Heterogeneous regional behavior during forced expiration before and after histamine inhalation in dogs

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.

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)


1982 ◽  
Vol 53 (5) ◽  
pp. 1175-1183 ◽  
Author(s):  
R. Castile ◽  
J. Mead ◽  
A. Jackson ◽  
M. E. Wohl ◽  
D. Stokes

Tien et al. (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 46: 565–570, 1979) found reproducible details in the configuration of averaged maximal expiratory flow-volume curves and suggested that these details may correspond to sudden relocations of airway choke points. The occurrence of choke points depends on factors affecting local airway pressure-diameter behavior. We postulated that changes in posture as they affect the distribution of lung recoil on airways might change the locations of choke points and thereby alter flow-volume configuration. Twenty normal adults performed five flow-volume curves in each of four postures (standing, supine, right, and left lateral recumbent). Volume was measured with a Krogh spirometer and airflow with a Fleisch No. 4 pneumotachometer. Curves were digitally filtered and plotted relative to upright total lung capacity. Five curves in each posture were averaged at increments of 0.1 l/s of flow and average volumes at given flows were compared using the Student's t test. Significant differences (P less than 0.01) in mean volumes at given flows occurred in all subjects from standing to supine and/or right to left lateral postures. Large changes in configuration were apparent in one of the two postural pairs in eight subjects. We conclude that changes in posture result in significant changes in flow-volume configuration in most normal adults. These findings are consistent with the wave-speed theory of flow limitation and suggest that small changes in local airway stresses can significantly alter the location and motion of airway choke points during forced expiration.


1981 ◽  
Vol 60 (1) ◽  
pp. 11-15 ◽  
Author(s):  
T. Higenbottam ◽  
T. J. H. Clark

1. Forced exhalations performed from volumes below total lung capacity, so-called partial expiratory flow-volume curves, are suggested to be more sensitive in detecting airways bronchoconstriction than maximal expiratory flow-volume curves begun at total lung capacity. 2. In eight healthy men both maximal and partial expiratory flow-volume curves were measured where breath was held at total lung capacity or 70% of vital capacity respectively, for either 0 or 15 s before performing the forced exhalation. An histamine aerosol was used to provoke bronchoconstriction. 3. The results showed that the 15 s breath hold caused greater reduction in expiratory flow rates after histamine for both maximal and partial expiratory flow-volume curves than either manoeuvres performed with no breath hold. 4. A breath hold of 15 s at total lung capacity appeared to make the maximal expiratory flow-volume curve as sensitive as a partial expiratory flow-volume curve in detecting the response to histamine as well as providing measurements of forced expiratory volume in 1 s and vital capacity. Forced spirometry after a 15 s breath hold at total lung capacity therefore provides an easy and sensitive technique for detecting bronchoconstriction.


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 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.


1982 ◽  
Vol 52 (2) ◽  
pp. 357-369 ◽  
Author(s):  
O. F. Pedersen ◽  
B. Thiessen ◽  
S. Lyager

Bronchial pressure measured by means of a Pitot static probe, esophageal pressure, and airflow were monitored during forced lung deflations in six anesthetized dogs. Dynamic transmural pressure-cross-sectional area area curves (Ptm-A curves) were constructed for three intrathoracic tracheal positions and one right lower lobal bronchial position. From the Ptm-A curves the maximal possible flow (Vmax) through the airways at each of the four positions was calculated and compared with the overall maximal flow obtained during the same deflation. The peak of the maximal expiratory flow-volume curve (MEFV curve) equaled the calculated Vmax at more than one position in the trachea but did not reach the Vmax calculated for the more peripheral position. During the transition between the peak and the plateau of the MEFV curve, the Ptm-A curve often changed shape, indicating an abrupt change in the “tube law,” probably due to changes in axial tension of the airway. During the flow-volume curve plateau, measured flow was near an estimated Vmax at a single point in the trachea. At lower lung volumes where the MEFV curve descends from the plateau, measured flow equaled Vmax calculated for the right lower lobe position. This indicates that after an initial period with no localized choking a “choke point” develops and eventually moves toward the periphery. We conclude that measurement of dynamic Ptm-A curves allows a precise prediction of maximal expiratory flows from the properties of the airways.


2000 ◽  
Vol 161 (3) ◽  
pp. 899-905 ◽  
Author(s):  
FRANCESCO PISTELLI ◽  
MATTEO BOTTAI ◽  
GIOVANNI VIEGI ◽  
FRANCESCO DI PEDE ◽  
LAURA CARROZZI ◽  
...  

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.


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