(Chest. 2000;118:976-980.)
© 2000
American College of Chest Physicians
Maximal Inspiratory Flow Rates in Patients With COPD*
Dan St
nescu, MD, PhD;
Claude Veriter, MA and
Karel P. Van de Woestijne, MD, PhD
*
From the Pulmonary Laboratory and Division (Drs. Stnescu and Veriter), Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, Brussels; and Laboratorium voor Pneumologie (Dr. Van de Woestijne), Universiteit Ziekenhuis Gasthuisberg, Leuven, Belgium.
Correspondence to: Dan Stnescu, MD, PhD, Cliniques Universitaires Saint-Luc, avenue Hippocrate, 10, 1200 Bruxelles, Belgium; e-mail: stanescu{at}pneu.ucl.ac.be
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Abstract
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Objectives: To assess the relevance of maximal
inspiratory flow rates (MIFR) in the assessment of airway obstruction
in COPD.
Setting: University teaching hospital.
Participants: Ten consecutive COPD patients (O group; mean
[± SD] age, 58.5 ± 8.3 years) and 10 matched healthy subjects (H
group; mean age, 58.7 ± 7.4 years).
Measurements:
Lung volumes, FEV1, specific airway conductance,
single-breath lung diffusing capacity, MIFR, and maximal expiratory
flow rates (MEFR).
Results: Mean
FEV1/vital capacity (VC) was 74.7% in the H group and
37.8% in the O group (p < 0.001). Total lung capacity was higher
(p < 0.001) in the O group compared with the H group. Lung diffusing
capacity was less than half in the O group compared with the H group
(p < 0.001). MEFR at all lung volumes were lower in the O group
(p < 0.001). MIFR were comparable in the two groups, except at 25%
inspired VC, where MIFR were lower in the O group (p < 0.05).
Conclusion: MIFR are less sensitive than MEFR to detect
airway obstruction in COPD patients. Yet, the interest of MIFR lay in
the possibility to separate intrinsic from extrinsic involvement of
airways. A normal MIFR associated with low MEFR, as in the present
study, suggests either a lack of parenchymal support, an increased
collapsibility of the airways, or a reversible peripheral airway
narrowing. A fixed, generalized airway narrowing would be associated
with a decrease of both MIFR and MEFR.
Key Words: airway obstruction • COPD • maximal inspiratory and expiratory flow rates
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Introduction
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Maximal
expiratory flow rates (MEFR) measured from a flow-volume curve are
currently used to assess expiratory flow limitation. However, except in
studies on upper-airways abnormalities, maximal inspiratory flow rates
(MIFR) are rarely recorded.1
2
3
4
5
There are only
three articles, published some 30 to 40 years ago, that systematically
assessed both MIFR and MEFR in patients with COPD.1
2
3
In the three studies, MIFR and MEFR were significantly less than
in normal subjects, and MEFR were lower than MIFR.
In contrast to these data, it has been our experience that in patients
with pulmonary emphysema, MIFR were often normal or close to normal.
Since, to the best of our knowledge, the above studies1
2
3
are the only ones comparing MIFR and MEFR in COPD, we decided to
repeat them. Taking the influence of gas compression into account,
changes in lung volumes were measured by body plethysmography.
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Materials and Methods
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We studied 10 male, consecutive patients with COPD (mean
[± SD] age, 58.5 ± 8.3 years), who were treated in the
pneumology division of our hospital. The diagnosis of COPD was based on
the standard criteria of the European Respiratory Society and the
American Thoracic Society.6
7
All patients were long-term
regular cigarette smokers, with a smoking history of 57.4 ± 41.8
pack-years. None of them had chronic expectoration. All medication was
stopped 24 h before the measurements. We also studied 10 healthy
subjects (mean age, 58.7 ± 7.4 years) recruited from the staff or
from hospital volunteers. The volunteers were all asymptomatic,
in good health, and without any upper-respiratory infection in the
preceding 3 months. Six of them were nonsmokers.
Slow vital capacity (VC) and FEV1 were measured
with a water spirometer (Pulmonet III; SensorMedics; Yorba Linda, CA).
