Aerosol-derived lung morphometry: comparisons with a lung model and lung function indexes

1991 ◽  
Vol 71 (4) ◽  
pp. 1216-1224 ◽  
Author(s):  
J. D. Blanchard ◽  
J. Heyder ◽  
C. R. O'Donnell ◽  
J. D. Brain
Keyword(s):  
Vital Capacity ◽  
Total Lung Capacity ◽  
Lung Model ◽  
Breath Holding ◽  
Small Airways ◽  
Lung Capacity ◽  
Air Space ◽  
Power Law Function ◽  
Lung Morphometry ◽  
The Relationship

This study evaluated the ability of aerosol-derived lung morphometry to noninvasively probe airway and acinar dimensions. Effective air-space diameters (EAD) were calculated from the time-dependent gravitational losses of 1-microns particles from inhaled aerosol boluses during breath holding. In 17 males [33 +/- 7 (SD) yr] the relationship between EAD and volumetric penetration of the bolus into the lungs (Vp) could be expressed by the linear power-law function, log (EAD) alpha beta log (Vp). Our EAD values were consistent with Weibel's symmetric lung model A for small airways and more distal air spaces. As lung volume increased from 57 to 87% of total lung capacity (TLC), EAD at Vp of 160 and 550 cm3 increased 70 and 41%, respectively. At 57% TLC, log (EAD) at 160 cm3 was significantly correlated with airway resistance (r = -0.57, P less than 0.0204) but not with forced expired flow between 25 and 75% of vital capacity. Log (EAD) at 400 cm3 was correlated with deposition of 1-micron particles (r = -0.73, P less than 0.0009). We conclude that aerosol-derived lung morphometry is a responsive noninvasive probe of peripheral air-space diameters.

Fast vs. slow exhalation before O2 inhalation alters subsequent phase III slope

1984 ◽  
Vol 56 (1) ◽  
pp. 52-56 ◽  
Author(s):  
T. S. Hurst ◽  
B. L. Graham ◽  
D. J. Cotton
Keyword(s):  
Total Lung Capacity ◽  
Normal Subjects ◽  
Phase Iii ◽  
Breath Holding ◽  
Small Airways ◽  
Residual Volume ◽  
Lung Capacity ◽  
Single Breath ◽  
Subsequent Phase ◽  
Phase Iii Slope

We studied 10 symptom-free lifetime non-smokers and 17 smokers all with normal pulmonary function studies. All subjects performed single-breath N2 washout tests by either exhaling slowly (“slow maneuver”) from end inspiration (EI) to residual volume (RV) or exhaling maximally (“fast maneuver”) from EI to RV. After either maneuver, subjects then slowly inhaled 100% O2 to total lung capacity (TLC) and without breath holding, exhaled slowly back to RV. In the nonsmokers seated upright phase III slope of single-breath N2 test (delta N2/l) was lower (P less than 0.01) for the fast vs. the slow maneuver, but this difference disappeared when the subjects repeated the maneuvers in the supine position. In contrast, delta N2/l was higher for the fast vs. the slow maneuver (P less than 0.01) in smokers seated upright. For the slow maneuver, delta N2/l was similar between smokers and nonsmokers but for the fast maneuvers delta N2/l was higher in smokers than nonsmokers (P less than 0.01). We suggest that the fast exhalation to RV decreases delta N2/l in normal subjects by decreasing apex-to-base differences in regional ratio of RV to TLC (RV/TLC) but increases delta N2/l in smokers, because regional RV/TLC increases distal to sites of small airways obstruction when the expiratory flow rate is increased.

scholarly journals Features of glossopharyngeal breathing in breath-hold divers

2006 ◽  
Vol 101 (3) ◽  
pp. 799-801 ◽  
Author(s):  
Leigh M. Seccombe ◽  
Peter G. Rogers ◽  
Nghi Mai ◽  
Chris K. Wong ◽  
Leonard Kritharides ◽  
...  
Keyword(s):  
Vital Capacity ◽  
Total Lung Capacity ◽  
Breath Hold ◽  
Lung Capacity ◽  
Diving Depth ◽  
Highly Correlated ◽  
Pressure Changes ◽  
Air Compression ◽  
The Relationship ◽  
Measured Volume

