Physiological Factors Affecting Airway Resistance in Normal Subjects and in Patients With Obstructive Respiratory Disease*

Abstract

Although the airway conductance1 increases at larger lung volumes in normal subjects (1), it is reduced in patients with asthma or emphysema who are breathing with a large functional residual capacity (FRC) (2). We have therefore tried to assess the influence of other factors which might affect the airway conductance in both normal subjects and in patients with asthma, bronchitis and emphysema. These include the interrelationship of lung volume, lung elastic pressure and airway conductance, the effect of exercise, forced breathing and normal aging, and the composition of the respired gas and bronchomotor drugs. We investigated the balance of forces regulating the diameter of the airway lumen, i.e., the tone of the airway wall, directed inward, opposed by the traction of the lung tissues, directed outward. We studied whether, in normal subjects, this balance was altered by bronchmotor drugs or by a change in lung elastic pressure following chest strapping, and whether in patients with asthma, the airway conductance/lung volume relationship was altered after forced breathing or exercise. Patterns of disturbance leading to air trapping § Established Investigator of the American Heart Association.1 Airway conductance, the reciprocal of airway resistance, is defined as the rate of airflow at the mouth for unit pressure difference between alveolus and mouth. It was measured over the range of 0 to 0.5 L per second of inspiratory airflow.were studied in patients who had emphysema or bronchitis of toxic etiology. METHODSAirway resistance and thoracic gas volume were measured during panting2 using an upright body plethysmograph (2). The methods hinge on Boyle's law for compression of gases. Volume change owing to compression of gas inside the thorax is measured by -the equal and opposite small displacement of gas around the body. After appropriate calibrations, the intrathoracic gas volume changes found when rebreathing the air of the chamber through a heated flowmeter are converted mathematically to alveolar pressure changes, thence to airway resistance and airway conductance; or, when breathing against a closed shutter and manometer, to thoracic gas volume. In practice, these values are read directly from a precalibrated scale and protractor on the face of an oscilloscope, thus reducing labor. Esophageal pressure and mouth pressures were measured alternately using a capacitance manometer and Brush recorder. Lung elastic pressure (3) at each lung volume was measured as mean esophageal pressure, while panting (4). Chest constriction was accomplished by binding the subj ect's chest or abdomen, in the expiratory position, with adhesive tape or a long strip of rubber (4). Other tests of pulmonary function were performed according to generally accepted methods. All measurements were made with the subj ect in the sitting position. Lung volumes are expressed at BTPS. RESULTS ON HEALTHY SUBJECTSSpontaneous variation of airway resistance with time. The airway resistance of six healthy subjects was studied at 20 minute intervals o...

Acute effects of inhaled isoproterenol on the mechanical characteristics of the lungs in normal man

“…On theoretical grounds, however, it is possible to visualize situations where changes in maximum expiratory flow occur without there being a change in airways resistance measured in the body plethysmograph, or conversely, where changes in resistance do not result in a change in maximum expiratory flow. A striking example of this type of discrepancy has been observed in normal subjects after the inhalation of isoproterenol, in whom it has been shown that, despite a considerable fall in airway resistance and rise in anatomical dead space (1)(2)(3)(4), there is very little change in the FEV1 (4). In the present study we have examined in detail the alterations in pulmonary mechanics that occur in normal subjects after isoproterenot in an effort to determine the causes of this particularpattern of change.…”

Dr. Henderson, et al reply

“…However, we suggest that the physiology described is unlikely to be the major determinant of the SLS phenotype. As Dr. Eberlein notes, impairment of compliance by chest strapping is quickly reversed -a few deep breaths are sufficient to restore normal compliance measures 3,4 . This was not the case with our patients with SLS, in whom compliance remained low through the course of pulmonary testing that included maximal respiratory efforts.…”

Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma

“…The static conditions under which the interdependence was assessed by NOBLE et al [289] do not represent the real environfment of the lung [297]. The viscoelastic lung parenchyma under dynamic conditions interacts with the airways very differently [298,299], and this should be kept in mind if the experiments of NOBLE et al [289] are revisited.…”