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1 Department of Human Anatomy and Physiology, University College, Dublin 2, Ireland; 2 Department of Cardiopulmonary Medicine, Charing Cross and Westminster Medical School, London W6 8RP, United Kingdom; and 3 Division of Pulmonary and Critical Care Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215
Multiple factors may contribute to the dyspnea
associated with restrictive ventilatory disease (RVD).
Simple models that examine specific features of this problem are likely
to provide insight into the mechanisms. Previous models of RVD
utilizing elastic loads may not represent completely the impact on
pulmonary and chest wall receptors derived from breathing at low
thoracic volumes. The purpose of this study was to
investigate the sensory consequences of breathing at low lung volumes
induced by external thoracic restriction in an attempt to further
elucidate the etiology of dyspnea in this setting. Ten men were
studied, with and without an inelastic corset applied at residual
volume (restriction resulted in mean reductions in vital capacity,
functional residual capacity, residual volume, and forced expired
volume in 1 s of 44, 31, 12.5, and 42%, respectively). During 10-min
steady-state exercise tests (at a workload set to achieve ~65%
maximum heart rate), restriction resulted in significant increases,
compared with control, in minute ventilation (61 vs. 49 l/min),
respiratory frequency (43 vs. 23 breaths/min), and visual analog scale
measurements of respiratory discomfort (65 vs. 20 mm). Alveolar
hyperventilation (end-tidal PCO2 = 39 vs. 44 Torr for control) and mild
O2 desaturation (arterial blood
O2 saturation = 93 vs. 95% for
control) occurred. Hypoxemia, atelectasis, increased work and effort of
breathing, or a decrease in the volume-related feedback from chest wall
and/or lungs could be responsible for the increased dyspnea
reported. External thoracic restriction provides a useful model to
study mechanisms of dyspnea in RVD.
restrictive disease; mechanisms
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