Effect of lung volume on forced expiratory flows during rapid thoracoabdominal compression in infants

1995 ◽  
Vol 78 (5) ◽  
pp. 1993-1997 ◽  
Author(s):  
J. Hammer ◽  
C. J. Newth
Keyword(s):  
Lung Volume ◽  
Vital Capacity ◽  
Forced Expiration ◽  
Flow Volume ◽  
Older Children ◽  
Lung Volumes ◽  
Volume Segment ◽  
Forced Expiratory Flow ◽  
Residual Capacity ◽  
End Tidal

The rapid thoracoabdominal compression (RTC) technique is commonly used in pulmonary function laboratories to assess flow-volume relationships in infants unable to produce a voluntary forced expiration maneuver. This technique produces forced expiratory flows over only a small lung volume segment (i.e., tidal volume). It has been argued that the RTC technique should be modified to measure flow-volume relationships over a larger portion of the vital capacity range to imitate the voluntary maximal forced expiratory maneuver obtained in older children and adults. We examined the effect of volume history on forced expiratory flows by generating forced expiratory flow-volume curves by RTC from well-defined inspiratory volumes delineated by inspiratory pressures of 10, 20, 30, and 40 cmH2O down to residual volume (i.e., the reference volume) in seven intubated and anesthetized infants with normal lungs [age 8.0 +/- 2.0 (SE) mo, weight 6.7 +/- 0.6 kg]. We compared maximal expiratory flows at isovolume points (25 and 10% of forced vital capacity) and found no significant differences in maximal isovolume flow rates measured from the different lung volumes. We conclude that there is no obvious need to initiate RTC from higher lung volumes if the technique is used for flow comparisons. However, compared with measurements of maximal flows at functional residual capacity by RTC from end-tidal inspiration, the initiation of RTC from a defined and reproducible inspiratory level appears to decrease the intrasubject variability of the maximal expiratory flows at low lung volumes.

Pressure transmission across the respiratory system at raised lung volumes in infants

1994 ◽  
Vol 77 (2) ◽  
pp. 1015-1020 ◽  
Author(s):  
D. J. Turner ◽  
C. J. Lanteri ◽  
P. N. LeSouef ◽  
P. D. Sly
Keyword(s):  
Lung Volume ◽  
Dynamic Pressure ◽  
Esophageal Pressure ◽  
Tidal Range ◽  
Lung Volumes ◽  
Pressure Transmission ◽  
Airway Opening ◽  
Forced Expiratory Flow ◽  
End Tidal ◽  
Volume Range

Forced expiratory flow-volume (FEFV) curves can be generated from end-tidal inspiration in infants with use of an inflatable jacket. We have developed a technique to raise lung volume in the infant before generation of FEFV curves. Measurements of pressure transmission to the airway opening by use of static maneuvers have shown no change with increasing lung volume above end-tidal inspiration. The aim of this study was to determine, under dynamic conditions (i.e., during rapid thoracic compression), whether the efficiency of pressure transmission across the chest wall is altered by raising lung volume above the tidal range. Dynamic pressure transmission (Ptx,dyn) was measured in five infants (age 6–17 mo). Jacket pressure (Pj), esophageal pressure, and volume were measured throughout passive and FEFV curves at lung volumes set by 10, 15, and 20 cmH2O preset pressure. The group mean Ptx,dyn was 37 +/- 6% (SE) of Pj at end-tidal inspiration, and no change was seen with further increases in lung volume. However, a mean decrease in Ptx,dyn of 42% was evident throughout the tidal volume range (i.e., from end-tidal inspiration to end expiration). Isovolume static pressure transmission (Ptx,st) was measured in three of the five infants by inflation of the jacket in a stepwise manner with the airway closed. Measurements were made at end-tidal inspiration and lung volumes at 10, 15, and 20 cmH2O preset pressure. Resulting changes in Pj, esophageal pressure, and airway opening pressure were compared using linear regressions to determine Ptx,st.(ABSTRACT TRUNCATED AT 250 WORDS)

Location of flow-limiting segments via airway catheters near residual volume in humans

