Download Respiratory Rate during Acute Asthma

Respiratory
Steven
Kesten,
Rate during
M.D.;
M. Reza
Maleki-Yazdi,
Bnwe
R. Sander
M.D.;
Janet A. Well
Kenneth
R. Chapman,
M.D.
F. C. C.P;
patients
hyperventilate
during
M.D.;
B. Sc.; Susan
and Anthony
,
Asthmatic
Acute Asthma*
acute
attacks,
L. McKillop,
S. Rebuck,
but
controversy
persists
as to whether
they breathe
rapidly,
deeply or both. We monitored
respiratory
rate under the
three following
conditions:
(1) asthma
treated
in the emergency room; (2) airways
obstruction
provoked
by methacholine inhalation;
and (3) airways
obstruction
provoked
by
exercise.
In 47 acutely
ill asthmatic
patients,
respiratory
rate was higher than in 42 nonasthmatic
control patients
in
the emergency
room. Pretreatment
respiratory
rate correlated with peak expiratory
flow
rate and forced expired
volume
in one second.
In 17 asthmatic
patients
and
16
healthy
volunteers,
breathing
pattern
was monitored
by
respiratory
inductance
plethysmography.
Methacholine
inhalation
and exercise
provoked
significant
airways
obstruc-
H
yperventilation
is a characteristic
asthma.
In all but the most
ening
marked
Perhaps
episodes,
increased
by lowered
arterial
for this
emergency
reason,
room
respiratory
rate
feature
of acute
severe,
life-threat-
alveolar
carbon
respiratory
charts.
in asthma
However,
have
investigations
not shown
clearly
while
Camazine3
was the most
pattern.
thought
appropriate
pattern
in asthmatic
three
conditions:
(1)
asthma
treated
in the emergency
line-induced
bronchospasm;
and
that slow,
deep
and commonly
patients
under
the
spontaneous
severe
room;
(2) methacho(3) exercise-induced
study,
inductance
studies
ventilatory
pattern
during
was
rate
was
control
emergency
known
noted
asthmatic
were
performed
on asthmatic
Medicine
and Asthma
Centre,
Services
in 47
RIP
the
in
during
third
stable
study,
asthmatic
Methacholine
were
sitting
to the
and had
on admission
and
ill asthmatic
minutes
and
of their
on
42
arrival
a standard
with bronchitis,
emphysema,
excluded.
Where possible,
in
spirometry
was
measured
in the emergency
room. The
flow-volume
symptoms
by an observer
acutely
a few
they
hour after therapy
had been admitted
noncardiorespiratory
one
emergency
respiratory
hour
with
mom
rate
monitored
later.
Challenge
A separate
and ten
challenge
group
healthy
testing.
RIP
medications
All
were
ofnine
and
stable,
nonasthmatic
Respiratory
subjects
asymptomatic
subjects
asthmatic
underwent
rate and tidal
were
withdrawn
methacholine
spirometer
with
each dose
of methacholine
volume
asymptomatic
for at least
challenge
test
co-workers.
were
an automated
one-second
The
prior
a 20 percent
at 0.03
30 and
reduction
of FEV,
method
solution,
mg/mI.
stopped
All
to testing.
saline
measured
was
testing.
by the
given
timer
test
monitored
to
was administered
ofmethacholine.
or when
were
prior
12 hours
Subjects
subjects
methacholine
Forced
by a wedge
90 seconds
at 16 mg/nil
occurred.
Exercise
Eight
399 Bath-
In the
respiratory
subjects
In
by
within
while
patients,
and one
subjects
The
by
exercise.
subjects
room
asthmatic
using
room.
monitored
stable
monitored
observed
emergency
was
stretcher.
Patients
lung diseases
were
room
or other
before
control
in
surreptitiously
the
Room
emergency
the
pattern
and following
nonasthmatic
the
was
in
bronchoconstriction.
Respiratory
in
rate
subjects
then doubling doses ofmethacholmne,
starting
expiratory
volume in one second
(FEy,)
was
Canada.
Supported
in part
by a grant
from
the
Physicians
Incorporated
Foundation
(PSI) of Ontario.
Manuscript
received
May 8; accepted
June 16.
Reprint requests:
Dt Rebuck,
Toronto
Western
Hospital,
urst Street,
Toronto,
Ontario,
Canada
M5T 2S8
58
respiratory
plethysmography
Emergency
after
*From the Division of Respiratory
Toronto Western
Hospital, Toronto,
first,
methacholine-induced
of Juniper
but related,
bronchoconstriction
ill asthmatic
second
subjects
METHODS
separate,
In the
of
bronchospasm.
Three
respiratory-induced
ventilatory
The present
study was designed
to see whether
we
could reconcile
these conflicting
opinions.
