scholarly journals Lung elastic recoil during breathing at increased lung volume

1999 ◽  
Vol 87 (4) ◽  
pp. 1491-1495 ◽  
Author(s):  
Joseph R. Rodarte ◽  
Gassan Noredin ◽  
Charles Miller ◽  
Vito Brusasco ◽  
Riccardo Pellegrino ◽  
...  

During dynamic hyperinflation with induced bronchoconstriction, there is a reduction in lung elastic recoil at constant lung volume (R. Pellegrino, O. Wilson, G. Jenouri, and J. R. Rodarte. J. Appl. Physiol. 81: 964–975, 1996). In the present study, lung elastic recoil at control end inspiration was measured in normal subjects in a volume displacement plethysmograph before and after voluntary increases in mean lung volume, which were achieved by one tidal volume increase in functional residual capacity (FRC) with constant tidal volume and by doubling tidal volume with constant FRC. Lung elastic recoil at control end inspiration was significantly decreased by ∼10% within four breaths of increasing FRC. When tidal volume was doubled, the decrease in computed lung recoil at control end inspiration was not significant. Because voluntary increases of lung volume should not produce airway closure, we conclude that stress relaxation was responsible for the decrease in lung recoil.

Author(s):  
Billy L. Luu ◽  
Rhys J. McDonald ◽  
Bart Bolsterlee ◽  
Martin E. Heroux ◽  
Jane E. Butler ◽  
...  

An object tracking algorithm was used on computed tomography (CT) images of the thorax from six healthy participants and nine participants with chronic obstructive pulmonary disease (COPD) to describe the movement of the ribs between the static lung volumes of functional residual capacity (FRC) and total lung capacity (TLC). The continuous motion of the ribs during tidal breathing was also described using four-dimensional CT datasets from seven participants with thoracic esophageal malignancies. Rib motion was defined relative to a local joint coordinate system where rotations about the axes that predominantly affected the anteroposterior and transverse diameters of the rib cage were referred to as pump-handle and bucket-handle movements, respectively. Between TLC and FRC, pump-handle movements were 1.8 times larger in healthy participants than in participants with COPD, in line with their 1.6 times larger inspiratory capacities. However, when rib motion was normalized to the change in lung volume, pump-handle movements were similar for healthy and COPD participant groups. We found no differences in bucket-handle movements between participant groups before and after normalization. Pump-handle movement was the dominant rib motion between FRC and TLC, on average four times greater than bucket-handle movement in healthy participants. For expiratory tidal volume, pump-handle movements were 20% smaller than bucket-handle movements. When normalized to tidal volume and compared to inspiratory capacity, pump-handle movements were smaller and bucket-handle movements were larger during tidal breathing. The findings suggest that the pump-handle and bucket-handle components of rib motion vary for small and large changes in lung volume.


1990 ◽  
Vol 68 (4) ◽  
pp. 1732-1738 ◽  
Author(s):  
J. L. Werchowski ◽  
M. H. Sanders ◽  
J. P. Costantino ◽  
F. C. Sciurba ◽  
R. M. Rogers

The respiratory inductance plethysmograph (RIP) has recently gained popularity in both the research and clinical arenas for measuring tidal volume (VT) and changes in functional residual capacity (delta FRC). It is important however, to define the likelihood that individual RIP measurements of VT and delta FRC would be acceptably accurate (+/- 10%) for clinical and investigational purposes in spontaneously breathing individuals on continuous positive airway pressure (CPAP). Additionally, RIP accuracy has not been compared in these regards after calibration by two commonly employed techniques, the least squares (LSQ) and the quantitative diagnostic calibration (QDC) methods. We compared RIP with pneumotachographic (PTH) measurements of delta FRC and VT during spontaneous mouth breathing on 0-10 cmH2O CPAP. Comparisons were made after RIP calibration with both the LSQ (6 subjects) and QDC (7 subjects) methods. Measurements of delta FRC by RIPLSQ and RIPQDC were highly correlated with PTH measurements (r = 0.94 +/- 0.04 and r = 0.98 +/- 0.01 (SE), respectively). However, only an average of 30% of RIPQDC determinations per subject and 31.4% of RIPLSQ determinations per subject were accurate to +/- 10% of PTH values. An average of 55.2% (QDC) and 68.8% (LSQ) of VT determinations per subject were accurate to +/- 10% of PTH values. We conclude that in normal subjects, over a large number of determinations, RIP values for delta FRC and VT at elevated end-expiratory lung volume correlate well with PTH values. However, regardless of whether QDC or LSQ calibration is used, only about one-third of individual RIP determinations of delta FRC and one-half of two-thirds of VT measurements will be sufficiently accurate for clinical and investigational use.