One technique employed by competitive breath-hold divers to increase diving depth is to hyperinflate the lungs with glossopharyngeal breathing (GPB). Our aim was to assess the relationship between measured volume and pressure changes due to GPB. Seven healthy male breath-hold divers, age 33 ( 8 ) [mean (SD)] years were recruited. Subjects performed baseline body plethysmography (TLCPRE). Plethysmography and mouth relaxation pressure were recorded immediately following a maximal GPB maneuver at total lung capacity (TLC) (TLCGPB) and within 5 min after the final GPB maneuver (TLCPOST). Mean TLC increased from TLCPRE to TLCGPB by 1.95 (0.66) liters and vital capacity (VC) by 1.92 (0.56) liters ( P < 0.0001), with no change in residual volume. There was an increase in TLCPOST compared with TLCPRE of 0.16 liters (0.14) ( P < 0.02). Mean mouth relaxation pressure at TLCGPB was 65 (19) cmH2O and was highly correlated with the percent increase in TLC ( R = 0.96). Breath-hold divers achieve substantial increases in measured lung volumes using GPB primarily from increasing VC. Approximately one-third of the additional air was accommodated by air compression.

Previous volume history of the lung and regional distribution of residual volume

1981 ◽  
Vol 51 (2) ◽  
pp. 313-316 ◽  
Author(s):  
F. Ruff ◽  
R. R. Martin ◽  
J. Milic-Emili
Keyword(s):  
Vital Capacity ◽  
Total Lung Capacity ◽  
Regional Distribution ◽  
Breath Hold ◽  
Small Airways ◽  
Residual Volume ◽  
Lung Capacity ◽  
Lower Lung ◽  
History Of ◽  
Collateral Ventilation

By use of 133Xe, the regional distribution of residual volume (RV) was measured in six seated healthy men, following a fast vital capacity (VC) expiration a) without and b) with a breath hold at residual volume of approximately 30 s and c) following a slow (greater than 30 s) VC expiration from total lung capacity (TLC) without a breath hold at RV. After the breath hold at RV, regional RV/TLC in the lower lung zones decreased significantly compared wih results obtained with fast expiratory VC and no breath hold at RV. At lung top the opposite was true. The distribution of regional RV/TLC was the same following the slow VC expiration with no breath hold at RV as with the fast expiration with the breath hold at RV. The different regional distribution of RV in b and c relative to a was probably due mainly to collateral ventilation, i.e., during the breath hold at RV and the slow expiration some of the gas that was trapped in the dependent lung zones behind closed airways escaped into the upper regions of the lung where the small airways had remained patent, leading to increased expansion of upper alveoli.

scholarly journals Diaphragm thickening during inspiration

1997 ◽  
Vol 83 (1) ◽  
pp. 291-296 ◽  
Author(s):  
David Cohn ◽  
Joshua O. Benditt ◽  
Scott Eveloff ◽  
F. Dennis McCool
Keyword(s):  
Lung Volume ◽  
Vital Capacity ◽  
Total Lung Capacity ◽  
Diaphragm Thickness ◽  
Lung Volumes ◽  
One Dimensional ◽  
Lung Capacity ◽  
The Mean ◽  
Definition Of ◽  
The Relationship

