Density-Dependence of Maximal Expiratory Flow Rates before and after Bronchodilators in Patients with Obstructive Airways Disease

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.

1986 ◽  
Vol 60 (3) ◽  
pp. 1060-1066 ◽  
Author(s):  
R. G. Castile ◽  
O. F. Pedersen ◽  
J. M. Drazen ◽  
R. H. Ingram

The effect of carbachol-induced central bronchoconstriction on density dependence of maximal expiratory flow (MEF) was assessed in five dogs. MEFs were measured on air and an 80% He-20% O2 mixture before and after local application of carbachol to the trachea. Airway pressures were measured using a pitot-static probe, from which central airway areas were estimated. At lower concentrations of carbachol the flow-limiting site remained in the trachea over most of the vital capacity (VC), and tracheal area and compliance decreased in all five dogs. In four dogs, decreases in choke point area predominated and produced decreases in flows. In one dog the increase in airway “stiffness” apparently offset the fall in area to account for an increase in MEF. Density dependence measured as the ratio of MEF on HeO2 to MEF on air at 50% of VC increased in all five dogs. Increases in density dependence appeared to be related to increases in airway stiffness at the choke point rather than decreases in gas-related airway pressure differences. Lower concentrations produced a localized decrease in tracheal area and extended the plateau of the flow-volume curve to lower lung volumes. Higher concentrations caused further reductions in tracheal area and greater longitudinal extension of bronchoconstriction, resulting in upstream movement of the site of flow limitation at higher lung volumes. Density dependence increased if the flow-limiting sites remained in the trachea at mid-VC but fell if the flow-limiting site had moved upstream by that volume.


1982 ◽  
Vol 52 (4) ◽  
pp. 874-878 ◽  
Author(s):  
J. W. Weiss ◽  
E. R. McFadden ◽  
R. H. Ingram

Using normal human subjects we have measured maximal expiratory flow rates with air (Vmaxair) and after a washin of 80% He-20% O2 (VmaxHeO2) and static elastic recoil pressures of the lung [Pst(L)] both before and after administration of a beta-agonist, terbutaline. The effects of inhaled drug were compared with those of the subcutaneously administered agent, each given in doses to produce maximal bronchodilatation as assessed by increases in Vmaxair in the mid-vital capacity. Although there was a significant yet modest decrease in Pst(L) only after injection of the agent, density dependence (DD), assessed as the ratio of VmaxHeO2 to Vmaxair, increased significantly and comparably after either route of administration. A modest decrease in Pst(L), therefore, did not affect the changes in DD.


1995 ◽  
Vol 78 (4) ◽  
pp. 1421-1424 ◽  
Author(s):  
E. Thorsen ◽  
B. K. Kambestad

To assess the contribution of hyperoxia to reduced pulmonary function after a deep saturation dive, a shallow saturation dive to a pressure of 0.25 MPa with the same profile of hyperoxic exposure as in a deep saturation dive to 3.7 MPa was conducted. The PO2 was 40 kPa, with periods of 75 kPa for 2 h every 2nd day during the first 14 days, 50 kPa the next 12 days, and a gradual fall to 21 kPa over the last 2 days in decompression. Seven submariners and one professional diver aged 22–27 yr participated. Pulmonary function, including static and dynamic lung volumes and flows and transfer factor for carbon monoxide (TLCO), were measured twice before, immediately after, 1 mo after, and 1 and 3 yr after the dive. As reported previously, there was a significant reduction in TLCO and in maximal expiratory flow rates at low lung volumes immediately after the dive. At the follow-up examinations 1 and 3 yr after, there was no recovery of the maximal expiratory flow rates. Forced midexpiratory flow rate was still reduced by 8.7 +/- 5.6% (P < 0.05) and 9.3 +/- 7.1% (P < 0.01), respectively. Forced expired volume in 1 s and forced vital capacity were not significantly reduced. There was a complete recovery of the TLCO. The findings are consistent with the studies indicating development of airway obstruction in divers, and the findings indicate that exposure to hyperoxia contributes to this effect.