Residual volume (RV) was measured by the He closed circuit method. MEFR
and MIFR were recorded at the mouth, in this order, with a heated
Fleisch No. 4 pneumotachograph (Fleisch; Lausanne, Switzerland). The
pneumotachograph was connected to a differential pressure transducer
(Statham PM 15 TC, 0.04 pounds per square inch; Oxnard, CA). Its
output was amplified (Hewlett-Packard 8805 B carrier amplifier; Hewlett
Packard; Waltham, MA) and recorded on a Gould TA 11 recorder (Gould;
Valley View, OH). MEFR and MIFR were measured at 75%, 50%, and 25%
of VC. Lung volume changes were measured in a pressure-corrected flow
body plethysmograph (homemade).8
To take into account
differences in body size, MEFR and MIFR were normalized by dividing
them by the cubic height of the patient. Specific airway conductance
(sGaw) was measured during panting (two cycles per second) by
dividing airway conductance (the inverse of airway resistance) by the
thoracic lung volume. Airway resistance was measured between 0 L/s and
0.2 L/s inspiratory and expiratory flow. The diffusing capacity of the
lung for carbon monoxide (DLCO) was measured by the
single-breath method, using the Morgan benchmark transfer test.
Data are reported as mean (SD) and were compared using the Student’s
t test for independent variables. The linear correlation
coefficient was calculated. A p value < 0.05 was considered
significant.
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Results
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Table 1
presents physical and functional data in both healthy and COPD
subjects. Age and height were comparable in both groups. Spirographic
tests were within predicted limits9
for healthy subjects,
but sharply decreased in COPD patients. The
FEV1/VC was 74.7% in healthy subjects and 37.8%
in COPD patients (p < 0.001). Total lung capacity (TLC) and RV/TLC
ratio were significantly higher in the latter compared with the former
group. DLCO was less than half in COPD subjects compared
with healthy ones (p < 0.001). sGAW was lower in obstructive
patients than in healthy ones (p < 0.001). Within the investigated
limits of airflows (± 0.2 L/s), inspiratory and expiratory
conductance were similar. The average expiratory and inspiratory
flow-volume curves for healthy and COPD subjects are presented in
Figure 1 . Values of MEFR and MIFR at different lung volumes are shown in the
Table 1
. MEFR at all lung volumes were significantly lower in the
COPD group (p < 0.001). MIFR were comparable (p > 0.05) in the two
groups, except at 25% inspired VC, where MIFR were lower in COPD
subjects than in healthy ones (p < 0.05). As shown in Figure 2
, a highly significant correlation was found in normal and COPD subjects
between sGaw and MEFR measured at 50% of VC (MEFR50).
There was also a significant correlation between sGaw and
MEFR50 in the COPD patients only (r = 0.92).
No correlation was found between sGaw and MIFR at 50% of VC in either
COPD patients alone or in both COPD and healthy subjects (Fig 3
).
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Figure 1.. Expiratory (upper) and inspiratory
(lower) flow-volume curves in the healthy (continuous
line) and COPD subjects (interrupted line). Flow rate was measured at
the mouth, and lung volume changes with the body plethysmograph (Vbox)
(vertical bars indicate SEM). MEFR were measured at 75%, 50%, and
25% of VC. MIFR were measured at 25%, 50%, and 75% of VC. MEFR and
MIFR were normalized by dividing flow rates by the cubic height (H) of
subjects.
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Figure 2.. Relationship between sGaw and MEFR at 50% of VC
(MEFR50 divided by the cubic height) in healthy subjects
(open circles) and COPD patients (closed circles). The coefficient of
correlation r is highly significant (p < 0.001). See
Figure 1
for abbreviation.
