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The association between emphysema and weight loss is well known. Severe α1-antitrypsin deficiency is an important risk factor for the development of emphysema.

Pulmonary embolism (PE) leads to an abnormal alveolar deadspace that is expired in synchrony with gas from normally perfused alveoli. This feature of PE separates it from pulmonary diseases affecting the airways, which are characterized by nonsynchronous emptying of compartments with an uneven ventilation/perfusion relationship. An analysis of the single breath test (SBT) for CO2, SBT-CO2, focusing on the late tidal expirate, was made in order to evaluate the feasibility to use the SBT-CO2for the diagnosis of PE. The test was evaluated in 38 patients with suspected PE where pulmonary angiography showed that nine had PE and 29 did not. It was also tested in a reference population consisting of patients with normal lung function, obstructive lung disease and interstitial lung disease. Previously suggested gas exchange measurements for the diagnosis of PE, ie, the physiologic deadspace fraction, VDphys/VT, and the arterial-to-end-tidal CO2gradient, P(a-E')CO2, were also evaluated in the groups. SBT-CO, achieved a nearly complete separation between the patients with PE and those without. The other measurements, however, showed a substantial overlap between patients with PE and those with obstructive or interstitial lung disease. The SBT-CO2is simple and potentially widely available and warrants further study as a routine technique for the diagnosis of PE. (Chest 1989; 96:357–62)

We examined the relationship between pulmonary density, measured with computerized tomography, and pulmonary mechanics (static pulmonary volume; pulmonary resistance) in 39 normal subjects (20 nonsmokers and 19 smokers). Pulmonary density decreased with increasing static elastic recoil pressure, and smokers consistently showed higher pulmonary density than nonsmokers. Pulmonary density, measured at full inspiration, correlated inversely with total lung capacity. Pulmonary density showed a ventrodorsal gradient, which was greater at low elastic recoil pressure than at high recoil pressure. The study shows that pulmonary density is related to the mechanical properties of the lung in normal subjects. Increased pulmonary density appears to be a sensitive indicator of pulmonary damage induced by smoking. Further studies of the relationship between pulmonary density and pulmonary mechanics in disease seem warranted.

To clarify how lung function at exercise is affected in sarcoidosis, and to analyze how exercise studies compare to esting measurements, 63 patients with pulmonary sarcoidosis were examined with lung mechanics and arterial blood gases during exercise. These findings were compared with simultaneously obtained, but previously reported results of the static lung pressure/volume curve and the lung resistance/static lung pressure curve. While mechanical variables at maximal exercise were as sensitive as those determined by measuring the PstL/V and RL/PstL curves, mechanics during spontaneous breathing at rest was less sensitive. The derangement of mechanics was more evident than that of arterial blood gases. No measurement at rest was a good predictor of working capacity or of arterial PaOs. A comprehensive exercise examination may be an alternative to resting investigations, which are either more elaborate or less sensitive. (Chest 1991; 99:572–78)

The clinical effect of inhaled radio-labeled (Technetium-99m diethylenetriamine-pentaacetic acid) methacholine was studied in two separate experiments performed in eight symptom-free asthmatics with bronchial hyperresponsiveness. Aerosols were formed by two different nebulizers, producing either mainly small aerosol particles (2-μm mass median aerodynamic diameter [MMAD]) for peripheral, or mainly large aerosol particles (9-μm MMAD) for large airway deposition. The intended site of deposition was confirmed by gamma camera recordings. Changes in specific airway conductance (sGaw) were set as an index of central airway constriction, and functional alterations in the gas exchanging parts of the lung were estimated by multiple inert gas elimination technique (MIGET) and arterial blood gas analyses. The main finding was that the responses, as measured by the changes in arterial blood gases and by MIGET, were similar in the two experiments, while the fall in sGaw was significantly larger after deposition in the main bronchi than in the peripheral airways (p<0.05). The time courses of the abnormalities in the gas exchanging elements were much longer than those of the responses of the central airways, and the abnormalities were recorded still at the end of the experiment 2 h after challenge in most patients. A discrepancy in dose dependency and time courses suggests differences in mechanism and/or dynamics of the responses exerted by the various target organs. Interaction in the process of clearance from the lung of inhaled methacholine by the bronchial circulation may have contributed to the observed discrepancies.

We measured lung density by means of x-ray computed tomography and lung mechanics in 33 workers exposed to asbestos cement and in 39 normal subjects. The exposed group showed evidence of lung fibrosis with reduced static lung volumes and lung compliance, although only three subjects had signs of interstitial fibrosis at standard chest radiography. Lung density was significantly increased in the exposed workers compared to control subjects, with greater differences between nonsmokers than between smokers. Lung density correlated inversely with static lung volumes. There was no appreciable difference in the regional distribution of lung density between exposed workers and control subjects. We conclude that lung density is often increased in workers with mild asbestosis, even in the presence of a normal chest radiograph. Measurement of lung density may be of value in the evaluation of asbestos-exposed workers for assessment of the extent of parenchymal disease.

The purpose of the study was to investigate whether a constant submaximal exercise challenge affected the plasma pharmacokinetics of an inhaled ß2-adrenoceptor agonist, terbutaline sulfate. Eight healthy nonsmokers participated in a study comprising measurements of plasma concentrations of terbutaline on two separate study days. Plasma samples were frequently collected at rest during study day 1, and on the second study day, during and after a 30-min exercise challenge, which was performed immediately after inhalation of the drug. The rate of increase of plasma concentrations and the maximal plasma concentrations were higher during exercise than during rest (p<0.01 and p<0.05, respectively). The plasma concentration fell rapidly after cessation of the exercise and approached those obtained at rest. We suggest that increased pulmonary and/or bronchial blood flow and altered surface tension of the liquid lining of the air space may contribute to the enhancement of absorption of this hydrophilic compound during exercise. Based on the levels of the maximal plasma concentrations reached during exercise in this study, the results would be to increase the frequency of administration of the drug, rather than to increase the administered doses, if the aim is to prevent or ameliorate exercise-induced asthma and potential systemic side effects.