1985 ◽  
Vol 59 (2) ◽  
pp. 502-508 ◽  
Author(s):  
G. C. Smaldone ◽  
P. L. Smith
Keyword(s):  
Lateral Pressure ◽  
Human Subjects ◽  
Forced Expiration ◽  
Flow Limitation ◽  
Residual Volume ◽  
Flow Volume ◽  
Maximal Flow ◽  
Lung Volumes ◽  
Residual Capacity ◽  
Lung Periphery

Previous studies have demonstrated sites of flow limitation in the central airways of dogs and humans. At low lung volumes, however, during a forced expiration, it is not clear whether flow-limiting segments (FLS) move into the lung periphery. Using intrabronchial lateral pressure catheters, we located FLS in human subjects at all lung volumes between functional residual capacity (FRC) and residual volume (RV). Three individuals with severe intracranial hemorrhage maintained on ventilators were studied. Partial maximal flow-volume curves were generated from 1 liter above FRC to RV by lowering downstream pressure and using the interrupter technique. Sites of FLS were defined as the most downstream points where lateral pressure did not change with driving pressure. FLS were found in all subjects in the central airways. In one subject, FLS moved from segmental bronchi to the first subsegmental bronchus as RV was approached but not beyond. In the other two subjects, FLS remained fixed in location at all measured lung volumes. At constant volume, multiple FLS were located, all in parallel, e.g., fixed in left upper, left lower, and right middle lobar bronchi. In conclusion, sites of flow limitation remain in the central airways as lung volume approaches RV. FLS may move peripherally within the central airways but not beyond proximal subsegmental bronchi.

scholarly journals Large Lung Volumes Delay the Onset of the Physiological Breaking Point During Simulated Diving

2021 ◽  
Vol 12 ◽  
Author(s):  
Paul F. McCulloch ◽  
B. W. Gebhart ◽  
J. A. Schroer
Keyword(s):  
Lung Volume ◽  
Blood Gases ◽  
Breaking Point ◽  
Breath Holding ◽  
Breath Hold ◽  
Lung Volumes ◽  
Arterial Blood ◽  
Face Immersion ◽  
Residual Capacity ◽  
End Tidal

During breath holding after face immersion there develops an urge to breathe. The point that would initiate the termination of the breath hold, the “physiological breaking point,” is thought to be primarily due to changes in blood gases. However, we theorized that other factors, such as lung volume, also contributes significantly to terminating breath holds during face immersion. Accordingly, nine naïve subjects (controls) and seven underwater hockey players (divers) voluntarily initiated face immersions in room temperature water at Total Lung Capacity (TLC) and Functional Residual Capacity (FRC) after pre-breathing air, 100% O2, 15% O2 / 85% N2, or 5% CO2 / 95% O2. Heart rate (HR), arterial blood pressure (BP), end-tidal CO2 (etCO2), and breath hold durations (BHD) were monitored during all face immersions. The decrease in HR and increase in BP were not significantly different at the two lung volumes, although the increase in BP was usually greater at FRC. BHD was significantly longer at TLC (54 ± 2 s) than at FRC (30 ± 2 s). Also, with each pre-breathed gas BHD was always longer at TLC. We found no consistent etCO2 at which the breath holding terminated. BDHs were significantly longer in divers than in controls. We suggest that during breath holding with face immersion high lung volume acts directly within the brainstem to actively delay the attainment of the physiological breaking point, rather than acting indirectly as a sink to produce a slower build-up of PCO2.

scholarly journals Exercise-induced bronchodilation in natural and induced asthma: effects on ventilatory response and performance

2002 ◽  
Vol 92 (6) ◽  
pp. 2353-2360 ◽  
Author(s):  
Emanuele Crimi ◽  
Riccardo Pellegrino ◽  
Attilio Smeraldi ◽  
Vito Brusasco
Keyword(s):  
Tidal Volume ◽  
Functional Residual Capacity ◽  
Lung Volume ◽  
Forced Vital Capacity ◽  
Vital Capacity ◽  
Breathing Frequency ◽  
Forced Expiratory Flow ◽  
Residual Capacity ◽  
Group 2 ◽  
Group 1

