Abstract

The mechanism of airflow obstruction was investigated in 21 patients with tracheal stenosis using tantalung tracheograms and pulmonary function studies, including flow-volume (FV) loops. In 4 patients with severe obstructive pulmonary disease, FV loops failed to demonstrate radiographically visible tracheal stenosis. In 17 patients, both FV loops and tracheograms demonstrated central airway obstruction. In three of the 17 patients, the stenotic segment was a rigid lesion at the thoracic outlet with similar limitation of inspiratory and expiratory flow. In nine of the 17 patients, the lesion was extrathoracic (rigid in 6 patients and pliable in 3). The 3 pliable extrathoracic lesions produced marked limitation of inspiratory flow but normal expiratory flow. Three rigid extrathoracic lesions produced inspiratory flow that was more limited than expiratory flow, suggesting dynamic inspiratory compression of the normal extrathoracic trachea. The one rigid intrathoracic lesion caused expiratory flow limitation greater than inspiratory flow limitation, suggesting dynamic compression of the intrathoracic trachea on expiration. The position of the obstructing lesion and dynamic compression of the normal, compliant trachea may be the major determinants of the difference in flow limitation between expiration and inspiration in some patients.

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