Breathing at low lung volumes and chest strapping: a comparison of lung mechanics

1981 ◽  
Vol 50 (3) ◽  
pp. 650-657 ◽  
Author(s):  
N. J. Douglas ◽  
G. B. Drummond ◽  
M. F. Sudlow

In six normal subjects forced expiratory flow rates increased progressively with increasing degrees of chest strapping. In nine normal subjects forced expiratory flow rates increased with the time spent breathing with expiratory reserve volume 0.5 liters above residual volume, the increase being significant by 30 s (P less than 0.01), and flow rates were still increasing at 2 min, the longest time the subjects could breathe at this lung volume. The increase in flow after low lung volume breathing (LLVB) was similar to that produced by strapping. The effect of LLVB was diminished by the inhalation of the atropinelike drug ipratropium. Quasistatic recoil pressures were higher following strapping and LLVB than on partial or maximal expiration, but the rise in recoil pressure was insufficient to account for all the observed increased in maximum flow. We suggest that the effects of chest strapping are due to LLVB and that both cause bronchodilatation.

1985 ◽  
Vol 59 (6) ◽  
pp. 1879-1885 ◽  
Author(s):  
W. S. Beckett ◽  
W. F. McDonnell ◽  
D. H. Horstman ◽  
D. E. House

We conducted an ozone (O3) exposure study using atropine, a muscarinic receptor blocker, to determine the role of the parasympathetic nervous system in the acute response to O3. Eight normal subjects with predetermined O3 responsiveness were randomly assigned an order for four experimental exposures. For each exposure a subject inhaled either buffered saline or atropine aerosol followed by exposure either to clean air or 0.4 ppm O3. Measurements of lung mechanics, ventilatory response to exercise, and symptoms were obtained before and after exposure. O3 exposure alone resulted in significant changes in specific airway resistance, forced vital capacity (FVC), forced expiratory flow rates, tidal volume (VT), and respiratory rate (f). Atropine pretreatment prevented the significant increase in airway resistance with O3 exposure and partially blocked the decrease in forced expiratory flow rates but did not prevent a significant fall in FVC, changes in f and VT, or the frequency of reported respiratory symptoms after O3. These results suggest that the increase in pulmonary resistance during O3 exposure is mediated by a parasympathetic mechanism and that changes in other measured variables are mediated, at least partially, by mechanisms not dependent on muscarinic cholinergic receptors of the parasympathetic nervous system.


PEDIATRICS ◽  
1968 ◽  
Vol 41 (3) ◽  
pp. 560-573
Author(s):  
Robert B. Mellins ◽  
O. Robert Levine ◽  
Roland H. Ingram ◽  
Alfred P. Fishman

A study of the interrelationships of instantaneous air flow, lung volume, and transpulmonary pressure over the range of the vital capacity has demonstrated striking differences in the determinants of maximum expiratory flow in cystic fibrosis and asthma. At high lung volumes, maximum expiratory flow rates in asthma are limited by the mechanical characteristics of the lungs and airways, whereas in cystic fibrosis and in the normal they are dependent on effort. At lower lung volumes, maximum expiratory flow rates are relatively more reduced in cystic fibrosis than in asthma and pressures in excess of those required to produce maximum flow actually depress flow. Also, forced expiration is associated with a transient reversal in the slope of the single breath nitrogen curve in cystic fibrosis and not in asthma. From these studies it is concluded that: (1) airway obstruction is less uniform and involves larger airways in cystic fibrosis than in asthma, and (2) increased expiratory pressure is associated with collapse of some of the larger airways over most of the range of the vital capacity in cystic fibrosis. A major clinical implication of these studies is that the effectiveness of cough is impaired by large airway collapse in cystic fibrosis.


