Density dependence of maximal flow in dogs with central and peripheral obstruction

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 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)


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.


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.


1987 ◽  
Vol 63 (4) ◽  
pp. 1648-1657 ◽  
Author(s):  
J. J. McNamara ◽  
R. G. Castile ◽  
G. M. Glass ◽  
J. J. Fredberg

Several lines of evidence suggest that the healthy mammalian lung empties homogeneously during a maximally forced deflation. Nonetheless, such behavior would appear to be implausible if for no other reason than that airway structure is known to be substantially heterogeneous among parallel pathways of gas conduction. To resolve this paradox we reexamined the degree to which lung emptying is homogeneous, and considered mechanisms that might control differential regional emptying. Twelve excised canine lungs were studied. Regional alveolar pressure relative to pleural pressure was used as an index of regional lung volume. By use of a capsule technique, alveolar pressure was measured simultaneously in each of six regions during flow-limited deflations; flow from the lung was measured plethysmographically. The standard deviation of interregional pressure differences, which was taken as an index of nonuniformity, was 0.0, 0.74, 0.64, and 0.90 cmH2O at mean recoil pressures of 30, 8.4, 4.5, and 2.1 cmH2O (0, 25, 50, and 75% expired vital capacity), indicating that interregional pressure differences increased more rapidly earlier in the deflation. When we examined the time rate of change of regional alveolar pressure as an index of regional flow, we observed an intricate pattern of differential regional behavior that was inapparent in the maximum expiratory flow-volume (MEFV) curve. The most plausible interpretation of these findings is that regions of the healthy excised canine lung empty heterogeneously to a small degree, but in an interdependent compensatory pattern that is inapparent in the configuration of the maximum expiratory flow-volume curve.


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

2021 ◽  
Vol 30 (162) ◽  
pp. 210081
Author(s):  
Andrew Kouri ◽  
Ronald J. Dandurand ◽  
Omar S. Usmani ◽  
Chung-Wai Chow

175 years have elapsed since John Hutchinson introduced the world to his version of an apparatus that had been in development for nearly two centuries, the spirometer. Though he was not the first to build a device that sought to measure breathing and quantify the impact of disease and occupation on lung function, Hutchison coined the terms spirometer and vital capacity that are still in use today, securing his place in medical history. As Hutchinson envisioned, spirometry would become crucial to our growing knowledge of respiratory pathophysiology, from Tiffeneau and Pinelli's work on forced expiratory volumes, to Fry and Hyatt's description of the flow–volume curve. In the 20th century, standardization of spirometry further broadened its reach and prognostic potential. Today, spirometry is recognized as essential to respiratory disease diagnosis, management and research. However, controversy exists in some of its applications, uptake in primary care remains sub-optimal and there are concerns related to the way in which race is factored into interpretation. Moving forward, these failings must be addressed, and innovations like Internet-enabled portable spirometers may present novel opportunities. We must also consider the physiologic and practical limitations inherent to spirometry and further investigate complementary technologies such as respiratory oscillometry and other emerging technologies that assess lung function. Through an exploration of the storied history of spirometry, we can better contextualize its current landscape and appreciate the trends that have repeatedly arisen over time. This may help to improve our current use of spirometry and may allow us to anticipate the obstacles confronting emerging pulmonary function technologies.


1995 ◽  
Vol 17 (5) ◽  
pp. 332-336 ◽  
Author(s):  
S. Abboud ◽  
O. Barnea ◽  
A. Guber ◽  
N. Narkiss ◽  
I. Bruderman

Sign in / Sign up

Export Citation Format

Share Document