Changes in flow-volume curve configuration with bronchoconstriction and bronchodilation

1986 ◽  
Vol 61 (6) ◽  
pp. 2243-2251 ◽  
Author(s):  
C. R. O'Donnell ◽  
R. G. Castile ◽  
J. Mead

Changes in the configuration of maximum expiratory flow-volume (MEFV) curves following mild degrees of bronchodilation or bronchoconstriction were studied in five normal and five asthmatic subjects. In a volume-displacement plethysmograph, MEFV curves were performed before and after inhalation of aerosolized isoproterenol (I) or histamine (H). Five filtered MEFV curves were averaged, and slope ratio vs. volume (SR-V) plots were obtained from averaged curves. Following I, maximal flows at 75% of the vital capacity (VC) were decreased in asthmatics but not in normal subjects. Flows at 50 and 25% of the VC increased in normal subjects and asthmatics, whereas VC′s were unchanged. In asthmatics, sudden large decreases in flow (bumps) occurred at lower lung volumes following I. H reduced flows over the entire VC, with greater reductions occurring in asthmatics than in normals, particularly at low lung volumes. In asthmatics, VC was slightly reduced, and bumps in MEFV curve configuration occurred at higher lung volumes or were abolished entirely following H. A reduction in the amount of configurational detail appreciable in MEFV curves following histamine in asthmatics was best seen in SR-V plots. Following H, SR′s decreased regularly with decreasing lung volume in all the asthmatics but in none of the normals. This was the single most striking finding of this study. Mild I- and H-induced perturbations of airway bronchomotor tone produced small but consistent changes in MEFV curve configuration.(ABSTRACT TRUNCATED AT 250 WORDS)

1983 ◽  
Vol 55 (3) ◽  
pp. 717-725 ◽  
Author(s):  
R. G. Castile ◽  
O. F. Pedersen ◽  
J. M. Drazen ◽  
R. H. Ingram

In 12 anesthetized, tracheotomized, vagotomized, open-chested, mongrel dogs we measured end and side hole airway pressures during forced expiration using a Pitot static probe. Volume was obtained as the integral of flow from a dog plethysmograph with frequency response adequate to 20 Hz. Equal pressure points (EPPs) and choke points (CPs) were located with dogs breathing air or a mixture of 80% helium-20% oxygen (HeO2) before and after partial obstruction of the trachea and intravenous histamine and propranolol. At 50% of vital capacity (VC) the CP was in the trachea in 11 of 12 dogs. Partial obstruction of the trachea decreased flow during the plateau of the maximum expiratory flow-volume curve (MEFVC) with the CP remaining in the trachea. The MEFVC plateau was extended to a lower lung volume. At 50% of VC the EPP moved downstream and density dependence remained high. Histamine and propranolol caused EPPs and CPs to move towards the periphery and density dependence to decrease. The shape of the MEFVC changed as the plateau was shortened and, in some instances, abolished. A plateau on the MEFVC could be regenerated by partial obstruction of the trachea. This was accompanied by return of the CP to the trachea and an increase in density dependence. Changes in density dependence were found to be a result of both the relocation of sites of flow limitation and differences in local CP areas with HeO2 and air.


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.


2019 ◽  
Vol 68 (2) ◽  
pp. 403-411 ◽  
Author(s):  
Octavian C Ioachimescu ◽  
James K Stoller

Previous work has shown that area under the expiratory flow–volume curve (AEX) performs well in diagnosing and stratifying respiratory physiologic impairment, thereby lessening the need to measure lung volumes. Extending this prior work, the current study assesses the accuracy and utility of several geometric approximations of AEX based on standard instantaneous flows. These approximations can be used in spirometry interpretation when actual AEX measurements are not available. We analysed 15 308 spirometry tests performed on subjects who underwent same-day lung volume assessments in the Pulmonary Function Laboratory. Diagnostic performance of four AEX approximations (AEX1–4) was compared with that of actual AEX. All four computations included forced vital capacity (FVC) and various instantaneous flows: AEX1 was derived from peak expiratoryflow (PEF); AEX2 from PEF and forced expiratoryflow at 50% FVC (FEF50); AEX3 from FVC, PEF, FEF at 25% FVC (FEF25) and at 75% FVC (FEF75), while AEX4 was computed from all four flows, PEF, FEF25, FEF50 and FEF75. Mean AEX, AEX1, AEX2, AEX3 and AEX4 were 6.6, 8.3, 6.7, 6.3 and 6.1 L2/s, respectively. All four approximations had strong correlations with AEX, that is, 0.95–0.99. Differences were the smallest for AEX–AEX4, with a mean of 0.52 (95% CI 0.51 to 0.54) and a SD of 0.75 (95% CI 0.74 to 0.76) L2/s. In the absence of AEX and in addition to the usual spirometric variables used for assessing functional impairments, parameters such as AEX4 can provide reasonable approximations of AEX and become useful new tools in future interpretative strategies.


1994 ◽  
Vol 76 (1) ◽  
pp. 356-360 ◽  
Author(s):  
J. J. McNamara ◽  
R. G. Castile ◽  
M. S. Ludwig ◽  
G. M. Glass ◽  
R. H. Ingram ◽  
...  