1976 ◽  
Vol 41 (2) ◽  
pp. 153-158 ◽  
Author(s):  
J. J. Wellman ◽  
R. Brown ◽  
R. H. Ingram ◽  
J. Mead ◽  
E. R. McFadden

In normal subjects, the second of two successive partial expiratory flow-volume (PEFV 2) curves often had higher isovolume maximal expiratory flow rates (Vmax) than the first (PEFV 1) (mean increase 30.2 +/- 13%). The higher Vmax on PEFV 2 was present only when there was a greater lung elastic recoil pressure (Pst(L)). In eight subjects the Pst(L) derived from sequential partial quasi-static pressure-volume curves, from interruption of the flow-volume maneuvers and at the start of the PEFV curves showed that isovolume upstream resistance increased although Vmax also increased after going to residual volume (RV). In four subjects the RV volume history did not change the pressure flow relationship across the upstream airways. If airways dimensions were the sole determinant of Vmax, then Vmax on PEFV 2 would be the same or smaller than on PEFV 1. That the opposite was observed in our study indicates that the increase in Pst(L), which results from parenchymal hysteresis, offsets any dimensional decrease in upstream airways due to airways hysteresis.


1975 ◽  
Vol 39 (1) ◽  
pp. 60-65 ◽  
Author(s):  
J. R. Rodarte ◽  
R. E. Hyatt ◽  
D. A. Cortese

Single-breath oxygen (SBO2) tests at expiratory flow rates of 0.2, 0.5, and 1.01/s were performed by 10 normal subjects in a body plethysmograph. Closing capacity (CC)--the absolute lung volume at which phase IV began--increased significantly with increases in flow. Five subjects were restudied with a 200-ml bolus of 100% N2 inspired from residual volume after N2 washout by breathing 100% O2 and similar results were obtained. An additional five subjects performed SBO2 tests in the standing, supine, and prone positions; closing volume (CV)--the lung volume above residual volume at which phase IV began--also increased with increases of expiratory flow. The observed increase in CC with increasing flow did not appear to result from dependent lung regions reaching some critical “closing volume” at a higher overall lung volume. In normal subjects, the phase IV increase in NI concentration may be caused by the asynchronous onset of flow limitation occurring initially in dependent regions.


1999 ◽  
Vol 87 (4) ◽  
pp. 1532-1542 ◽  
Author(s):  
Anthony P. Pietropaoli ◽  
Irene B. Perillo ◽  
Alfonso Torres ◽  
Peter T. Perkins ◽  
Lauren M. Frasier ◽  
...  

Human airways produce nitric oxide (NO), and exhaled NO increases as expiratory flow rates fall. We show that mixing during exhalation between the NO produced by the lower, alveolar airways (V˙l NO) and the upper conducting airways (V˙u NO) explains this phenomenon and permits measurement ofV˙l NO,V˙u NO, and the NO diffusing capacity of the conducting airways (Du NO). After breath holding for 10–15 s the partial pressure of alveolar NO (Pa) becomes constant, and during a subsequent exhalation at a constant expiratory flow rate the alveoli will deliver a stable amount of NO to the conducting airways. The conducting airways secrete NO into the lumen (V˙u NO), which mixes with Pa during exhalation, resulting in the observed expiratory concentration of NO (Pe). At fast exhalations, Pa makes a large contribution to Pe, and, at slow exhalations, NO from the conducting airways predominates. Simple equations describing this mixing, combined with measurements of Pe at several different expiratory flow rates, permit calculation of Pa,V˙u NO, and Du NO.V˙l NOis the product of Pa and the alveolar airway diffusion capacity for NO. In seven normal subjects, Pa = 1.6 ± 0.7 × 10−6 (SD) Torr,V˙l NO= 0.19 ± 0.07 μl/min,V˙u NO= 0.08 ± 0.05 μl/min, and Du NO = 0.4 ± 0.4 ml ⋅ min−1 ⋅ Torr−1. These quantitative measurements ofV˙l NOandV˙u NOare suitable for exploring alterations in NO production at these sites by diseases and physiological stresses.