1998 ◽  
Vol 84 (6) ◽  
pp. 1872-1881 ◽  
Author(s):  
Steven R. McClaran ◽  
Craig A. Harms ◽  
David F. Pegelow ◽  
Jerome A. Dempsey

We subjected 29 healthy young women (age: 27 ± 1 yr) with a wide range of fitness levels [maximal oxygen uptake (V˙o 2 max): 57 ± 6 ml ⋅ kg−1 ⋅ min−1; 35–70 ml ⋅ kg−1 ⋅ min−1] to a progressive treadmill running test. Our subjects had significantly smaller lung volumes and lower maximal expiratory flow rates, irrespective of fitness level, compared with predicted values for age- and height-matched men. The higher maximal workload in highly fit (V˙o 2 max > 57 ml ⋅ kg−1 ⋅ min−1, n = 14) vs. less-fit (V˙o 2 max < 56 ml ⋅ kg−1 ⋅ min−1, n = 15) women caused a higher maximal ventilation (V˙e) with increased tidal volume (Vt) and breathing frequency (fb) at comparable maximal Vt/vital capacity (VC). More expiratory flow limitation (EFL; 22 ± 4% of Vt) was also observed during heavy exercise in highly fit vs. less-fit women, causing higher end-expiratory and end-inspiratory lung volumes and greater usage of their maximum available ventilatory reserves. HeO2 (79% He-21% O2) vs. room air exercise trials were compared (with screens added to equalize external apparatus resistance). HeO2 increased maximal expiratory flow rates (20–38%) throughout the range of VC, which significantly reduced EFL during heavy exercise. When EFL was reduced with HeO2, Vt, fb, andV˙e (+16 ± 2 l/min) were significantly increased during maximal exercise. However, in the absence of EFL (during room air exercise), HeO2 had no effect onV˙e. We conclude that smaller lung volumes and maximal flow rates for women in general, and especially highly fit women, caused increased prevalence of EFL during heavy exercise, a relative hyperinflation, an increased reliance on fb, and a greater encroachment on the ventilatory “reserve.” Consequently, Vt andV˙e are mechanically constrained during maximal exercise in many fit women because the demand for high expiratory flow rates encroaches on the airways’ maximum flow-volume envelope.


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.


CHEST Journal ◽  
1992 ◽  
Vol 102 (5) ◽  
pp. 1636-1637
Author(s):  
Sema Umut ◽  
Bilun Gemicioğlu ◽  
Nurhayat Yildirim

1982 ◽  
Vol 53 (2) ◽  
pp. 392-396 ◽  
Author(s):  
J. W. Weiss ◽  
E. R. McFadden ◽  
R. H. Ingram

Using forced vital capacity maneuvers, we measured maximal expiratory flow rates (Vmax) and static elastic recoil pressures of the lung [Pst(L)] using quasi-static maneuvers in normal nonsmoking human subjects who were breathing air and after a washing of 80% helium-20% oxygen before and after both inhaled and intravenously administered atropine sulfate. By both routes there were equivalent increases in Vmaxair but different effects on density dependence (DD) of Vmax (DD = ratio of VmaxHeO2 to Vmaxair) and on Pst(L). At 30% of vital capacity, DD decreased from an average of 1.47 to 1.32 (P less than 0.01, paired t test) after inhaled drug and did not change after parenteral administration [1.44 vs. 1.48 (P greater than 0.2)]. After inhalation Pst(L) did not change, but after parenteral administration Pst(L) significantly decreased. We interpret these findings to indicate a predominantly large-airway effect with the inhalation route and a more uniform dilatation after the parenteral dose. These results contrast with beta-adrenergic dilatation following which small-airway effects predominate regardless of route of administration.


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.


1981 ◽  
Vol 50 (3) ◽  
pp. 575-579 ◽  
Author(s):  
K. P. Strohl ◽  
C. F. O'Cain ◽  
R. H. Ingram ◽  
M. A. Yanta ◽  
W. D. Kaplan ◽  
...  

To determine the relationship between changes in density dependence of maximal expiratory flow and changes in the predominant site of bronchoconstriction, we altered the pattern of inhalation of a methacholine aerosol to achieve deposition either centrally (by short choppy breaths) or peripherally (by slow deep breaths). Partial expiratory flow volume curves on air and on 80% helium-20% oxygen (HeO2) were recorded in six healthy subjects before and after each pattern of methacholine inhalation. We varied concentrations of methacholine and number of inhalations to achieve equivalent degrees of bronchoconstriction as assessed by decreases in maximal flow (Vmax) on air, which fell 27% from control values. Vmax on HeO2 also fell after both inhalation patterns. Density dependence (Vmax on HeO2 divided by Vmax on air) decreased following slow deep breaths of bronchoconstrictor aerosol, and increased following short choppy breaths. In three subjects, inhalation of radiolabeled methacholine aerosol confirmed that the slow deep pattern was associated with a diffuse, more peripheral deposition, whereas the short choppy pattern led to central deposition. We conclude that changes in density dependence reflect the predominant site of obstruction after acute methacholine aerosol challenge in healthy subjects.


1970 ◽  
Vol 38 (3) ◽  
pp. 18P-19P
Author(s):  
A. J. S. Gardiner ◽  
L. Wood ◽  
P. Gayrard ◽  
H. Menkes ◽  
P. T. Macklem

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