Paul P Walker

University of Liverpool, Liverpool, England, United Kingdom

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Publications (7)17.05 Total impact

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    ABSTRACT: The change in forced expiratory volume in 1 s (FEV1) after administration of a short-acting bronchodilator has been widely used to identify patients with chronic obstructive pulmonary disease (COPD) who have a potentially different disease course and response to treatment. Despite the apparent simplicity of the test, it is difficult to interpret or rely on. Test performance is affected by the day of testing, the severity of baseline lung-function impairment, and the number of drugs given to test. Recent data suggest that the response to bronchodilators is not enhanced in patients with COPD and does not predict clinical outcomes. In this Review we will discuss the insight that studies of bronchodilator reversibility have provided into the nature of the COPD, and how the abnormal physiology seen in patients with this disorder can be interpreted.
    09/2013; 1(7):564-73. DOI:10.1016/S2213-2600(13)70086-9
  • American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans; 05/2010
  • American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans; 05/2010
  • American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans; 05/2010
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    ABSTRACT: The non-specific bronchial hyper-responsiveness reported in mild to moderate COPD is usually attributed to reduced airway calibre accentuating the effect of airway smooth muscle shortening. We hypothesized that in more severe COPD the fall in forced expiratory volume in 1 second (FEV(1)) seen during methacholine challenge would result from an increase in residual volume and decrease in vital capacity rather than an increase in airways resistance. Twenty-five subjects with moderate to severe COPD and 10 asthmatic subjects had spirometry and oscillatory mechanics measured before methacholine challenge and at a 20% fall from baseline post challenge (PC(20)FEV(1)). In the COPD subjects median PC(20) was 0.35mg/mL. Comparing baseline to PC(20) there were significant falls in forced vital capacity (FVC) (2.91 vs. 2.2L; p<0.001), slow vital capacity (3.22 vs. 2.58L; p<0.001) and IC (2.21 vs. 1.75L; p<0.001) without change in FEV(1)/FVC ratio (0.52 vs. 0.52; not significant) or in total lung capacity where this was measured. Total respiratory system resistance (R(5)) was unchanged (0.66 vs. 0.68; not significant) but total respiratory system reactance decreased significantly (-0.33 vs. -0.44; p<0.001). In contrast, the asthmatics became more obstructed and showed a proportionally smaller fall in lung volume with increase in R(5) (0.43 vs. 0.64; p<0.01). In moderate to severe COPD the fall in FEV(1) with methacholine is mainly due to increases in residual volume, which may represent airway closure and new-onset expiratory flow limitation.
    Respiratory medicine 12/2008; 103(4):535-41. DOI:10.1016/j.rmed.2008.11.002 · 2.33 Impact Factor
  • Paul P Walker, Peter M A Calverley
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    ABSTRACT: A significant proportion of patients with COPD show post-bronchodilator improvement in lung volume even though this response is rarely considered when classifying subjects as having reversible or irreversible airway disease. We studied 266 patients with a clinical and physiological diagnosis of COPD who underwent pulmonary function testing and had their spirometric response to 5 mg salbutamol assessed. After the bronchodilator 125 (47%) patients increased their forced vital capacity by more than the known variability of the test while 60 (23%) showed only a volume response without improvement in expiratory flow. These 'volume responders' had greater degrees of airflow obstruction-lower FEV(1) (p < 0.001) and FEV(1)/FVC (p < 0.05)-and a higher residual volume at rest (p = 0.005) with similar degrees of emphysema measured by K(CO). Subjects with evidence of greater dynamic airway collapse, assessed by the ratio of early to mid expiratory flow, were less likely to have a flow response but more likely to have a volume response after salbutamol (p < 0.005). This would be compatible with volume response being commoner in patients who exhibit tidal expiratory flow limitation. We suggest that post-bronchodilator absolute change in FVC provides important additional physiological information when interpreting bronchodilator reversibility testing.
    COPD Journal of Chronic Obstructive Pulmonary Disease 07/2008; 5(3):147-52. DOI:10.1080/15412550802092928 · 2.73 Impact Factor
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    ABSTRACT: Exacerbation of chronic obstructive pulmonary disease commonly causes hospitalization. The change in lung mechanics during exacerbation and its relationship to symptoms in spontaneously breathing individuals has not been described. We hypothesized that changes in both airflow and lung volumes would occur during an exacerbation, but that only volume change would relate to symptomatic improvement. Lung mechanics and resting dyspnea were recorded in 22 hospitalized patients during recovery from exacerbation. Spirometry, inspiratory capacity, respiratory system resistance and reactance, tidal breathing patterns, and expiratory flow limitation were recorded after nebulized bronchodilator therapy on the first 3 d after admission, at discharge, and 6 wk postadmission (Day 42). Prebronchodilator measurements were taken on Day 2, at discharge, and on Day 42. Postbronchodilator inspiratory capacity increased 0.23 +/- 0.07 L by discharge and 0.42 +/- 0.1 L by Day 42, FEV1 rose 0.09 +/- 0.04 and 0.2 +/- 0.05 L at discharge and Day 42, respectively, and FVC increased 0.21 +/- 0.08 and 0.47 +/- 0.09 L at discharge and Day 42 (all p < 0.05). Consistent reduction in dyspnea was seen as the exacerbation resolved. Respiratory system resistance, FEV1/FVC, and expiratory flow limitation were unchanged throughout, indicating that changes in lung volume rather than airflow resistance predominated. Improvement in operating lung volumes is the principal change seen as a chronic obstructive pulmonary disease exacerbation resolves and increase in inspiratory capacity is a useful guide to a reduction in dyspnea.
    American Journal of Respiratory and Critical Care Medicine 12/2005; 172(12):1510-6. DOI:10.1164/rccm.200504-595OC · 11.99 Impact Factor

Publication Stats

118 Citations
17.05 Total Impact Points


  • 2008
    • University of Liverpool
      • Department of Clinical Sciences
      Liverpool, England, United Kingdom
  • 2005
    • Aintree University Hospital NHS Foundation Trust
      Liverpool, England, United Kingdom