Am. J. Respir. Crit. Care Med., Vol 153, No. 3, 03 1996, 967-975.
Inhaled bronchodilators reduce dynamic hyperinflation during exercise in patients with chronic obstructive pulmonary disease
MJ Belman, WC Botnick and JW Shin
Division of Pulmonary Medicine, Cedars Sinai Medical Center, Los Angeles, California 90048, USA.
Dynamic hyperinflation (DH) is a major pathophysiologic consequence of
airflow limitation during exercise in patients with chronic obstructive
pulmonary disease (COPD) and an important contributing factor to
breathlessness. In this study we aimed to examine the effect of inhaled
beta agonist therapy on DH during exercise in these patients and the
relationship between changes in DH and breathlessness. In 13 COPD patients
(mean age 65.1 +/- 2.0, FEV1 1.20 +/- 0.17, FEV1/FVC 40 +/- 3) we measured
pulmonary function tests, exercise breathlessness by Borg score, and
exercise flow volume and pressure volume loops on two separate days. Prior
to testing, patients randomly received inhaled placebo or albuterol on the
first test day and the alternative medication on the second test day. From
measurements of exercise inspiratory capacity (IC), we calculated the
end-expiratory and end- inspiratory lung volumes (EELV, EILV). We used
esophageal pressure recordings to measure peak inspiratory esophageal
pressure (Pesins) during exercise and this was related to the maximal
capacity for pressure generation taking into account lung volume and
airflow changes (Pcapi). Bronchodilator caused significant increase in both
FEV1 and FVC (+0.23 and +0.51, p<0.01). Comparisons of breathlessness,
exercise volumes, and pressures were made at the highest equivalent work
load. There was a significant reduction in the peak exercise EELV/TLC (80
+/- 0.02% to 76 +/- 0.02%, p<0.05) while the peak EILV/TLC decreased by
2% (97 +/- 1% to 95 +/- 1%, p<0.05). The peak Pesins/Pcapi decreased
(0.79 +/- 0.10 to 0.57 +/- 0.05, p<0.05), and the Pcapi - Pesins
increased (7.4 +/- 3 to 13.0 +/- 3 cm H2O, p<0.05). There was
significant improvement in neuroventilatory coupling for volume change
(Pesins/Pcapi/VT/TLC 5.45 +/- 0.5 to 3.25 +/- 1.0, p<0.05). There was a
significant reduction in breathlessness as measured by Borg score (4.5 +/-
0.7 to 3.1 +/- 0.5, p<0.05) and there was a significant correlation
between delta Borg and delta EILV/TLC (r=0.771, p<0.01) with a trend for
Pesins/Pcapi/VT/TLC (r=0.544, p=0.067). There was also a significant
correlation between delta EELV/TLC and delta Pesins/Pcapi/VT/TLC (r=0.772,
p<0.01). The relationships between delta Borg, delta resting volumes,
and flow rates were not significant. We conclude that in patients with
COPD, inhaled bronchodilator reduces exercise DH and improves inspiratory
pressure reserve and neuroventilatory coupling. Changes in DH and
neuroventilatory coupling were the main determinants of reduced
breathlessness.
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