Effects of posture on flow-volume curve configuration in normal humans

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.

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.


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.


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.


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.


1989 ◽  
Vol 111 (3) ◽  
pp. 192-199 ◽  
Author(s):  
D. Elad ◽  
R. D. Kamm

Numerical calculations were performed to study the influence of several physiologic parameters on a forced expiration. It was found that the axial distribution of airway compliance produced profound changes in the detailed flow pattern, as characterized by the axial distributions of speed index and area ratio, but had little effect on the flow-volume curve. Similar results were obtained when the expression for frictional losses was changed to reflect new experimental results. In contrast, changes in airway size and geometry altered both the detailed flow pattern and the mean expiratory flow rate. The shape of the flow-volume curve remained unchanged.


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.


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.


1979 ◽  
Vol 46 (5) ◽  
pp. 867-871 ◽  
Author(s):  
A. Vinegar ◽  
E. E. Sinnett ◽  
D. E. Leith

Awake mice (22.6--32.6 g) were anesthetized intravenously during head-out body plethysmography. One minute after pentobarbital sodium anesthesia, tidal volume had fallen from 0.28 +/- 0.04 to 0.14 +/- 0.02 ml and frequency from 181 +/- 20 to 142 +/- 8. Functional residual capacity (FRC) decreased by 0.10 +/- 0.02 ml. Expiratory flow-volume curves were linear, highly repeatable, and submaximal over substantial portions of expiration in awake and anesthetized mice; and expiration was interrupted at substantial flows that abruptly fell to and crossed zero as inspiration interrupted relaxed expiration. FRC is maintained at a higher level in awake mice due to a higher tidal volume and frequency coupled with expiratory braking (persistent inspiratory muscle activity or increased glottal resistance). In anesthetized mice, the absence of braking, coupled with reductions in tidal volume and frequency and a prolonged expiratory period, leads to FRCs that approach relaxation volume (Vr). An equation in derived to express the difference between FRC and Vr in terms of the portion of tidal volume expired without braking, the slope of the linear portion of the expiratory flow-volume curve expressed as V/V, the time fraction of one respiratory cycle spent in unbraked expiration, and respiratory frequency.


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