Inspiratory Flow Rate and Ventilation Distribution in Normal Subjects and in Patients with Simple Chronic Bronchitis

1972 ◽  
Vol 43 (5) ◽  
pp. 583-595 ◽  
Author(s):  
J. M. B. Hughes ◽  
B. J. B. Grant ◽  
R. E. Greene ◽  
L. D. Iliff ◽  
J. Milic-Emili
Keyword(s):  
Airway Resistance ◽  
Bolus Injection ◽  
Normal Subjects ◽  
Breath Holding ◽  
Ventilation Distribution ◽  
Inspiratory Flow Rate ◽  
Flow Rates ◽  
History Of ◽  
Fast Flow ◽  
Volume History

1. Seated subjects stopped ventilation briefly at end expiration while a 5 ml bolus of 133Xe was injected close to the mouth. They then inspired air at different flow rates and the distribution of radioactivity in the lungs was measured with a scanning technique during a period of breath-holding at maximal inspiration. 2. In five normal subjects the dependent zones received a greater fraction of the 133Xe bolus than the apex during slow inspirations, but apical distribution exceeded basal for fast inspirations. The volume history of the lungs before the bolus injection had no effect on the slow/fast difference in four out of five subjects. 3. In five patients with clinical bronchitis but normal forced expired volume, dependent zone ventilation was much reduced on a slow inspiration compared with normals, but at fast flow rates the distribution was normal. 4. Insofar as the bolus in the fast inspiration was distributed according to regional airway conductances, these results suggest that in normal subjects differences in airway resistance exist between the upper and lower zones of the upright lung. An early abnormality in bronchitis appears to be a reduction of compliance in the dependent zones, as judged from the decrease in basal ventilation on a slow inspiration.

scholarly journals Simultaneous measurement of nitric oxide production by conducting and alveolar airways of humans

1999 ◽  
Vol 87 (4) ◽  
pp. 1532-1542 ◽  
Author(s):  
Anthony P. Pietropaoli ◽  
Irene B. Perillo ◽  
Alfonso Torres ◽  
Peter T. Perkins ◽  
Lauren M. Frasier ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Normal Subjects ◽  
Breath Holding ◽  
No Production ◽  
Large Contribution ◽  
Flow Rates ◽  
Expiratory Flow ◽  
Human Airways ◽  
Conducting Airways ◽  
Expiratory Flow Rates

Human airways produce nitric oxide (NO), and exhaled NO increases as expiratory flow rates fall. We show that mixing during exhalation between the NO produced by the lower, alveolar airways (V˙l NO) and the upper conducting airways (V˙u NO) explains this phenomenon and permits measurement ofV˙l NO,V˙u NO, and the NO diffusing capacity of the conducting airways (Du NO). After breath holding for 10–15 s the partial pressure of alveolar NO (Pa) becomes constant, and during a subsequent exhalation at a constant expiratory flow rate the alveoli will deliver a stable amount of NO to the conducting airways. The conducting airways secrete NO into the lumen (V˙u NO), which mixes with Pa during exhalation, resulting in the observed expiratory concentration of NO (Pe). At fast exhalations, Pa makes a large contribution to Pe, and, at slow exhalations, NO from the conducting airways predominates. Simple equations describing this mixing, combined with measurements of Pe at several different expiratory flow rates, permit calculation of Pa,V˙u NO, and Du NO.V˙l NOis the product of Pa and the alveolar airway diffusion capacity for NO. In seven normal subjects, Pa = 1.6 ± 0.7 × 10−6 (SD) Torr,V˙l NO= 0.19 ± 0.07 μl/min,V˙u NO= 0.08 ± 0.05 μl/min, and Du NO = 0.4 ± 0.4 ml ⋅ min−1 ⋅ Torr−1. These quantitative measurements ofV˙l NOandV˙u NOare suitable for exploring alterations in NO production at these sites by diseases and physiological stresses.

