Pulmonary mechanics during exercise in subjects with chronic airflow obstruction

1980 ◽  
Vol 49 (3) ◽  
pp. 511-515 ◽  
Author(s):  
D. G. Stubbing ◽  
L. D. Pengelly ◽  
J. L. Morse ◽  
N. L. Jones

A body plethysmograph was used to measure pulmonary mechanics in six subjects with chronic airflow obstruction during steady states at rest and during exercise at 200 and 400 kpm . min-1. The mean forced expired volume in 1 s was 1.32 liters (39.2% predicted). The flow rates during tidal breathing reached the maximum expiratory flow-volume (MEFV) curve in all but one subject, and on exercise they all reached the MEFV curve. Total lung capacity did not change significantly, but functional residual capacity increased to 104% of the control value (P less than 0.05) and residual volume increased to 113.3% of the control value (P less than 0.02). The MEFV curves did not change and tidal flow rates in excess of th MEFV curve were not seen. Dynamic compliance fell with increasing exercise to 52.8% (P less than 0.01) and static expiratory pulmonary compliance to 90.2% of the control value. Transpulmonary pressures during tidal breathing when expiratory flow reached the MEFV curve increased to progressively higher values as the work load increased. At low work loads there were several subjects with negative transpulmonary pressure when maximum flow rates were present. In patients with chronic airflow obstruction, little change occurs during exercise in pulmonary mechanics; the tidal flow patterns are dominated by the expired flow-volume curve, which is not changed by exercise; maximum flow occurs in some patients when transpulmonary pressure is still negative.

PEDIATRICS ◽  
1971 ◽  
Vol 48 (1) ◽  
pp. 64-72
Author(s):  
Alois Zapletal ◽  
Etsuro K. Motoyama ◽  
Lewis E. Gibson ◽  
Arend Bouhuys

Maximum expiratory flow rates on flow-volume curves are often decreased below normal limits in children with asthma or cystic fibrosis who are clinically well and whose standard spirometric tests are within normal limits. In particular, maximum flow rates at small lung volumes (25% of vital capacity) are decreased. Maximum expiratory flow-volume (MEFV) curves provide a sensitive and quantitative assessment of small airway obstruction in these and other obstructive lung conditions.


1982 ◽  
Vol 52 (2) ◽  
pp. 346-351 ◽  
Author(s):  
N. Berend ◽  
W. M. Thurlbeck

Pressure-volume and maximum expiratory flow-volume curves with air and a He-O2 mixture were performed in 25 excised human lungs. Small airway dimensions were measured, and the degree of various small airway lesions and emphysema was graded. Correlations were then made between the maximum flow (Vmax) at a transpulmonary pressure (PL) of 5 cmH2O and these measurements and scores. Small airway dimensions correlated poorly with Vmax. However, significant correlations were obtained between Vmax and the inflammation score (P less than 0.05), fibrosis score (P less than 0.05), and emphysema grade (P less than 0.01) but not smooth muscle hyperplasia or pigmentation. Neither the increase in flow with He-O2 nor the volume of flow correlated significantly with any small airway measurement or score.


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.


1980 ◽  
Vol 49 (3) ◽  
pp. 506-510 ◽  
Author(s):  
D. G. Stubbing ◽  
L. D. Pengelly ◽  
J. L. Morse ◽  
N. L. Jones

A body plethysmograph adapted to contain the pedals of an electrically braked cycle ergometer was used to measure pulmonary mechanics during steady-state exercise in 12 normal male subjects aged 22-65 yr. During exercise there was a progressive increase in residual volume to 119% of the value at rest (P less than 0.01), but functional residual capacity and total lung capacity did not change. The maximum expiratory flow-volume (MEFV) curves did not change and flow rates during tidal breathing did not exceed the MEFV curve. Dynamic pulmonary compliance fell to 91.3% of the control value and static expiratory pulmonary compliance fell to 76.9% of the control value (P less than 0.05). Pulmonary resistance did not change during exercise. Transpulmonary pressure during tidal breathing was negative even at the highest power outputs. The fall in compliance may be due to an increase in pulmonary capillary blood volume. These results demonstrate the importance of measuring absolute thoracic gas volume and the elastic properties of the lung when comparing pulmonary mechanics at rest and during exercise.