Cohn, David, Joshua O. Benditt, Scott Eveloff, and F. Dennis McCool. Diaphragm thickening during inspiration. J. Appl. Physiol. 83(1): 291–296, 1997.—Ultrasound has been used to measure diaphragm thickness ( T di) in the area where the diaphragm abuts the rib cage (zone of apposition). However, the degree of diaphragm thickening during inspiration reported as obtained by one-dimensional M-mode ultrasound was greater than that predicted by using other radiographic techniques. Because two-dimensional (2-D) ultrasound provides greater anatomic definition of the diaphragm and neighboring structures, we used this technique to reevaluate the relationship between lung volume and T di. We first established the accuracy and reproducibility of 2-D ultrasound by measuring T diwith a 7.5-MHz transducer in 26 cadavers. We found that T di measured by ultrasound correlated significantly with that measured by ruler ( R 2 = 0.89), with the slope of this relationship approximating a line of identity ( y = 0.89 x + 0.04 mm). The relationship between lung volume and T di was then studied in nine subjects by obtaining diaphragm images at the five target lung volumes [25% increments from residual volume (RV) to total lung capacity (TLC)]. Plots of T di vs. lung volume demonstrated that the diaphragm thickened as lung volume increased, with a more rapid rate of thickening at the higher lung volumes [ T di = 1.74 vital capacity (VC)2 + 0.26 VC + 2.7 mm] ( R 2= 0.99; P < 0.001) where lung volume is expressed as a fraction of VC. The mean increase in T di between RV and TLC for the group was 54% (range 42–78%). We conclude that 2-D ultrasound can accurately measure T di and that the average thickening of the diaphragm when a subject is inhaling from RV to TLC using this technique is in the range of what would be predicted from a 35% shortening of the diaphragm.

Growth of the small airways and alveoli from childhood to the adult lung measured by aerosol-derived airway morphometry

2006 ◽  
Vol 100 (3) ◽  
pp. 965-971 ◽  
Author(s):  
Kirby L. Zeman ◽  
William D. Bennett
Keyword(s):  
Lung Volume ◽  
Space Dimension ◽  
Total Lung Capacity ◽  
Small Airways ◽  
Anatomical Features ◽  
Lung Capacity ◽  
Air Space ◽  
The Mean ◽  
Age Range

Understanding the human development of pulmonary air spaces is important for calculating the dose from exposure to inhaled materials as a function of age. We have measured, in vivo, the air space caliber of the small airways and alveoli at their natural full distension [total lung capacity (TLC)] by aerosol-derived airway morphometry in 53 children of age 6–22 yr and 59 adults of age 23–80 yr. Aerosol-derived airway morphometry utilizes the gravitational settling time of inhaled inert particles to infer the vertical distance necessary to produce the observed loss of particles to the airway surfaces at sequential depths into the lung. Previously, we identified anatomical features of the lung: the caliber of the transitional bronchioles [transitional effective air space dimension (EADtrans)]; the mean linear dimension of the alveoli (EADmin); and a measure of conducting airway volume [volumetric lung depth (VLDtrans)]. In the present study, we found that EADmin increased with age, from 184 μm at age 6 to 231 μm at age 22, generally accounting for the increase in TLC observed over this age range. EADtrans did not increase with TLC, averaging 572 μm, but increased with subject age and height when the entire age range of 6–80 yr is included {EADtrans (μm) = 0.012[height (cm)] × [age (yr)] + 508; P = 0.007}. VLDtrans scaled linearly with lung volume, but VLDtrans relative to TLC did not change with age, averaging 7.04 ± 1.55% of TLC. The data indicate that from childhood (age of 6 yr) to adulthood a constant number of respiratory units is maintained while both the smallest bronchioles and alveoli expand in size to produce the increased lung volume with increased age and height.

Pulmonary resistance and state of inflation of lungs in normal subjects and in patients with airway obstruction

1959 ◽  
Vol 14 (5) ◽  
pp. 727-732 ◽  
Author(s):  
Tsung O. Cheng ◽  
Malcolm P. Godfrey ◽  
Richard H. Shepard
Keyword(s):  
High Resistance ◽  
Lung Volume ◽  
Vital Capacity ◽  
Total Lung Capacity ◽  
Normal Subjects ◽  
Viscous Resistance ◽  
Pulmonary Resistance ◽  
Lung Capacity ◽  
Normal Resistance ◽  
The Relationship

