Influence of expiratory flow on closing capacity at low expiratory flow rates

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.

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.


1975 ◽  
Vol 38 (2) ◽  
pp. 199-207 ◽  
Author(s):  
R. Begin ◽  
A. D. Renzetti ◽  
A. H. Bigler ◽  
S. Watanabe

The influence of expiratory flow rate and age on the results of measurement of closing volume (CV) of the lung have been studied by a nitrogen single-breath method in 66 asymptomatic lifetime nonsmoking normal subjects between 20 and 82 yr of age. Normal was defined as having values for spirometric measurements within a 95% tolerance interval of reported predicted normal mean values. For the CV determination, inspiratory flow rate was held constant at 0.51/s and studies were carried out at expiratory flow rates of 0.25, 0.5, 1.0, and 1.5 1/s. Our results show that CV expressed as a percentage of vital capacity (VC) and the slope of the alveolar plateau increases with increasing flow rate and age. Dynamic compliance (Cdyn) at frequencies corresponding to peak flow rates of 0.5 and 1.5 1/s was also measured and correlated well with the CV results. Frequency dependence of compliance with aging was demonstrated. Nine smokers with normal spirometric measurements and abnormal CV %VC were also studied. Since the results of Cdyn measurement differentiated only two-thirds of the smokers from the normal population, we suggest that the CV method is probably more sensitive than the Cdyn method for the detection of small airway obstruction.


1982 ◽  
Vol 52 (1) ◽  
pp. 34-43 ◽  
Author(s):  
G. M. Nichol ◽  
D. B. Michels ◽  
H. J. Guy

A downward-deflecting phase V is often seen following the phase IV terminal rise in the single-breath N2 washout test (SB N2). This phase V was studied in eight normal nonsmoking subjects aged 27–41, using both the SB N2 test and single-breath washouts of boluses of inert tracer gas slowly inhaled from residual volume (RV). All of the subjects showed a distinct phase V in both tests. Expiratory flow rates between 0.1 and 2.0 1/s were used; at each flow rate phase V appeared shortly after expiration became flow limited. Thus the volume above RV at which phase V began increased with increasing expiratory flow rate. The difference between the exhaled volumes at which flow became limited and phase V appeared was shown to be approximately equal to the anatomic dead space. This behavior is predicted by a model of lung emptying in a gravitational field. As expiration proceeds, flow limitation occurs first in the (tracer-poor) lower lung regions and then progresses toward the (tracer-rich) upper lung regions causing phase IV. When all lung regions have finally become flow limited, the amount of flow from the upper regions decreases relative to that of the lower regions, thereby causing phase V.


1979 ◽  
Vol 46 (5) ◽  
pp. 1011-1015 ◽  
Author(s):  
D. P. Osmanliev ◽  
P. K. Popov

The influence of expiratory flow rate (VE) on the onset of phase IV was studied in 15 normal subjects. VE was controlled voluntarily and varied between 0.2 and 2.5 l/s. All subjects showed significantly higher values for CV/VC, % at expiratory flow rate of 1.0 and 1.5 l/s, compared to those estimated at 0.2 l/s. The correlation between CV and volume of flow limitation (VFL) was also studied. For most of the subjects a considerable disagreement between the two values at very low VE was found. At higher flows, however, CV and VFL agreed well. Our results indicate that CV measurement is markedly influenced by VE in the range 0.2--1.5 l/s. This finding gives further support to the hypothesis that CV is determined in part by dynamic flow-limiting properties of the lung as well as by true airway closure.


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.


1979 ◽  
Vol 46 (1) ◽  
pp. 24-30 ◽  
Author(s):  
L. Forkert ◽  
S. Dhingra ◽  
N. R. Anthonisen

Using boluses of radioactive Xe we compared regional N2O uptake with regional perfusion distribution during open glottis breath hold in five seated men. Measurements were made near residual volume, at closing volume (CV), above CV and when possible, between CV and residual volume (RV). At low lung volumes basal N2O uptake was small whereas basal blood flow was not. This discrepancy was interpreted as evidence of airway closure and was quantitated. All subjects showed extensive basal closure near RV. At closing volume four of five subjects demonstrated closure and some closure was evident in these subjects at volumes in excess of CV. The increase in airway closure with decreasing lung volume was much greater below CV than above it. Conventional CV tracings were obtained using helium boluses; the height of phase IV was positively correlated with the change in airway closure between CV and RV as assessed by the N2O technique. The slope of phase III did not correlate with the amount of airway closure measured at CV. We concluded that the conventionally measured CV is not the volume at which airway closure begins but that the onset of phase IV reflects an increase in basal airway closure and the height of phase IV reflects the amount of basal closure between CV and RV.


1982 ◽  
Vol 53 (2) ◽  
pp. 361-366
Author(s):  
L. Delaunois ◽  
R. Boileau ◽  
J. Diodatti ◽  
J. Gauthier ◽  
R. R. Martin

The regional distribution of a bolus of gas inhaled at residual volume (RV) is attributed to regional airway closure and is responsible for the phase IV of the single-breath washout during the following deflation. As bronchospasm increases the range of airway opening pressures through the lung, the regional distribution of the bolus could change with effects on the shape of the single-breath washout. We investigated the regional distribution of boluses inhaled at RV and their single-breath washouts during methacholine-induced bronchospasm in prone dogs. With increasing total lung resistance (RL) we first observed in five out of eight animals a preferential “redistribution” of the bolus to the upper caudal regions of the lung, which could be partially attributed to the increased lung volume at RV. When maximal RL was attained, the bolus was evenly distributed through all regions of the lung in these animals with disappearance of phase IV and increased slope of phase III, and a final decrease of tracer concentration at low lung volumes was observed. We conclude from these data that increased bronchomotor tone in dogs results in a less homogeneous intraregional distribution of the bolus with increased slope of phase III and in a more even interregional distribution leading to disappearance of phase IV. In severe bronchospasm the downward slope at low lung volume suggests intraregional closed lung units emptying through collateral pathways into still open neighboring units.


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.


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

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.


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