC, which is a measure of obstruction—PEF cannot differentiate between restrictive and obstructive impairments.
• Spirometry can be performed by patients at any level of severity of airway obstruction with similar reproducibility.
• There are well-defined normal ranges that allow for the effects of age, ethnicity and sex, against which the severity of the impairment can be calculated.
• The level of the FEV1 predicts future mortality and to the severity of breathlessness.
• The variance of repeated measurements is lower than for PEF. In COPD, the variability of the FEV1 between testing occasions is about 170mL  Hence, if values change by more than an absolute value of 200 mL, it is unlikely that the difference is due to chance.
• Serial measurements (over several years) are evidence of the rate of progression.
Against these advantages must be set the disadvantage that the equipment is significantly more expensive, and good measurement depends on having a good technician operating the spirometer .
There is one more important reason for preferring spirometry in COPD. The physiological processes causing the airflow limitation differ between COPD and asthma. This leads to an altered relationship between FEV1 and PEF. The airway narrowing of asthma is mostly from bronchospasm of major airways. During expiration in COPD, it is due to a combination of bronchospasm in larger to medium airways, small-airway narrowing and obliteration, and collapsibility of the segmental airway secondary to the loss of elastic tissue within the lungs. It is probably the latter feature that upsets the relationship. Fig. 3.1 shows the expiratory flow volume loop for a patient with severe COPD compared with that for a healthy person. The patient's FEV1 is reduced to 0.8 L or 33% of the normal example, whereas the PEF is relatively preserved at 5.7L/s (340L/min) (80% of predicted).
As normal expiration begins (point 'a'), there is a rapid increase in expiratory flow until the flow becomes limited by the airway dimensions and peak flow is reached (point 'b'). As expiration continues in the healthy subject (upper trace), flow decreases slowly and progressively until the person reaches their residual volume when flow ceases (point 'd').
Fig. 3.1 Expiratory flow volume traces from a healthy person (solid line) and someone with emphysema (dashed line). Timings refer to the elapsed time from onset of the expiratory effort.
In the COPD patient, the initial rapid rise in expiratory flow is similar, but to a lower peak (point 'b'); then, as intrathoracic pressure increases in the early part of expiration, that pressure is transmitted to the segmental airways, which have lost the elastic attachments that enable normal airways to resist compression . The airways therefore 'collapse' and obstruct the passage of air through those airways. This results in the rapid reduction in flow after the peak has been attained (point 'c'). Flow in the remainder of the expiration remains low, limited by the collapsed airways. A feature of severe COPD such as this is that airflow during tidal breathing (when the patient is generating less intrathoracic pressure) may be better than in the forced expiratory manoeuvre.
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