1976 ◽  
Vol 51 (2) ◽  
pp. 133-139
Author(s):  
J. J. Wellman ◽  
E. R. McFadden ◽  
R. H. Ingram

1. Gas-density-dependence of maximal expiratory flow rates (V̇max), defined as the ratio of V̇max while breathing helium/oxygen (80:20) to V̇max. while breathing air at the same lung volume, was examined in relation to other measurements of airways obstruction in patients with obstructive airways disease before and after administration of bronchodilators. 2. Seventeen patients showed a 45% or greater increase in specific conductance(sGaw) after bronchodilator therapy (group A) and thirteen patients demonstrated a lesser response (group B). 3. Before the administration of bronchodilators, the degree of obstruction in the two groups was not different as measured by lung volumes, sGaw, forced expiratory volume in 1 s, and flow rates high in the vital capacity; yet the maximal mid-expiratory flow rate and the degree of density-dependence were significantly lower in group B. 4. After bronchodilators, both groups of patients showed significant improvements in sGaw flow rates and lung volumes. However, group A patients showed a significant increase in density-dependence whereas group B patients did not. 5. Increased density-dependence after bronchodilators in the group A patients was associated with an increase in the computed resistance of the upstream segment with air and a decrease in resistance with helium/oxygen. These changes could be explained by a more mouthward movement of equal pressure points, and therefore a further increase in the relative contribution of the larger density-dependent airways to limitation of flow. 6. The fact that density-dependence was not altered after bronchodilators in the group B patients suggests that the site of limitation of flow did not change appreciably. The shift in the pressure—flow curve for the upstream airways was such that the computed resistance of these airways fell. Thus it appears that the airways comprising the upstream segment were dilated.


PEDIATRICS ◽  
1971 ◽  
Vol 48 (1) ◽  
pp. 64-72
Author(s):  
Alois Zapletal ◽  
Etsuro K. Motoyama ◽  
Lewis E. Gibson ◽  
Arend Bouhuys

Maximum expiratory flow rates on flow-volume curves are often decreased below normal limits in children with asthma or cystic fibrosis who are clinically well and whose standard spirometric tests are within normal limits. In particular, maximum flow rates at small lung volumes (25% of vital capacity) are decreased. Maximum expiratory flow-volume (MEFV) curves provide a sensitive and quantitative assessment of small airway obstruction in these and other obstructive lung conditions.


1976 ◽  
Vol 40 (3) ◽  
pp. 320-323 ◽  
Author(s):  
C. Prefaut ◽  
E. Lupi-h ◽  
N. R. Anthonisen

We measured lung volumes, static deflation pressure-volume curves of the lung, maximum expiratory flow-volume curves, and closing capacities in five men standing immersed to the neck in water. FRC was decreased 27%, while other lung volumes did not change significantly. At high lung volumes immersion tended to increase lung elastic recoil while recoil was decreased at low lung volumes, changes compatible with vascular congestion. Maximum expiratory flow was increased at high lung volumes, probably because of hydrostatic pressure. At low lung volumes maximum expiratory flow was decreased. This was probably due to decreased recoil since the relationship between elastic recoil and maximum flow was unchanged. Closing capacities by the N2 technique were unchanged but the slope of the alveolar plateau and the amplitude of cardiogenic oscillations were decreased in some individuals. Static and dynamic lung properties were unchanged by 5 min of immersion with tidal volume restricted to 0.5 liter. Though immersion produced volume restriction comparable with that reported with chest strapping, it did not produce similar changes in lung mechanics.


2015 ◽  
Vol 115 (8) ◽  
pp. 1645-1652 ◽  
Author(s):  
Joshua R. Smith ◽  
Sam R. Emerson ◽  
Stephanie P. Kurti ◽  
Kirti Gandhi ◽  
Craig A. Harms

PLoS ONE ◽  
2015 ◽  
Vol 10 (12) ◽  
pp. e0145476 ◽  
Author(s):  
Craig M. Riley ◽  
Sally E. Wenzel ◽  
Mario Castro ◽  
Serpil C. Erzurum ◽  
Kian Fan Chung ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document