We studied whether bronchodilatation occurs with exercise during the late asthmatic reaction (LAR) to allergen ( group 1, n = 13) or natural asthma (NA; group 2, n = 8) and whether this is sufficient to preserve maximum ventilation (V˙e max), oxygen consumption (V˙o 2 max), and exercise performance (W˙max ). In group 1, partial forced expiratory flow at 30% of resting forced vital capacity increased during exercise, both at control and LAR. W˙max was slightly reduced at LAR, whereasV˙e max, tidal volume, breathing frequency, and V˙o 2 max were preserved. Functional residual capacity and end-inspiratory lung volume were significantly larger at LAR than at control. In group 2, partial forced expiratory flow at 30% of resting forced vital capacity increased greatly with exercise during NA but did not attain control values after appropriate therapy. Compared with control, W˙max was slightly less during NA, whereas V˙o 2 maxand V˙e max were similar. Functional residual capacity, but not end-inspiratory lung volume at maximum load, was significantly greater than at control, whereas tidal volume decreased and breathing frequency increased. In conclusion, remarkable exercise bronchodilation occurs during either LAR or NA and allowsV˙e max andV˙o 2 max to be preserved with small changes in breathing pattern and a slight reduction inW˙max.

Lung volumes of singers

1960 ◽  
Vol 15 (1) ◽  
pp. 40-42 ◽  
Author(s):  
Stanley S. Heller ◽  
William R. Hicks ◽  
Walter S. Root
Keyword(s):  
Lung Volume ◽  
Vital Capacity ◽  
Total Lung Capacity ◽  
Residual Volume ◽  
Inspiratory Capacity ◽  
Lung Volumes ◽  
Lung Capacity ◽  
Vocal Training ◽  
Professional Singers ◽  
Residual Capacity

Lung volume determinations (tidal volume, inspiratory capacity, inspiratory reserve volume, expiratory reserve volume, vital capacity, maximum breathing capacity, functional residual capacity, residual volume, and total lung capacity) were carried out on 16 professional singers and 21 subjects who had had no professional vocal training. No differences were found between the two groups of subjects, whether recumbent or standing, which could not be explained upon the basis of age, size, or errors involved in making the measurements. Submitted on March 24, 1959

Dependence of maximal flow-volume curves on time course of preceding inspiration

1993 ◽  
Vol 75 (3) ◽  
pp. 1155-1159 ◽  
Author(s):  
E. D'Angelo ◽  
E. Prandi ◽  
J. Milic-Emili
Keyword(s):  
Time Course ◽  
Vital Capacity ◽  
Normal Subjects ◽  
Forced Expiratory Volume ◽  
Flow Volume ◽  
Maximal Flow ◽  
Lung Volumes ◽  
Residual Capacity ◽  
Expiratory Flow ◽  
Volume Range

Thirteen normal subjects, sitting in a body plethysmograph and breathing through a pneumotachograph, performed forced vital capacity maneuvers after a rapid inspiration without or with an end-inspiratory pause (maneuvers 1 and 2) and after a slow inspiration without or with an end-inspiratory pause (maneuvers 3 and 4), the pause lasting 4–6 s. Inspirations were initiated close to functional residual capacity. At all lung volumes, expiratory flow was larger with maneuver 1 than with any other maneuver and, over the upper volume range, larger with maneuver 3 than with maneuver 4, whereas it was similar for maneuvers 2 and 4. Relative to corresponding values with maneuver 4, peak expiratory flow was approximately 16 and approximately 4% larger with maneuvers 1 and 3, respectively, whereas forced expiratory volume in 1 s increased by approximately 5% only with maneuver 1. The time dependence of maximal flow-volume curves is consistent with the presence of viscoelastic elements within the respiratory system (D'Angelo et al. J. Appl. Physiol. 70: 2602–2610, 1991).

Changes in regional emptying sequence need not change maximum expiratory flow

1986 ◽  
Vol 60 (6) ◽  
pp. 1834-1838 ◽  
Author(s):  
R. B. Filuk ◽  
N. R. Anthonisen
Keyword(s):  
Vital Capacity ◽  
Total Lung Capacity ◽  
Young Men ◽  
Forced Expiration ◽  
Flow Volume ◽  
Lung Volumes ◽  
Lung Capacity ◽  
Maximum Expiratory Flow ◽  
Expiratory Flow