“Alveolar plateau” of the single breath nitrogen elimination curve in normal subjects

1959 ◽  
Vol 14 (1) ◽  
pp. 105-108 ◽  
Author(s):  
Ingemar Kjellmer ◽  
Lars Sandqvist ◽  
Erik Berglund
Keyword(s):  
Flow Rate ◽  
Normal Subjects ◽  
Holding Time ◽  
Breath Holding ◽  
Flow Rates ◽  
Alveolar Plateau ◽  
Single Breath ◽  
The Difference ◽  
Nitrogen Elimination ◽  
Elimination Curve

The single breath N2 elimination test, as standardized by Comroe and Fowler, has been used in normal subjects. The N2 difference, i.e. the difference in N2 concentration between Ve = 1250 and Ve = 750 ml, showed a tendency to increase with increasing volumes of inspired O2 and with increasing inspiratory flow rates. It decreased with increasing breath-holding time and was not consistently influenced by expiratory flow rate. The findings are compared with those of Fowler and of Shephard on normal subjects; different results were obtained, largely depending on different analytical procedures. These factors must be considered when evaluating results in patients. Submitted on July 21, 1958

Importance of inspiratory flow rate in the cough response to citric acid inhalation in normal subjects

1990 ◽  
Vol 78 (5) ◽  
pp. 521-525 ◽  
Author(s):  
Manuel J. Barros ◽  
Stefano J. Zammattio ◽  
P. John Rees
Keyword(s):  
Citric Acid ◽  
Flow Rate ◽  
Geometric Mean ◽  
Normal Subjects ◽  
Forced Expiratory Volume ◽  
Inspiratory Flow ◽  
Inspiratory Flow Rate ◽  
Flow Rates ◽  
Cough Response ◽  
The Mean

1. The cough response to inhalation of citric acid is produced mainly by irritation of the larynx and trachea. Variations in the inspiratory flow rate might lead to changes in deposition of the drug, and consequently in the cough threshold. 2. We have studied the effect of three different inspiratory flow rates in 11 normal, non-smoking subjects (nine males, aged 23–39 years), who inhaled nebulized citric acid (2.5–640 mg/l). The test finished when a cough. was produced at each inhalation (cough threshold) or the maximum concentration was reached. 3. The inspiratory flow rate was limited with a fixed resistance and displayed on a screen so that the subjects could reach a constant inspiratory flow rate of 50, 100 and 150 l/min with a submaximal inspiratory effort. 4. The mean (sd) inspiratory flow rates achieved were 51.4 (5.3), 86.2 (16.6) and 134.4 (22.9) l/min. Baseline forced expiratory volume in 1 s and functional vital capacity were not different on the 3 study days. 5. The cough threshold (geometric mean and 95% confidence intervals) was 21 (9–54) mg/l at an inspiratory flow rate of 50 l/min and 43 (13–141) mg/l at 150 l/min (P <0.05). The amount of drug tolerated by the subjects before the cough threshold was achieved was 5.2 (2.0–13.8) mg at an inspiratory flow rate of 50 l/min and 11.6 (3.4–39.8) mg at 150 l/min (P <0.05). The number of coughs per inhalation was 1.6 (1.1–2.0) at an inspiratory flow rate of 50 l/min and 1.1 (0.7–1.5) at 150 l/min (P <0.05). 6. We conclude that lower inspiratory flow rates were associated with a greater cough stimulus in the citric acid challenge procedure used in this study. This may be related to increased laryngeal deposition. The inspiratory flow rate is a variable which should be controlled in the performance of cough challenges with citric acid.

Influence of passive changes of lung volume on upper airways

1990 ◽  
Vol 68 (5) ◽  
pp. 2159-2164 ◽  
Author(s):  
F. Series ◽  
Y. Cormier ◽  
M. Desmeules
Keyword(s):  
Lung Volume ◽  
Airway Resistance ◽  
Upper Airway ◽  
Normal Subjects ◽  
Base Line ◽  
Nasal Resistance ◽  
Inspiratory Flow Rate ◽  
Upper Airways ◽  
Lung Volumes ◽  
Bias Flow

The total upper airway resistances are modified during active changes in lung volume. We studied nine normal subjects to assess the influence of passive thoracopulmonary inflation and deflation on nasal and pharyngeal resistances. With the subjects lying in an iron lung, lung volumes were changed by application of an extrathoracic pressure (Pet) from 0 to 20 (+Pet) or -20 cmH2O (-Pet) in 5-cmH2O steps. Upper airway pressures were measured with two low-bias flow catheters, one at the tip of the epiglottis and the other in the posterior nasopharynx. Breath-by-breath resistance measurements were made at an inspiratory flow rate of 300 ml/s at each Pet step. Total upper airway, nasal, and pharyngeal resistances increased with +Pet [i.e., nasal resistance = 139.6 +/- 14.4% (SE) of base-line and pharyngeal resistances = 189.7 +/- 21.1% at 10 cmH2O of +Pet]. During -Pet there were no significant changes in nasal resistance, whereas pharyngeal resistance decreased significantly (pharyngeal resistance = 73.4 +/- 7.4% at -10 cmH2O). We conclude that upper airway resistance, particularly the pharyngeal resistance, is influenced by passive changes in lung volumes, especially pulmonary deflation.