The relationship between pulmonary resistance and the state of inflation of the lung was estimated throughout the expired vital capacity, using the multiple interrupter of Clements and Elam and a servo-spirometer. In normal subjects the pulmonary resistance was lowest near full inflation and remained relatively constant until about 80% of the vital capacity had been expired. It then rose abruptly and approached infinity at full expiration. In patients with obstructed airways, this relationship was altered in one of several ways: 1) normal resistance near full inflation increasing to high levels early in the expired vital capacity, 2) high resistance near full inflation with little further rise until late in expiration and 3) various combinations of the above. The first pattern probably reflects changes in the small, relatively flaccid airways while the second pattern probably reflects changes in the large, relatively rigid airways or in pulmonary viscous resistance. The type of relationship between resistance and lung volume also appears to influence the partition of the total lung capacity. Submitted on February 17, 1959

STUDIES OF RESPIRATORY PHYSIOLOGY IN CHILDREN

PEDIATRICS ◽  
1959 ◽  
Vol 24 (2) ◽  
pp. 181-193
Author(s):  
C. D. Cook ◽  
P. J. Helliesen ◽  
L. Kulczycki ◽  
H. Barrie ◽  
L. Friedlander ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Vital Capacity ◽  
Total Lung Capacity ◽  
Lung Compliance ◽  
Respiratory Physiology ◽  
Residual Volume ◽  
Lung Volumes ◽  
Lung Capacity ◽  
Residual Capacity

Tidal volume, respiratory rate and lung volumes have been measured in 64 patients with cystic fibrosis of the pancreas while lung compliance and resistance were measured in 42 of these. Serial studies of lung volumes were done in 43. Tidal volume was reduced and the respiratory rate increased only in the most severely ill patients. Excluding the three patients with lobectomies, residual volume and functional residual capacity were found to be significantly increased in 46 and 21%, respectively. These changes correlated well with the roentgenographic evaluation of emphysema. Vital capacity was significantly reduced in 34% while total lung capacity was, on the average, relatively unchanged. Seventy per cent of the 61 patients had a signficantly elevated RV/TLC ratio. Lung compliance was significantly reduced in only the most severely ill patients but resistance was significantly increased in 35% of the patients studied. The serial studies of lung volumes showed no consistent trends among the groups of patients in the period between studies. However, 10% of the surviving patients showed evidence of significant improvement while 15% deteriorated. [See Fig. 8. in Source Pdf.] Although there were individual discrepancies, there was a definite correlation between the clinical evaluation and tests of respiratory function, especially the changes in residual volume, the vital capacity, RV/ TLC ratio and the lung compliance and resistance.

Airway responses to inhaled histamine in asymptomatic smokers and nonsmokers

1977 ◽  
Vol 42 (4) ◽  
pp. 508-513 ◽  
Author(s):  
N. E. Brown ◽  
E. R. McFadden ◽  
R. H. Ingram
Keyword(s):  
Vital Capacity ◽  
Total Lung Capacity ◽  
Aerosol Deposition ◽  
Flow Volume ◽  
Maximal Flow ◽  
Airway Reactivity ◽  
Lung Capacity ◽  
Large Airway ◽  
Airway Response ◽  
Airway Responses

Bronchia reactivity to inhaled histamine was assessed in asymptomatic cigarette smokers and in nonsmoking atopic and nonatopic subjects. The only prechallenge between-group difference was the ratio of maximal flow on 80% helium-20% oxygen (Vmax HeO2) to maximal flow on air (Vmax air) from partial expiratory flow volume curves at 25% vital capacity (25% VC PEFV): Mean +/- SEM for smokers 1.18 /+- 0.06, atopics 1.45 +/- 0.08, nonatopics 1.51 +/- 0.03. This suggests that prior to inhalation to total lung capacity, the predominant site of resistance at flow limitation was in smaller airways of the smokers and in larger airways of both groups of nonsmokers. Following inhalation of histamine, smokers and nonatopics had similar changes in lung volumes and Vmax air which were less than in atopics. The Vmax HeO2/Vmax air ratios at 25% VC PEFV increased in smokers and decreased in nonsmokers: smokers 1.48 +/- 0.08, atopics 1.22 +/- 0.10, nontopics 1.16 +/- 0.06. This suggests a predominant large airway response in smokers and a prominent small airway response in nonsmokers. These responses may reflect differences in the predominant site of aerosol deposition rather than in airway reactivity.

