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1 Department of Medicine,
Pulmonary Section, Baylor College of Medicine, Houston, Texas 77030;
2 Dipartimento di Scienze Motorie
e Riabilitative, 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.
hyperinflation; elastic recoil; asthma
IN A RECENT STUDY OF INDUCED bronchoconstriction by
Pellegrino et al. (13), when maximal flow impinged on the control tidal flow-volume curve, functional residual capacity (FRC) increased. The
breathing pattern remained essentially constant except for the increase
in lung volume (13). Before the increase in FRC, bronchoconstriction
produced an increase in elastance with no consistent effect on lung
elastic recoil at control FRC. Bronchoconstriction severe enough to
produce an increase in FRC was associated with a further increase in
elastance, but lung recoil at the elevated FRC was systematically less
than predicted than the elastance at the initial FRC. This phenomenon
occurred in both asthmatic patients and normal subjects who achieved
sufficient bronchoconstriction to increase their FRC. The decreased
lung elastic recoil reduced the increase of elastic work of breathing
produced by the hyperinflation. There was no statistically significant
change in lung elastic recoil from static deflation pressure-volume
(P-V) curves from total lung capacity (TLC). The less-than-expected
increase in lung recoil that occurred with the increase in mean lung
volume could have been caused by airway closure induced by
bronchoconstrictor agents or by stress relaxation produced by the
increased mean lung volume. Voluntary increases in FRC should not
produce airway closure. If voluntary increases in lung volume produced
a reduction in lung elastic recoil, it would suggest that stress
relaxation was responsible. Therefore, we studied the effects on lung
recoil of voluntary increases of FRC and mean lung volume.
Eight normal men, age 29-39 yr, were studied in a
pressure-corrected, integrated flow-volume displacement
plethysmograph. Anthropometric data are shown in Table
1. The frequency response of this
plethysmograph is adequate up to 10 Hz. Volume measurements were
obtained by measuring the pressure difference across a resistance element located in the wall of the plethysmograph with an MP45 Validyne
pressure transducer (±2
cmH2O). This signal was then integrated and corrected for the phase lag because of the pneumatic capacitance of the plethysmograph to obtain volume. The characteristics of this type of plethysmograph are described elsewhere (11, 14).
Respiratory flow was measured by a no. 3 Fleisch pneumotachograph connected to an MP45 Validyne pressure transducer (±2
cmH2O). Transpulmonary pressure
(Ptp) was measured by a 10-cm-long thin latex balloon positioned in the
lower one-third of the esophagus, 38-45 cm from the nostril, and
connected to a Statham 131 pressure transducer (±5 psi). The
balloon was filled with ~1 ml of air. Ptp was estimated as the
difference between mouth and esophageal pressure. Placement of the
balloon was considered correct if Ptp remained constant while subjects
made gentle respiratory efforts against a small orifice. Oral pressure
changes confirmed respiratory efforts. Signals of flow, volume, and Ptp
were recorded on a strip-chart recorder (HP-7758A) and digitally
collected with a computer (DEC11/73) at a sample rate of 50 Hz for
subsequent analysis.
ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
Table 1.
Anthropometric characteristics of subjects
Protocol.
Subjects were instructed to breathe through the mouthpiece continuously
throughout the study to assist in achieving a steady-state heat
transfer and to minimize thermal drift during measurements. Subjects
breathed quietly for 3-5 min without specific instructions, except
to avoid taking a deep breath while the integrator was adjusted to
minimize thermal drift. The integrator was adjusted so that the reset
button would return the volume to control end inspiration, which was
recorded as zero volume by the on-line computer. The gain of a
time-based oscilloscope was adjusted so that volume during normal tidal
breathing fell between the first and second of three equally spaced
lines on the display. At the beginning of data collection, this
oscilloscope was placed so that subjects could see it, and they were
instructed to "breathe between the first two lines" for 1 min
[normal tidal volume
(VT)] and then perform
one of two experimental maneuvers.