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Discussion
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We have found in a group of COPD patients, compared with a matched
group of healthy volunteers, a decrease of MEFR and sGaw but normal or
near-normal MIFR. Since single-breath DLCO was markedly
reduced, it is likely that pulmonary emphysema was present in a
significant degree in these patients. Indeed, single-breath
DLCO is considered to be a good reflection of pulmonary
emphysema.10
A further argument in favor of
emphysema is the higher TLC in COPD patients (+ 30%) as compared with
the healthy volunteers. The decrease of MEFR is a typical finding in
COPD patients and is an expression of flow limitation. Two mechanisms
are advanced to explain expiratory flow limitation in COPD patients: an
intrinsic mechanism, ie, decrease of the caliber of the
small airways (inner diameter of < 2 mm) by inflammation, fibrosis,
and mucus plugging; and an extrinsic mechanism, one due to lack of
parenchymal support of the peripheral airways as a consequence of
disruption of the elastic network of the lung. In most COPD patients,
the two mechanisms coexist, though there are rare subjects with
exclusive intrinsic or extrinsic impairment of airways. Both peripheral
airway narrowing and lack of support also result in a decrease of
sGaw.11
12
This may explain the close
correlation we found between sGaw and MEFR50 in normal and
COPD subjects (Fig 2)
. A third mechanism explaining the reduction
of MEFR was previously advanced by Leaver et al12
: an
enhanced collapsibility of the flow-limiting airways, in keeping with
the wave-speed theory.13
MIFR at a given volume depends on airways caliber, as well as strength
and speed of shortening of the inspiratory muscles.14
Since we have found normal or near-normal values for MIFR, we can
conclude that neither an impairment of the shortening of the
inspiratory muscles nor a substantial narrowing of airways caliber was
operating in our COPD patients. Therefore, how can the difference
between MEFR and MIFR be explained? The basic difference between these
indexes is related to the different mechanical forces acting during
inspiration and expiration. During forced expiration, pleural pressure
(Ppl) has a dual action: it is, together with the elastic recoil of the
lung (Pel l), a component of alveolar pressure, the driving pressure
during expiration. It is also the main outside component of the
transmural pressure of the intrathoracic airways. A large increase in
Ppl results in negative transmural pressure and intrathoracic airway
compression, leading to flow limitation. When the latter is reached,
Ppl is neutralized as a driving pressure, the primary driving pressure
for expiration then being Pel l.15
If the latter is
reduced, the MEFR will decrease. A peripheral airway narrowing or an
increased collapsibility of the flow-limiting airways will amplify the
narrowing of the compressed airways, both resulting in a further
decrease of MEFR. In contrast, during forced inspiration, flow
limitation does not occur; the transmural pressure of the intrathoracic
airways is strongly positive over the largest part of the bronchial
tree, keeping the intrathoracic airways wide open. In addition, the
driving pressure (Ppl - Pel l) is much larger than Pel l. Therefore,
neither a reduction of Pel l (lack of support of the
intraparenchymatous airways) nor an increased collapsibility of the
intrathoracic airways will modify the MIFR. An airway narrowing at low
flow rates, evidenced by a decrease of airway conductance, would be
associated with a normal or near-normal MIFR (high flow rates), as the
result of a high positive transmural inspiratory pressure that restores
the airways caliber to a normal or near-normal size. One expects a
clear-cut decrease of MIFR only if there is a marked, generalized
airways narrowing not yielding to an increase in transmural pressure
(low compliance airways, fixed airway obstruction), either anatomic
(bronchiolitis obliterans) or functional (bronchial asthma). In a study
of 14 asymptomatic asthmatics, inhalation of histamine resulted in
decreased FEV1 (average decrease, 18%). There
was a decrease of MEFR50 of 0.9 L/s (- 40% with respect
to control values) and of MIFR50 of 1.1 L/s
(- 19%).16
Detailed assessment of MIFR in COPD patients was rarely done before. In
three reports in COPD patients, MIFR and MEFR were both significantly
lower than in normal subjects.1
2
3
In all three articles,
MEFR values were lower than MIFR. This pattern is compatible with a
generalized airway obstruction, with or without associated pulmonary
emphysema. In one of these articles,3
in patients with
chronic bronchitis, there was, as in our study, a decrease of MEFR, but
no decrease of MIFR. Unfortunately, these studies were published some
time ago, before generally recognized criteria for the diagnosis of
pulmonary emphysema became available.6
7
In our patients,
a lack of parenchymal support, associated probably with a reversible
peripheral airways narrowing, was responsible for the decrease of MEFR
and near-normal values of MIFR. An extreme example in a patient with
severe emphysema (DLCO, 15% of predicted) is presented in
Figure 4
.
In conclusion, MIFR is less sensitive than MEFR in detecting
airway narrowing. Yet, the interest of MIFR in COPD is in the
possibility of separating intrinsic from extrinsic involvement of the
airways, marked airways narrowing from lack of support. Normal MIFR
associated with low MEFR, as in the present study, suggests either a
lack of parenchymal support, an increased collapsibility, or reversible
narrowing of the airways. A fixed, generalized airways narrowing would
be associated with a decrease of both MIFR and MEFR.
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Footnotes
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Abbreviations:
DLCO = diffusing capacity of the lung for carbon
monoxide; MEFR = maximal expiratory flow rate;
MEFR50 = MEFR measured at 50% of vital capacity;
MIFR = maximal inspiratory flow rate; Pel l = elastic recoil of the
lung; Ppl = pleural pressure; RV = residual volume;
sGaw = specific airway conductance; TLC = total lung capacity;
VC = vital capacity
Received for publication October 22, 1999.
Accepted for publication May 24, 2000.
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Abstract
Introduction
