Air trapping and cardiopulmonary exercise testing in patients with mild to moderate bronchial obstruction: clinical role of trapped gas measurements.

UNLABELLED: In 14 patients with obstructive airways disease (7 atopic asthmatics, 7 COPD pts with stable disease, FEV1 < 65% pred., 11 m, 3 f, age 50.9 +/- 17.2 y) the effect of a beta mimetic agent on physical performance was studied. PROTOCOL: Inhalation of 2.5 ml normal saline (P) or salbutamol 0.1% (S) in double-blind random order on 2 successive days. Spirometry, body-plethysmography, single-breath helium dilution at rest. Spiroergometry with incremental workload to tolerance. The volume of trapped gas (D) was derived from: TLC Body-TLC Helium Single Breath. RESULTS: Base line values revealed mild to moderate airways obstruction (FEV1 2.04 +/- 0.81 L, FEV1/VC 60.2 +/- 8.5%). Subsequent to inhaling S FEV1 increased significant by 20% to 2.38 +/- 0.87 L. There was a concomitant substantial improvement of VC (3.37 +/- 1.09 L to 3.60 +/- 0.93 L). Rs declined sign. (2.37 +/- 1.43 to 1.69 +/- 0.8 kPa*s), and so did D (1.15 +/- 0.73 L to 0.55 +/- 0.89 L = -20% from base line). Despite clear-cut bronchodilation exercise performance did not improve in response to S (114.6 +/- 49.3 vs 112.5 +/- 50.0 Watt max, ns). Base line max. VO2 (19.78 +/- 6.36 ml/min/kg) and VO2 at anaerobic threshold (13.29 +/- 3.21 ml/min/kg) suggested only minimal impairment of physical performance. S induced a small but significant decrease in max. VO2 (19.78 +/- 6.36 to 18.43 +/- 6.27 ml/min/kg, p < 0.025). Gas exchange (derived from AaDO2) was impaired at rest (30.18 +/- 10.4 mmHg) and during exercise (28.07 +/- 13.03 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

Reversible volume changes of trapped gas in nonspecific bronchoprovocation tests.

Thirty patients with a history of asthma and ten patients with suspected bronchial hyperreactivity underwent nonspecific provocation testing. The control group consisted of ten normal volunteers without a history of lung disease. The patients' baseline FEV1 (percent predicted) revealed mild obstructive disease (72.9 +/- 8.9 percent and 74.6 +/- 7.7 percent) compared with controls (87.2 +/- 8.5 percent, p less than 0.001). The mean volume of trapped gas (D) (ie, TLCB-TLCHe) was not significantly different between groups (0.11 +/- 0.49 L vs 0.15 +/- 0.4 L vs 0.18 +/- 0.45 L), and no correlation was established with any of the remaining lung function data. Bronchial hyperreactivity in response to inhaling acetylcholine could be observed in the asthma group only. Their mean D increased significantly from 0.11 +/- 0.49 L to 0.62 +/- 0.66 L (p less than 0.001), and returned to baseline (0.26 +/- 0.55, NS) subsequent to inhaling salbutamol. D changes induced by acetylcholine correlated weakly with concurrent changes of FEV1 (r = -0.44, p = 0.01), RV (r = 0.59, p less than 0.001), and Rs (r = 0.59, p less than 0.001). In response to bronchodilating doses of salbutamol, however, D was changed in close correlation with FEV1 (r = -0.82, p less than 0.0001), RV (r = 0.85, p less than 0.0001), and Rs (r = 0.76, p less than 0.0001). Provided that D is a valid parameter of small airways function, these data may give a clue to the site of action of both drugs. Acetylcholine affects small and large airways alike with no clear-cut preference, whereas salbutamol's predominant target appears to be the small airways. These conclusions are only partially supported by the pertinent literature.