1)
VT was held
constant, but FRC was increased so that the initial end-inspiratory volume became the new FRC and volume excursion was from
lines 2-3 on the oscilloscope
(VT+1 pattern; Fig.
1A).
2) The
VT was doubled so that
VT excursion on the oscilloscope
was from lines 1-3 rather than
1-2
(2VT pattern; Fig.
1B). The sequence of the maneuvers
was random, and each lasted for ~1 min. At the end of each imposed
breathing pattern, the airway was occluded at the volume corresponding
to control end inspiration, which was end expiration for the
VT+1 pattern and
mid-VT for the
2VT pattern. Thoracic gas volume
was measured, and the subjects performed a maximal inspiration to TLC.
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Data analysis.
Ptp, flow, and volume for each breath were analyzed by the least
squares method. The start of inspiratory flow
(
I) was determined by searching back
from a definite inspiration to the first flow point >0.
End-expiratory flow is taken as the last point <0 in the expiratory
phase of the breath. Each breath was examined with one elastance term
and a separate pulmonary resistance for inspiration (RLi) and
expiration
(RLe)
(12). After the zero flow points are determined, the
I is forced to zero during expiration,
the expiratory flow (E) is forced to
zero during inspiration, and the data are fit to the following equation
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(1) |
Statistics. P0, RLi, RLe, and Edyn for breaths before and after the breathing pattern of each subject was changed were analyzed by repeated-measures ANOVA at each of the breathing patterns. TLC at the end of the two breathing patterns was compared by paired t-test.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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There were no differences in TLC measured after the two maneuvers or
P0, RLi,
RLe, and Edyn before the change in breathing pattern. Figure 1A
illustrates both the change in breathing pattern and changes in Ptp for
a representative subject when FRC was increased. The changes in lung
volume were not associated with proportionate changes in Ptp. This
effect occurred within the first few breaths. Corresponding
transpulmonary P-V loops and the fit for the dynamic pulmonary
elastance for representation breaths of this same subject are shown in
Fig. 2A.
For the VT+1 pattern, the
computed elastic component of the dynamic loop was reduced after the
increase of FRC relative to the extrapolation of the control breath.
The effect of doubling VT in the
same subject is shown in Fig. 2B. For
the 2VT pattern, the amplitude
of the pressure doubled, and there was essentially no change in
pressure at zero volume in this subject. There were no differences in
RLi and
RLe between
any of the breathing patterns. Elastic recoils and Edyn for each
subject are shown in Table 2. The
VT+1 pattern was associated with
a 10.6% decrease in mean elastic recoil at the common volume, control
end inspiration (P < 0.001). The
2VT pattern was associated with
a smaller mean decrease in elastic recoil at the same volume and was
not statistically significant (P < 0.27). There were small but statistically significant increases in
elastance with both VT+1 and
2VT patterns.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Comments on the methodology. Separating RLi and RLe provides a better fit for the dynamic P-V relationship than a single resistance. RLe is greater than RLi, as would be expected from the changes of intrathoracic airway transmural pressure and glottic aperture. If a single resistance is used when RLe and RLi are quite different, the regression analysis will accommodate by shifting the computed elastic P-V relationship away from the side of the loop with the higher resistance. Therefore, using both RLi and RLe provides a better estimate of the elastic pressure. The elastic component of the dynamic P-V loop over the tidal-breathing range is estimated by plotting PLFRC + EV, where PLFRC is Ptp at FRC. This line is essentially indistinguishable from the straight line connecting the P-V relationship at instants of zero flow but has less breath-to-breath variability. Because zero flow on every breath during the control and VT+1 pattern did not exactly occur at our mean control end-inspiratory volume, zero volume, this methodology allows us to estimate the dynamic elastic pressure at that volume with reduced variability. However, when we computed elastic recoil at end inspiration during control breathing and end expiration during the VT+1 pattern, virtually identical results were obtained because our subjects were quite skilled at accomplishing the requested respiratory pattern.