1988 ◽  
Vol 65 (6) ◽  
pp. 2679-2686 ◽  
Author(s):  
S. T. Kariya ◽  
S. A. Shore ◽  
W. A. Skornik ◽  
K. Anderson ◽  
R. H. Ingram ◽  
...  

The maximal effect induced by methacholine (MCh) aerosols on pulmonary resistance (RL), and the effects of altering lung volume and O3 exposure on these induced changes in RL, was studied in five anesthetized and paralyzed dogs. RL was measured at functional residual capacity (FRC), and lung volumes above and below FRC, after exposure to MCh aerosols generated from solutions of 0.1-300 mg MCh/ml. The relative site of response was examined by magnifying parenchymal [RL with large tidal volume (VT) at fast frequency (RLLS)] or airway effects [RL with small VT at fast frequency (RLSF)]. Measurements were performed on dogs before and after 2 h of exposure to 3 ppm O3. MCh concentration-response curves for both RLLS and RLSF were sigmoid shaped. Alterations in mean lung volume did not alter RLLS; however, RLSF was larger below FRC than at higher lung volumes. Although O3 exposure resulted in small leftward shifts of the concentration-response curve for RLLS, the airway dominated index of RL (RLSF) was not altered by O3 exposure, nor was the maximal response using either index of RL. These data suggest O3 exposure does not affect MCh responses in conducting airways; rather, it affects responses of peripheral contractile elements to MCh, without changing their maximal response.


1989 ◽  
Vol 67 (4) ◽  
pp. 1438-1442 ◽  
Author(s):  
G. A. Farkas ◽  
M. Estenne ◽  
A. De Troyer

A change from the supine to the head-up posture in anesthetized dogs elicits increased phasic expiratory activation of the rib cage and abdominal expiratory muscles. However, when this postural change is produced over a 4- to 5-s period, there is an initial apnea during which all the muscles are silent. In the present studies, we have taken advantage of this initial silence to determine functional residual capacity (FRC) and measure the subsequent change in end-expiratory lung volume. Eight animals were studied, and in all of them end-expiratory lung volume in the head-up posture decreased relative to FRC [329 +/- 70 (SE) ml]. Because this decrease also represents the increase in lung volume as a result of expiratory muscle relaxation at the end of the expiratory pause, it can be used to determine the expiratory muscle contribution to tidal volume (VT). The average contribution was 62 +/- 6% VT. After denervation of the rib cage expiratory muscles, the reduction in end-expiratory lung volume still amounted to 273 +/- 84 ml (49 +/- 10% VT). Thus, in head-up dogs, about two-thirds of VT result from the action of the expiratory muscles, and most of it (83%) is due to the action of the abdominal rather than the rib cage expiratory muscles.


1989 ◽  
Vol 66 (2) ◽  
pp. 606-612 ◽  
Author(s):  
S. Bellofiore ◽  
D. H. Eidelman ◽  
P. T. Macklem ◽  
J. G. Martin