Effect of volume history on successive partial expiratory flow-volume maneuvers

1976 ◽  
Vol 41 (2) ◽  
pp. 153-158 ◽  
Author(s):  
J. J. Wellman ◽  
R. Brown ◽  
R. H. Ingram ◽  
J. Mead ◽  
E. R. McFadden
Keyword(s):  
Static Pressure ◽  
Normal Subjects ◽  
Flow Volume ◽  
Elastic Recoil ◽  
Flow Rates ◽  
Recoil Pressure ◽  
Maximal Expiratory Flow ◽  
Expiratory Flow ◽  
Expiratory Flow Rates ◽  
Volume History

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.

Effect of airway closure on ventilation distribution

1989 ◽  
Vol 66 (6) ◽  
pp. 2511-2515 ◽  
Author(s):  
A. B. Crawford ◽  
D. J. Cotton ◽  
M. Paiva ◽  
L. A. Engel
Keyword(s):  
Normal Subjects ◽  
Phase Iii ◽  
Mixing Efficiency ◽  
Breath Holding ◽  
Airway Closure ◽  
Ventilation Distribution ◽  
Residual Capacity ◽  
Lung Periphery ◽  
Phase Iii Slope ◽  
Volume Range

We examined the effect of airway closure on ventilation distribution during tidal breathing in six normal subjects. Each subject performed multiple-breath N2 washouts (MBNW) at tidal volumes of 1 liter over a range of preinspiratory lung volumes (PILV) from functional residual capacity (FRC) to just above residual volume. All subjects performed washouts at PILV below their measured closing capacity. In addition five of the subjects performed MBNW at PILV below closing capacity with end-inspiratory breath holds of 2 or 5 s. We measured the following two independent indexes of ventilation maldistribution: 1) the normalized phase III slope of the final breaths of the washout (Snf) and 2) the alveolar mixing efficiency of those breaths of the washout where 80–90% of the initial N2 had been cleared. Between a mean PILV of 0.28 liter above closing capacity and that 0.31 liter below closing capacity, mean Snf increased by 132% (P less than 0.005). Over the same volume range, mean alveolar mixing efficiency decreased by 3.3% (P less than 0.05). Breath holding at PILV below closing capacity resulted in marked and consistent decreases in Snf and increases in alveolar mixing efficiency. Whereas inhomogeneity of ventilation decreases with lung volume when all airways are patent (J. Appl. Physiol. 66: 2502–2510, 1989), airway closure increases ventilation inequality, and this is substantially reduced by short end-inspiratory breath holds. These findings suggest that the predominant determinant of ventilation distribution below closing capacity is the inhomogeneous closure of airways subtending regions in the lung periphery that are close together.

Role of the parasympathetic nervous system in acute lung response to ozone

1985 ◽  
Vol 59 (6) ◽  
pp. 1879-1885 ◽  
Author(s):  
W. S. Beckett ◽  
W. F. McDonnell ◽  
D. H. Horstman ◽  
D. E. House
Keyword(s):  
Nervous System ◽  
Airway Resistance ◽  
Parasympathetic Nervous System ◽  
Normal Subjects ◽  
Lung Mechanics ◽  
Flow Rates ◽  
Forced Expiratory Flow ◽  
Expiratory Flow ◽  
Expiratory Flow Rates

We conducted an ozone (O3) exposure study using atropine, a muscarinic receptor blocker, to determine the role of the parasympathetic nervous system in the acute response to O3. Eight normal subjects with predetermined O3 responsiveness were randomly assigned an order for four experimental exposures. For each exposure a subject inhaled either buffered saline or atropine aerosol followed by exposure either to clean air or 0.4 ppm O3. Measurements of lung mechanics, ventilatory response to exercise, and symptoms were obtained before and after exposure. O3 exposure alone resulted in significant changes in specific airway resistance, forced vital capacity (FVC), forced expiratory flow rates, tidal volume (VT), and respiratory rate (f). Atropine pretreatment prevented the significant increase in airway resistance with O3 exposure and partially blocked the decrease in forced expiratory flow rates but did not prevent a significant fall in FVC, changes in f and VT, or the frequency of reported respiratory symptoms after O3. These results suggest that the increase in pulmonary resistance during O3 exposure is mediated by a parasympathetic mechanism and that changes in other measured variables are mediated, at least partially, by mechanisms not dependent on muscarinic cholinergic receptors of the parasympathetic nervous system.