Nine normal young men inhaled boluses of He at the onset of slow vital capacity (VC) inspirations. During the subsequent VC expirations, we measured expired flow, volume, and He concentrations. Expirations consisted of full or partial maximum expiratory flow-volume (MEFV) maneuvers. Full maneuvers were forced expirations from total lung capacity (TLC). Partial maneuvers were accomplished by expiring slowly from TLC to 70, 60, 50, and 40% VC and then initiating forced expiration. Expired He concentrations from full and partial maneuvers were compared with each other and with those resulting from slow expirations. At comparable volumes less than 50% VC, flow during partial and full MEFV maneuvers did not differ. Expired He concentrations were higher during partial maneuvers than during full ones; at the onset of partial maneuvers upper zone emptying predominated, whereas this was not the case at the same lung volumes during maneuvers initiated at TLC. We observed substantial differences in regional emptying sequence that did not influence maximum expiratory flow.

Methacholine-induced bronchoconstriction in dogs: effects of lung volume and O3 exposure

1988 ◽  
Vol 65 (6) ◽  
pp. 2679-2686 ◽  
Author(s):  
S. T. Kariya ◽  
S. A. Shore ◽  
W. A. Skornik ◽  
K. Anderson ◽  
R. H. Ingram ◽  
...  
Keyword(s):  
Lung Volume ◽  
Maximal Response ◽  
Maximal Effect ◽  
Response Curves ◽  
Lung Volumes ◽  
Before And After ◽  
Residual Capacity ◽  
Induced Changes ◽  
Conducting Airways ◽  
Concentration Response Curve

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.

Breathing at low lung volumes and chest strapping: a comparison of lung mechanics

1981 ◽  
Vol 50 (3) ◽  
pp. 650-657 ◽  
Author(s):  
N. J. Douglas ◽  
G. B. Drummond ◽  
M. F. Sudlow
Keyword(s):  
Lung Volume ◽  
Maximum Flow ◽  
Normal Subjects ◽  
Lung Mechanics ◽  
Lung Volumes ◽  
Flow Rates ◽  
Recoil Pressure ◽  
Forced Expiratory Flow ◽  
Expiratory Flow ◽  
Expiratory Flow Rates

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.

scholarly journals THE LUNG VOLUME IN HEART DISEASE

1923 ◽  
Vol 38 (4) ◽  
pp. 445-476 ◽  
Author(s):  
Carl A. L. Binger
Keyword(s):  
Heart Disease ◽  
Lung Volume ◽  
Vital Capacity ◽  
Lung Volumes ◽  
Total Lung Volume ◽  
Surface Areas ◽  
Normal Individuals ◽  
The Absolute ◽  
Total Capacity ◽  
Residual Air

The lung volumes in a group of individuals suffering from chronic cardiac disease have been studied by a method which is applicable to patients suffering from dyspnea. In a number of instances the same patients were investigated during various stages of decompensation and compensation. The values found have been compared with those determined in a group of normal subjects. Lung volumes have been considered from three points of view: (1) relative lung volumes or subdivisions of total lung volume expressed as percentage of total lung volume; (2) the absolute lung volumes of patients with heart disease have been compared with lung volumes calculated for normal individuals having similar surface areas or chest measurements; and (3) in individual cases absolute lung volumes have been measured in various stages of compensation and decompensation. (1) In patients with heart disease it has been observed that the vital capacity forms a portion of the total lung volume relatively smaller than in normal individuals, and that the mid-capacity and residual air form relatively larger portions. When the patient progresses from the compensated to the decompensated state these changes become more pronounced. (2) When the absolute lung volumes determined for patients are compared with volumes of the same sort, as calculated for normal individuals of the same surface areas and chest measurements, the following differences are found. The vital capacities are always smaller in the patients and the volumes of residual air are always larger. There is a tendency for middle capacity and total capacity to be smaller, though, when the patients are in a compensated state, these volumes may approximate normal. (3) When decompensation occurs the absolute lung volumes undergo changes as follows: (a) vital capacity, mid-capacity, and total capacity decrease in volume; and (b) the residual air may either increase or decrease according to the severity of the state of decompensation. The significance of these changes has been discussed and an explanation offered for the occurrence of a residual air of normal volume in patients with heart disease. It results from a combination of two tendencies working in opposite directions: one to increase the residual air—stiffness of the lungs (Lungenstarre); the other to decrease it—distended capillaries (Lungenschwellung), edema, round cell infiltration.

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