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The purpose of this study was to assess whether expiratory flow limitation (FL), as measured by applying negative pressure at the mouth during tidal expiration, is a better predictor of dyspnea than routine spirometry measurements. The study population consisted of 117 ambulatory patients with COPD. Dyspnea was assessed according to the ATS-DLD respiratory Questionnaire. Expiratory flow limitation was measured in supine and sitting positions, and expressed as a percentage of the expired control tidal volume affected by flow limitation (FL, % VT). Using Spearman's rank correlation (rs), we found that the correlation of dyspnea scale with FL was stronger (rs > 0.5) than with FVC (rs < -0.3) or FEV1 (rs < -0.4) in both positions. In a multiple regression analysis FL remained the best predictor of dyspnea scale even after adjustment for FEV1 (% pred). Finally, FL was almost as sensitive as FEV1 (% pred) but much more specific in assessing the severity of dyspnea scale. These findings suggest that expiratory flow limitation as measured by the negative expiratory pressure technique may be more useful in the evaluation of dyspnea in patients with COPD than spirometry measurements.

The increase in morbidity and mortality attributable to chronic obstructive pulmonary disease (COPD) has focused attention on environmental and host factors causally associated with the clinical entities included under the rubric of this term with a view to early preventive intervention. Despite the biologic plausibility of inhaled agents being causally implicated, only the role of tobacco smoke has been accepted beyond doubt. However, evidence implicating occupational exposures has accumulated, in particular over the last 2 yr, from: (1) community-based studies (in which larger study populations provide greater power than the usually smaller workforce based studies); (2) longitudinal studies of lung function (which enhance the signal of interest, namely the effects of the occupational exposures, and diminish the noise due to between-individual differences); (3) pathology studies (in which the outcome of interest is the quantitative measurement of emphysema), and (4) cohort mortality studies of all or specific causes of death. This evidence, reviewed here according to accepted criteria for establishing causality, leaves little doubt that occupational exposure to dust and/or to dust and fumes may be causally implicated in the genesis of COPD. As with tobacco exposure, both bronchitis (mucus hypersecretion) and airflow limitation are recognized as causally related to exposure, but not necessarily to each other. As with tobacco exposure, though effects are in general dose related to exposure, there is evidence for individual susceptibility. As with tobacco exposure, a possible host factor is the reactivity of airways to inhaled materials.(ABSTRACT TRUNCATED AT 250 WORDS)

Summary. Five women and three men, all obese and weighing 95 to 140 kg, were studied by routine pulmonary function tests and by a radioactive xenon technique, while seated upright at rest, to measure the regional ventilation and perfusion distribution in the lung.In four subjects in whom the expiratory reserve volume averaged 49% of predicted normal, the ventilation distribution as measured with 133xenon was normal. In the remaining four subjects, in whom the expiratory reserve volume was reduced to less than 0.4 L and averaged only 21% of predicted values, the distribution of a normal tidal breath was predominantly to the upper zones.In all subjects the perfusion distribution was predominantly to the lower lung zones but was slightly more uniform than in normal nonobese subjects. During tidal-volume breathing, therefore, in four subjects the ventilation and perfusion distribution was substantially normal, whereas in the remaining four perfusion was maximal in the lower zones, to which ventilation was significantly reduced.These findings show that there may be significant ventilation/perfusion abnormality on a regional basis in obese subjects, this abnormality bearing a close relationship to the reduction in expiratory reserve volume, a finding predictable from recently published data on normal nonobese subjects (1). The abnormalities of ventilation/perfusion relationships that were demonstrated in four of the eight obese subjects could cause a reduction in arterial oxygen tension during resting tidal ventilation. IntroductionThe term "Pickwickian syndrome" was introduced by Burwell, Robin, Whaley, and Bickelmann (2) to describe a patient with alveolar hypoventilation, polycythemia, and right heart failure. As the patient lost weight, his pulmonary and

The detrimental effects of smoking on lung function have been recognized for several decades. Evidence comes from cross-sectional studies which emphasize that damage, certainly at the level of the small airways, may be detectable after a relatively short smoking history, and from longitudinal studies which show that smoking is associated with an increased rate of function loss over time. Implicit in most published evaluations of the evidence has been the concept that smoking is a habit taken up at random by the general population, and that those who do and do not take up the habit start out with similar levels of lung function. Published material was reviewed for evidence to the contrary, consistent with a health selection process similar to that shown in relation to workplace exposures and labeled the ‘healthy worker’ effect. Despite the wealth of published data on the topic of lung function in relation to the smoking habit, much is presented in a way which does not permit the concept of the ‘healthy smoker’ to be addressed. Nevertheless, this review revealed sufficient evidence from cross-sectional studies, as well as evidence from one longitudinal study to support the concept of the ‘healthy smoker’ as an individual who takes up the habit because his/her lungs are relatively resistant to the effects of smoking. If correct, this means that previous studies, particularly those which were cross-sectional in design and focussed on younger persons, are likely to have underestimated the consequences of smoking on lung function. The concept of the ‘healthy smoker’ may also throw light on characteristics which identify the ‘susceptible smoker’

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The relationships of lung functions to maximal respiratory pressure relative to the role of other recognized determinants (height, weight, age, and smoking status) were examined in 924 healthy Caucasian urban residents, 369 males 15 to 35 yr of age and 555 females 13 to 35 yr of age. In subjects no longer thought to be growing in stature, height was the main determinant of most functions. After height, respiratory pressures were the main determinant of forced vital capacity (FVC), forced expiratory volume in one second (FEV), and peak flow in men and women, with weight also an important determinant in women. Age had no consistent effect, and, although functions in smokers were lower than in nonsmokers for several tests, the effects were only significant for FEV and forced expiratory flow during the middle half of the FVC in women. These findings indicate that, if required, between-subject variation in this age group can be reduced by taking into account the relatively simple measurement of maximal inspiratory and expiratory pressures.

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