Effect of volume history on changes in DLcoSB-3EQ with lung volume in normal subjects

1992 ◽  
Vol 73 (2) ◽  
pp. 434-439 ◽  
Author(s):  
D. J. Cotton ◽  
F. Taher ◽  
J. T. Mink ◽  
B. L. Graham
Keyword(s):  
Lung Volume ◽  
Normal Subjects ◽  
Breath Holding ◽  
Diffusing Capacity ◽  
Tidal Breathing ◽  
Inspiratory Capacity ◽  
Deep Breath ◽  
Residual Capacity ◽  
The Relationship ◽  
Volume History

The purpose of this study was to determine the relationship between the three-equation diffusing capacity for carbon monoxide (DLcoSB-3EQ) and lung volume and to determine how this relationship was altered when maneuvers were immediately preceded by a deep breath. DLcoSB-3EQ maneuvers were performed in nine healthy subjects either immediately after a deep breath or after tidal breathing for 10 min. The maneuvers consisted of slow inhalation of test gas from functional residual capacity to 25, 50, 75, or 100% of the inspiratory capacity and, without breath holding, slow exhalation to residual volume. After either a deep breath or tidal breathing, we found that DLcoSB-3EQ decreased nonlinearly with decreasing lung volume. At all lung volumes, DLcoSB-3EQ was significantly greater when measured after a deep breath than after tidal breathing. This effect increased as lung volume decreased, so that the greatest difference between DLcoSB-3EQ after a deep breath and that after tidal breathing occurred at the lowest lung volume. We conclude that a deep breath or spontaneous sigh has a role in reestablishing the pathway for gas exchange during tidal breathing.

Effect of breath holding on ventilation maldistribution during tidal breathing in normal subjects

1986 ◽  
Vol 61 (6) ◽  
pp. 2108-2115 ◽  
Author(s):  
A. B. Crawford ◽  
M. Makowska ◽  
S. Kelly ◽  
L. A. Engel
Keyword(s):  
Dead Space ◽  
Normal Subjects ◽  
Breath Holding ◽  
Constant Flow ◽  
Tidal Breathing ◽  
Flow Rates ◽  
Ventilation Inhomogeneity ◽  
Delta Sigma ◽  
Rate Of Increase ◽  
The Mean

To test the hypothesis that during the course of a multiple-breath N2 washout (MBNW) diffusion-dependent ventilation maldistribution is more apparent in the early breaths, whereas convection-dependent maldistribution predominates in the later breaths, we performed MBNW with 0-, 1-, and 4-s end-inspiratory breath holds (BH0, BH1, BH4, respectively) in five normal subjects. Each subject breathed with a constant tidal volume of 1 liter, at 10–12 breaths/min and at constant flow rates. For each breath we computed the slope of the alveolar plateau normalized by the mean expired N2 concentration (Sn), the Bohr dead space (VDB), and an index analogous to the Fowler dead space (V50). In all five subjects, Sn, VDB, and V50 decreased with breath holding, indicating diffusion dependence of these indexes. Over the first five breaths the rate of increase of Sn as a function of cumulative expired volume (delta Sn/delta sigma VE) decreased by 29 and 54% during BH1 and BH4, respectively, compared with BH0. In contrast, from breath 5 to the end of the washout there was no significant change in delta Sn/delta sigma VE during BH1 and BH4 compared with BH0. Our results provide further experimental support for the hypothesis that the increase of Sn as a function of cumulative expired volume after the fifth breath constitutes a diffusion-independent index of ventilation inhomogeneity. It therefore reflects alveolar gas inequalities among larger units.(ABSTRACT TRUNCATED AT 250 WORDS)

Stellar Evolution

1962 ◽  
Vol 11 (02) ◽  
pp. 137-143
Author(s):  
M. Schwarzschild
Keyword(s):  
Solar System ◽  
Stellar Evolution ◽  
Space Craft ◽  
New Techniques ◽  
Substantial Body ◽  
Individual Stars ◽  
The Past ◽  
Evolution Of Galaxies ◽  
History Of ◽  
Fast Flow

It is perhaps one of the most important characteristics of the past decade in astronomy that the evolution of some major classes of astronomical objects has become accessible to detailed research. The theory of the evolution of individual stars has developed into a substantial body of quantitative investigations. The evolution of galaxies, particularly of our own, has clearly become a subject for serious research. Even the history of the solar system, this close-by intriguing puzzle, may soon make the transition from being a subject of speculation to being a subject of detailed study in view of the fast flow of new data obtained with new techniques, including space-craft.

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