We studied the evolution of alveolar pressure (PA) heterogeneity during the course of forced expiration in the lungs of six anesthetized open-chest dogs. Using an alveolar capsule technique, we measured PA simultaneously in six lung regions during full maximal forced deflations before and after administering aerosolized histamine. Flow was measured plethysmographically with volume obtained by flow integration. Heterogeneity was expressed as the coefficient of variation (CV) of regional PA after 25% of the vital capacity had been expired from total lung capacity. The CV in in vivo open-chest canine lungs (21.3%) was significantly greater than that we measured previously in excised lungs (8.7%) (P < 0.02). Inhalation of aerosolized solutions of histamine produced significant increases in interregional heterogeneity (CV = 35.5 and 38.8% after 3 and 10 mg/ml of histamine, respectively; P < 0.025). After histamine, the vital capacity was reduced and the configuration of the flow-volume curve demonstrated some shortening of the flow plateau commonly observed in dogs. Changes in the flow-volume relationship failed, however, to reflect well the marked degree of heterogeneity of PA after histamine administration. These findings may be reconciled on the basis of interdependence of regional expiratory flows. Reductions in flow from obstructed regions appear to be compensated by increases in flow from unobstructed regions and thus mask upstream nonuniformities. These mechanisms may explain in part why the maximal expiratory flow-volume curve has been a relatively insensitive tool for the detection of early nonuniform airway disease.


1996 ◽  
Vol 81 (1) ◽  
pp. 33-43 ◽  
Author(s):  
A. R. Elliott ◽  
G. K. Prisk ◽  
H. J. Guy ◽  
J. M. Kosonen ◽  
J. B. West

Gravity is known to influence the mechanical behavior of the lung and chest wall. However, the effect of sustained microgravity (microG) on forced expirations has not previously been reported. Tests were carried out by four subjects in both the standing and supine postures during each of seven preflight and four postflight data-collection sessions and four times during the 9 days of microG exposure on Spacelab Life Sciences-1. Compared with preflight standing values, peak expiratory flow rate (PEFR) was significantly reduced by 12.5% on flight day 2 (FD2), 11.6% on FD4, and 5.0% on FD5 but returned to standing values by FD9. The supine posture caused a 9% reduction in PEFR. Forced vital capacity and forced expired volume in 1 s were slightly reduced (approximately 3-4%) on FD2 but returned to preflight standing values on FD4 and FD5, and by FD9 both values were slightly but significantly greater than standing values. Forced vital capacity and forced expiratory volume in 1 s were both reduced in the supine posture (approximately 8-10%). Forced expiratory flows at 50% and between 25 and 75% of vital capacity did not change during microG but were reduced in the supine posture. Analysis of the maximum expiratory flow-volume curve showed that microG caused no consistent change in the curve configuration when individual in-flight days were compared with preflight standing curves, although two subjects did show a slight reduction in flows at low lung volumes from FD2 to FD9. The interpretation of the lack of change in curve configuration must be made cautiously because the lung volumes varied from day to day in flight. Therefore, the flows at absolute lung volumes in microG and preflight standing are not being compared. The supine curves showed a subtle but consistent reduction in flows at low lung volumes. The mechanism responsible for the reduction in PEFR is not clear. It could be due to a lack of physical stabilization when performing the maneuver in the absence of gravity or a transient reduction in respiratory muscle strength.


2008 ◽  
pp. 91-97 ◽  
Author(s):  
G. A. Lyubimov ◽  
I. M. Skobeleva ◽  
G. M. Sakharova ◽  
A. V. Suvorov

This report introduces a mathematical model of forced expiration to analyze pulmonary function. Results of 3-year lung function monitoring of an ex-smoker have been shown in the paper. Actual values of lung volumes and airway resistance were used for modeling. The computerized data were compared to the flow-volume curve parameters and lung volumes measured during the forced expiration. Weak correlation between the "flow-volume" curve parameters and the time after quitting smoking together with significant change in the lung volumes and the airway resistance seen in the study could be due to some processes which have not been followed in this study (lung compliance, airway resistance at forced expiration, and elastic properties of airway walls).The results demonstrated that mathematical models could increase informative value of pulmonary functional tests. In addition, the model could emphasize additional functional tests for better diagnostic usefulness of functional investigations.


2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Jonathon Stickford ◽  
Marc Augenreich ◽  
Valesha Province ◽  
Nina Stute ◽  
Abigail Stickford ◽  
...  

CHEST Journal ◽  
1988 ◽  
Vol 94 (4) ◽  
pp. 799-806 ◽  
Author(s):  
Mary C. Kapp ◽  
E.Neil Schachter ◽  
Gerald J. Beck ◽  
Lucinda R. Maunder ◽  
Theodore J. Witek

1979 ◽  
Vol 46 (3) ◽  
pp. 565-570 ◽  
Author(s):  
Y. K. Tien ◽  
E. A. Elliott ◽  
J. Mead

With a computer technique variability of the configuration of maximum expiratory flow-volume (MEFV) curves was studied in terms of slope ratio, SR. SR = dV/dV divided by V/V, where V is the instantaneous flow and V is the volume increment above residual volume.) Approximately four SR-V curves, each based on three to five smoothed and averaged MEFV curves, were derived for each of 20 normal subjects (aged 23–55 yr) on a single occasion, and again at least 1 wk later. Individual curves were largely reproducible, the maximum difference in SR at most volumes being 0.3–1 U, but frequently showed substantial yet reproducible fluctuations with volume. These corresponeded to hitherto unrecognized irregularities of maximum expiratory flow that may reflect sudden changes in the location of flow limitation.


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