Interaction of inhaled LTC4 with histamine and PGD2 on airway caliber in asthma

1989 ◽  
Vol 66 (1) ◽  
pp. 304-312 ◽  
Author(s):  
G. D. Phillips ◽  
S. T. Holgate
Keyword(s):  
Time Course ◽  
Vital Capacity ◽  
Total Lung Capacity ◽  
Forced Expiratory Volume ◽  
Maximal Flow ◽  
Lung Capacity ◽  
Airway Caliber ◽  
Relevant Interaction

To investigate possible mediator interaction in asthma, the effect of inhaled leukotriene (LT) C4 on bronchoconstriction provoked by histamine and prostaglandin (PG) D2 was studied in nine asthmatic subjects. The provocation doses of histamine, PGD2, and LTC4 required to produce a 12.5% decrease in baseline forced expiratory volume in 1 s (FEV1, PD12.5) and to further this fall to 25% (PD25–12.5) were determined. On three subsequent occasions, subjects inhaled either the PD12.5 LTC4 plus vehicle or vehicle plus the PD25–12.5 of either histamine or PGD2, and FEV1 and maximal flow at 70% of vital capacity below total lung capacity after a forced partial expiratory maneuver (Vp30) followed for 45 min. From these results, predicted time-course curves for LTC4 with histamine and LTC4 with PGD2 were calculated. On two final occasions, airway caliber was followed for 45 min after inhalation of the PD12.5 LTC4 followed by the PD25–12.5 of either histamine or PGD2. During the first 9 min after LTC4-histamine and LTC4-PGD2, the decreases in airway caliber were greater than the calculated predicted response. This interaction, although small, was significant with LTC4-PGD2 for both FEV1 (P = 0.01) and Vp30 (P less than 0.05) and with LTC4-histamine for Vp30 (P less than 0.05) but not for FEV1 (P less than 0.05). We conclude that inhaled LTC4 interacts synergistically with histamine and PGD2 and that this effect, although small, may be a relevant interaction in asthma.

Effect of volume history on distribution of inspired gas in asthmatics

1987 ◽  
Vol 62 (3) ◽  
pp. 1179-1185 ◽  
Author(s):  
R. B. Filuk ◽  
N. R. Anthonisen
Keyword(s):  
Vital Capacity ◽  
Total Lung Capacity ◽  
Lung Parenchyma ◽  
Phase Iii ◽  
Ventilation Distribution ◽  
Lung Capacity ◽  
Beta Agonists ◽  
Airway Tone ◽  
Washout Curves ◽  
Volume History

Twelve stable adult asthmatics slowly inhaled boluses of He at 20, 40, or 60% vital capacity (VC); these volumes were achieved either by expiring from total lung capacity (TLC) or by inspiring from residual volume (RV). Inspirations were continued to TLC and then were followed by slow expirations to RV while expired He was measured as a function of expired volume. At 20% VC slopes of alveolar plateaus (phase III) were positive, at 40% VC they were flat, and at 60% VC they were negative; at 20 and 60% VC the slopes were steeper than those in normals. When boluses were administered at 40 and 60% VC, He washout curves were independent of lung volume history. However at 20% VC the slope of phase III was significantly less positive when boluses were given after inspiration from RV than after expiration from TLC. In eight subjects, who were given inhaled beta-agonists, slopes of all He washouts decreased and became independent of volume history at 20% VC. We conclude that in asthmatics at low lung volumes the airways that determine ventilation distribution behave as though they have less hysteresis than the lung parenchyma probably due to increased airway tone.

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