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

1993 ◽  
Vol 74 (6) ◽  
pp. 2681-2686 ◽  
Author(s):  
R. Pellegrino ◽  
B. Violante ◽  
E. Crimi ◽  
V. Brusasco

To investigate whether histamine (His) and methacholine (MCh) have different effects on airways and lung parenchyma, 11 healthy subjects were given aerosol MCh until a response plateau was obtained and then two doses of His. At the plateau, forced expiratory volume in 1 s and forced expiratory flow at 40% of vital capacity from partial flow-volume curves were reduced by 19 +/- 3 (SE) and 80 +/- 4%, respectively. Aerosol His decreased forced expiratory volume in 1 s by an additional 12 +/- 1% but left partial forced expiratory flow unchanged. The bronchodilator effect of deep inhalation, as inferred from the ratio of forced expiratory flow from maximal to that from partial flow-volume curves, increased after MCh and plateaued but decreased after His. Quasi-static transpulmonary pressure-volume area determined in seven subjects was unchanged after MCh but was increased by 57 +/- 10% after His. We conclude that adding His after the response to MCh plateaued does not increase the maximal degree of bronchoconstriction but may increase parenchymal hysteresis, thus blunting the bronchodilator effect of deep inhalation. These results suggest that His and MCh have similar effects on airway smooth muscle but different effects on lung tissue properties.


1990 ◽  
Vol 69 (4) ◽  
pp. 1413-1418 ◽  
Author(s):  
G. P. Topulos ◽  
G. J. Nielan ◽  
G. M. Glass ◽  
J. J. Fredberg

Wilson et al. (J. Appl. Physiol. 59:1924-28, 1985) have asserted that interdependence of regional expiratory flows could cause differences of interregional alveolar pressures to relax to time-independent limits during forced deflation. To test the hypothesis that such limiting differences do arise, we examined regional alveolar pressures during complete and partial maximally forced deflations of six excised canine lungs. Alveolar pressures were monitored using alveolar capsules on each of six lobes during forced deflations initiated at transpulmonary pressures of 30, 20, 15, and 10 cmH2O. In all lungs and in all maneuvers, interregional heterogeneity of alveolar pressure increased rapidly early in the deflation but much less so or not at all later in the deflation. When we compared complete with partial forced deflations, 16 of 24 maneuvers in six lungs showed clear evidence that as deflation progressed the degree of heterogeneity at isovolumic points became independent of the transpulmonary pressure from which the deflation was initiated. That is, alveolar pressures relaxed to limiting interregional differences that did not depend on time elapsed from the onset of the deflation. These data offer strong evidence of the existence of limiting differences. Such behavior implies that the sequence of regional emptying is controlled by a competition of opposing influences: nonuniformities of airway and parenchymal properties promoting nonuniformity of emptying vs. interdependence of regional expiratory flows promoting uniformity. As nonuniformity of regional pressures grows so do those factors that oppose that nonuniformity. These data underscore the insensitivity of maximum expiratory flow-volume curve configuration to the underlying inhomogeneous pattern of regional lung emptying.


1976 ◽  
Vol 41 (2) ◽  
pp. 153-158 ◽  
Author(s):  
J. J. Wellman ◽  
R. Brown ◽  
R. H. Ingram ◽  
J. Mead ◽  
E. R. McFadden

In normal subjects, the second of two successive partial expiratory flow-volume (PEFV 2) curves often had higher isovolume maximal expiratory flow rates (Vmax) than the first (PEFV 1) (mean increase 30.2 +/- 13%). The higher Vmax on PEFV 2 was present only when there was a greater lung elastic recoil pressure (Pst(L)). In eight subjects the Pst(L) derived from sequential partial quasi-static pressure-volume curves, from interruption of the flow-volume maneuvers and at the start of the PEFV curves showed that isovolume upstream resistance increased although Vmax also increased after going to residual volume (RV). In four subjects the RV volume history did not change the pressure flow relationship across the upstream airways. If airways dimensions were the sole determinant of Vmax, then Vmax on PEFV 2 would be the same or smaller than on PEFV 1. That the opposite was observed in our study indicates that the increase in Pst(L), which results from parenchymal hysteresis, offsets any dimensional decrease in upstream airways due to airways hysteresis.


1978 ◽  
Vol 45 (6) ◽  
pp. 840-845 ◽  
Author(s):  
E. C. Lucey ◽  
B. R. Celli ◽  
G. L. Snider

Maximum expiratory flow was measured in 19 normal, anesthetized, tracheostomized, supine hamsters from records of forced deflation produced by the application of varying degrees of negative pressure to the tracheostomies of animals whose lungs had been previously inflated to a transpulmonary pressure (PL) of 25 cmH2O. Flow was measured with a pneumotachograph, volume with a constant-volume pressure plethysmograph and pleural surface pressure (Ppl) with a water-filled esophageal catheter. The esophageal pressure measurement overestimated Ppl and a simple technique was based on an estimate of the resting volume of the chest wall. This volume, at which the Ppl is zero, was calculated for anesthetized supine hamsters from the measurement of respiratory-system pressure and PL made independently of esophageal pressure and was found to be about 30% of vital capacity (VC). Flow limitation was present below 70% of VC with a tracheal deflation pressure of -30cmH2O. Negative effort dependence of flow was seen in small segments of the flow-volume curves. Mean +/- SD maximum expiratory flow at 50% VC was 52 +/- 9.5 ml/s or 9.1 VC/s. Upstream resistance was 0.09 +/- 0.03 cmH2O/ml per s.


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