We examined the effects of elastase-induced emphysema on lung volumes, pulmonary mechanics, and airway responses to inhaled methacholine (MCh) of nine male Brown Norway rats. Measurements were made before and weekly for 4 wk after elastase in five rats. In four rats measurements were made before and at 3 wk after elastase; in these same animals the effects of changes in end-expiratory lung volume on the airway responses to MCh were evaluated before and after elastase. Airway responses were determined from peak pulmonary resistance (RL) calculated after 30-s aerosolizations of saline and doubling concentrations of MCh from 1 to 64 mg/ml. Porcine pancreatic elastase (1 IU/g) was administered intratracheally. Before elastase RL rose from 0.20 +/- 0.02 cmH2O.ml-1.s (mean +/- SE; n = 9) to 0.57 +/- 0.06 after MCh (64 mg/ml). A plateau was observed in the concentration-response curve. Static compliance and the maximum increase in RL (delta RL64) were significantly correlated (r = 0.799, P less than 0.01). Three weeks after elastase the maximal airway response to MCh was enhanced and no plateau was observed; delta RL64 was 0.78 +/- 0.07 cmH2O.ml-1.s, significantly higher than control delta RL64 (0.36 +/- 0.7, P less than 0.05). Before elastase, increase of end-expiratory lung volume to functional residual capacity + 1.56 ml (+/- 0.08 ml) significantly reduced RL at 64 mg MCh/ml from 0.62 +/- 0.05 cmH2O.ml-1.s to 0.50 +/- 0.03, P less than 0.05.(ABSTRACT TRUNCATED AT 250 WORDS)


1988 ◽  
Vol 64 (6) ◽  
pp. 2482-2489 ◽  
Author(s):  
P. Leblanc ◽  
E. Summers ◽  
M. D. Inman ◽  
N. L. Jones ◽  
E. J. Campbell ◽  
...  

The capacity of inspiratory muscles to generate esophageal pressure at several lung volumes from functional residual capacity (FRC) to total lung capacity (TLC) and several flow rates from zero to maximal flow was measured in five normal subjects. Static capacity was 126 +/- 14.6 cmH2O at FRC, remained unchanged between 30 and 55% TLC, and decreased to 40 +/- 6.8 cmH2O at TLC. Dynamic capacity declined by a further 5.0 +/- 0.35% from the static pressure at any given lung volume for every liter per second increase in inspiratory flow. The subjects underwent progressive incremental exercise to maximum power and achieved 1,800 +/- 45 kpm/min and maximum O2 uptake of 3,518 +/- 222 ml/min. During exercise peak esophageal pressure increased from 9.4 +/- 1.81 to 38.2 +/- 5.70 cmH2O and end-inspiratory esophageal pressure increased from 7.8 +/- 0.52 to 22.5 +/- 2.03 cmH2O from rest to maximum exercise. Because the estimated capacity available to meet these demands is critically dependent on end-inspiratory lung volume, the changes in lung volume during exercise were measured in three of the subjects using He dilution. End-expiratory volume was 52.3 +/- 2.42% TLC at rest and 38.5 +/- 0.79% TLC at maximum exercise.


1998 ◽  
Vol 84 (2) ◽  
pp. 726-732 ◽  
Author(s):  
Andy Adler ◽  
Norihiro Shinozuka ◽  
Yves Berthiaume ◽  
Robert Guardo ◽  
Jason H. T. Bates

Adler, Andy, Norihiro Shinozuka, Yves Berthiaume, Robert Guardo, and Jason H. T. Bates. Electrical impedance tomography can monitor dynamic hyperinflation in dogs. J. Appl. Physiol. 84(2): 726–732, 1998.—We assessed in eight dogs the accuracy with which electrical impedance tomography (EIT) can monitor changes in lung volume by comparing the changes in mean lung conductivity obtained with EIT to changes in esophageal pressure (Pes) and to airway opening pressure (Pao) measured after airway occlusion. The average volume measurement errors were determined: 26 ml for EIT; 35 ml for Pao; and 54 ml for Pes. Subsequently, lung inflation due to applied positive end-expiratory pressure was measured by EIT (ΔVEIT) and Pao (ΔVPao) under both inflation and deflation conditions. Whereas ΔVPaowas equal under both conditions, ΔVEITwas 28 ml greater during deflation than inflation, indicating that EIT is sensitive to lung volume history. The average inflation ΔVEITwas 67.7 ± 78 ml greater than ΔVPao, for an average volume increase of 418 ml. Lung inflation due to external expiratory resistance was measured during ventilation by EIT (ΔVEIT,vent) and Pes (ΔVPes,vent) and at occlusion by EIT (ΔVEIT,occl), Pes, and Pao. The average differences between EIT estimates and ΔVEIT,occlwere 5.8 ± 44 ml for ΔVEIT,ventand 49.5 ± 34 ml for ΔVEIT,occl. The average volume increase for all dogs was 442.2 ml. These results show that EIT can provide usefully accurate estimates of changes in lung volume over an extended time period and that the technique has promise as a means of conveniently and noninvasively monitoring lung hyperinflation.