Because the P-V relationship of the lung is not linear, elastance is an approximation of the P-V relationship. If the P-V relationship were a single exponent, then elastance would be a linear function of the mean lung volume. Thus the increase in elastance with both the VT+1 and 2VT patterns is expected. Use of a linear relationship slightly underestimates the lung recoil at both extremes of volume and should not systematically bias our comparison between the control and VT+1 data. Linear analysis would overestimate the elastic pressure at mid-VT of an exponential P-V relationship and would tend to underestimate any reduction recoil at zero volume when VT was doubled.Effects of increased VT.
Doubling VT produced the same
end-inspiratory lung volume but a lower mean volume than did increasing
FRC (Table 3). The decrease in
recoil at control end inspiration was smaller and more variable and did
not achieve statistical significance. The increase in elastance was
also smaller but was still significant. As noted above, linear analysis
of an exponential P-V curve tends to overestimate lung recoil at
mid-VT. Because zero volume is end inspiration under control conditions and is
mid-VT during increased
VT, there is a systematic bias
that would underestimate a decrease in elastic recoil associated with
this breathing pattern.
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E at constant volume (16). The
preponderance of evidence suggests that it is not due to atelectasis
but may be due to changes in lung surface tension (9, 15). Changes in
lung surface tension are one of the potential mechanisms for stress
adaptation that would produce an increase in lung recoil when lung
volume is reduced below its usual value and a reduction in lung recoil
when mean lung volume is increased.
We are unaware of any previous study reporting elastic recoil during
voluntary increases in mean lung volume. In a previous study of static
deflation P-V curves from TLC after subjects breathed for 45-60 s
at very high mean lung volumes, one of three normal subjects showed a
decrease in the static lung recoil pressure, but the other two did not
(8). Several studies have shown decreases in TLC and increases in
static deflation elastic recoil at constant lung volume after relief of
bronchoconstriction with beta agonist (4, 7). However, in these
studies, TLC and airway resistance were determined by body
plethysmography before the demonstration that high-frequency panting
causes overestimates of lung volume in patients with severe airway
obstruction (2). Therefore, artifact may contribute to these results.
However, high doses of beta agonist cause decreases in static lung
elastic recoil on deflation from TLC in normal individuals, presumably
due to relaxation of contractile tissue rather than changes in
surfactant (4, 10). Lung stretch is associated with a release of
surfactant in excised rat and dog lungs inflated proportionately to the
degree of inflation, and stretch causes release of surfactant from
alveolar type II cells in vitro (5, 6). The present study provides strong evidence that, when mean lung volume is increased, there is a
rapid decrease in lung recoil due to stress relaxation. It provides no
evidence as to whether this is due to a release of surfactant onto the
alveolar surface, relaxation of contractile elements, or a viscoplastic
deformation of other parenchymal elements.
In one subject, we administered methacholine in a dose sufficient to
increase mean resistance by 64%. This dose was not sufficient to cause
flow limitation in the tidal-breathing range or to increase FRC. The
computed elastic components of the dynamic P-V loops are shown in Fig.
3. In the control case, both
VT+1 and
2VT patterns were associated
with a decrease in lung elastic recoil and a minimal increase in
elastance. With bronchoconstriction, lung recoil at FRC and lung
elastance increased relative to control. The
VT+1 breathing pattern was
associated with a larger decrease in lung recoil at zero volume than
during the previous study. There was also a decrease in resistance with
the increased mean lung volume because of the bronchodilator effect of
increased mean lung volume in normal subjects during
bronchoconstriction. We cannot exclude the possibility that increased
elastance during bronchoconstriction with a normal breathing pattern in
the present or previous study (13) was due to parallel inhomogeneity up
to and including airway closure. In contrast to the situation in which
FRC is increased because of the airway constriction, the changes
occurring with voluntary increase in lung volume, both before and after
bronchoconstriction, cannot be due to airway closure. The data in this
study are most consistent with stress adaptation causing the reduction
in recoil.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: J. R. Rodarte, Dept. of Medicine - Pulmonary Section, Suite 520B, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030 (E-mail: rodarte{at}bcm.tmc.edu).
Received 5 March 1999; accepted in final form 3 June 1999.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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