1959 ◽  
Vol 14 (4) ◽  
pp. 499-506 ◽  
Author(s):  
K. Tokuyasu ◽  
A. Coblentz ◽  
H. R. Bierman

Estimation of pulmonary ventilation was attempted by measuring the elimination of nitrogen and helium with the mass spectrometer. Exhalatory concentrations of nitrogen and helium were continuously recorded in each of 12 normal subjects and 10 patients with pulmonary enphysema or space-occupying pulmonary lesions. Uniform values for both slow and rapid uneven ventilation were found in all normal subjects but always less than in emphysematous states. Ratios of effective tidal volume (Vt) and alveolar ventilation volume (f·Vt) to functional residual capacity P = Vt/Vr and Q = f·Vt/Vr were one half or less than those in the normal subject. Smaller values of uneven ventilation were found for helium than nitrogen. Data computed by the theory of 'periodic' ventilation gave greater values for uneven ventilation (Q) and more accurately represented the physiologic conditions than derived by ‘continuous’ ventilation. Submitted on August 7, 1958


1980 ◽  
Vol 48 (5) ◽  
pp. 794-798 ◽  
Author(s):  
T. C. Lloyd ◽  
J. A. Cooper

Using anesthetized spontaneously breathing dogs, we compared the respiratory effects of tracheal distension with the effects of changes in lung volume before and after vagotomy. We used an endotracheal tube with a long cuff to distend the trachea to pressures of 10, 20, and 40 cmH2O. Lung volume increases were imposed by expiratory threshold loading, and volume was decreased by abdominal compression, both of which caused outward rib cage displacement. During expiratory loading, the tidal volume was unchanged but respiratory frequency and minute volume fell and an active expiratory effort appeared; whereas frequency and minute volume rose, but tidal volume fell during abdominal compression. Tracheal distension evoked no discernible change in breathing. Following vagotomy, tidal volume and minute volume fell, and frequency rose slightly, during expiratory loading but abdominal compression was without effect. After vagotomy, 40 cmH2O tracheal distension caused a slight frequency increase. We concluded that the potential role of tracheal deformation in the reflex control of breathing is insignificant in comparison with the other airways.


1985 ◽  
Vol 68 (2) ◽  
pp. 215-225 ◽  
Author(s):  
A. J. Winning ◽  
R. D. Hamilton ◽  
S. A. Shea ◽  
C. Knott ◽  
A. Guz

1. The effect on ventilation of airway anaesthesia, produced by the inhalation of a 5% bupivacaine aerosol (aerodynamic mass median diameter = 4.77 μm), was studied in 12 normal subjects. 2. The dose and distribution of the aerosol were determined from lung scans after the addition to bupivacaine of 99mTc. Bupivacaine labelled in this way was deposited primarily in the central airways. The effectiveness and duration of airway anaesthesia were assessed by the absence of the cough reflex to the inhalation of three breaths of a 5% citric acid aerosol. Airway anaesthesia always lasted more than 20 min. 3. Resting ventilation was measured, by respiratory inductance plethysmography, before and after inhalation of saline and bupivacaine aerosols. The ventilatory response to maximal incremental exercise and, separately, to CO2 inhalation was studied after the inhalation of saline and bupivacaine aerosols. Breathlessness was quantified by using a visual analogue scale (VAS) during a study and by questioning on its completion. 4. At rest, airway anaesthesia had no effect on mean tidal volume (VT), inspiratory time (Ti), expiratory time (Te) or end-tidal Pco2, although the variability of tidal volume was increased. On exercise, slower deeper breathing was produced and breathlessness was reduced. The ventilatory response to CO2 was increased. 5. The results suggest that stretch receptors in the airways modulate the pattern of breathing in normal man when ventilation is stimulated by exercise; their activation may also be involved in the genesis of the associated breathlessness. 6. A hypothesis in terms of a differential airway/alveolar receptor block, is proposed to explain the exaggerated ventilatory response to CO2.


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