We wanted
to know
whether
or not the respiratory
rate was
increased
in asthma
and whether
the routine
monitoring of it might
be useful.
We therefore
assessed
breathing
following
RIP=
in
hyperventilation
is accompanied
by an increased
respiratory
rate. Tobin et al’ observed
normal
respiratory
rates in ambulatory,
symptomatic
asthmatic
patients;
Woolcock2
reported
that their breathing
was rapid and
shallow,
breathing
observed
I
in acutely
that
F.C. C.P
,
tion in asthmatic
patients
but not in control
subjects.
In
asthmatic
patients,
minute
ventilation
and tidal volume
increased
above that of control subjects
following
methacholine
and exercise,
but the rate was no higher than in
control
subjects
We conclude
that the respiratory
rate is
increased
in naturally
occurring
asthma,
but not when
acute
airways
obstruction
is induced
transiently
in the
laberator
In the former setting,
the respiratory
rate is
correlated
with spirometric
measures
ofairflow
obstruction,
but the weakness
of the correlation
does not allow the
respiratory
rate to be used as a substitute
for spirometry.
(Chest
19;
97:58-62)
subjects.
ventilation
is
dioxide
tension.
rate is recorded
B. Sc.;
M. D.
asthmatic
two weeks
minute
patients
and eight
treadmill
whose
healthy
exercise
testing.
Respiratory
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21605/ on 06/18/2017
asthma
nonasthmatic
Respiratory
Rate during
been stable for over
subjects underwent
six-
had
rate
Acute
and tidal
Asthma
volume
(Kesten eta!)
were
monitored
least
12 hours
The
exercise
under
km/h)
the
subjects
and
automated
were
withdrawn
(8 to
ofthe
no
FEy,
in an air.condifioned
conditions.
at least
could
13 percent)
challenge.
Exercise
continue
measured
timer
were
oftheir
before
and
adjusted
was
maximal
stopped
because
upon
each
recorder
calculated
the
two
the
sum
with
The
etry.
percent.
At the
measured
RIP
were
recorded
if there
methods
Calibration
with
tidal
procedure
and
on
tidal
was
w
volume
a mean
ofgreater
than
studies,
by
repeated
tidal
volume
by spirom-
if tidal
by
spirometry.
tidal
by comparing
measured
differed
of the
was
more
than
volume
The
volume
± 10
by RIP
trial
difference
was
data
were
between
the
acutely
ill asthmatic
into this study.
Seventeen
women
(mean age, 30 years,
patients
were
en-
were
men
and 30
range 16 to 65 years)
to the emergency
room for treatTechnically
satisfactory
values
for
within
a few minutes
of arriving
in
room,
were
obtained
satisfactory
spirometry
dilator
therapy
expiratory
flow
was obtained
in 26 patients.
Peak
rate (PEFR)
was obtained
in 31 of 47
in 27 of
postbroncho-
47
patients.
At the time of presentation,
the mean initial
FEY1 (1.43 ± 0.49 L) was 43 ± 16 percent
of predicted
for age, sex and height.5
Accordingly,
may be viewed,
as a group,
as having
had an episode
ofasthma
ofmoderate
severity.
Among
patients
for whom
initial
spirometry
was obtained,
there
were
inverse
correlations
between
respiratory
rate and several
indices
of airflow:
FEY1 (r =
0.45,
-
p<O.05),
PEFR
(r= -0.42,
p<O.O2)
(Fig 1), and flow
at 50 percent
of vital
capacity
(Y50) (r =
0.45,
p<O.OS).
One hour after initiation
ofinhalation
therapy
-
with
drugs
nebulized
sympathomimetic
or both,
respiratory
rate
26.8±6.8 to 20.6±4.3
breaths/min
that
was
still
10
higher
than
in the
20
30
RESPIRATORY
RATE
or anticholinergic
had
slowed
from
(p<0.001),
a level
42 control
subjects
40
(17.8
±
4.3
breaths/mm,
while
flow
rates
(FEY1=
1.43±0.49
piratory
measures
p<O.Ol)
Forty-two
(Fig
had increased
vs 2.10±0.70
rate
no longer
offlow
(FEY1,
peak
2).
presenting
were
also
the same emergency
room; 22 were men
women
and their
mean
age was 39 years
rate
a
5. 1 vs 17.9
subjects
mean
30
was
in asthmatic
breaths/mm,
not signfficantly
trol
The
(26.8
±
in
and 20 were
(range
1 1 to
of the asthmatic
that observed
in
6.8
±
vs
18.3
±
4.6
altered
by
methacholine
subjects
(16.0±3.7
vs
p>O.2)
or in control
subjects
4.7 breaths/mm,
different
after
decrease
not
between
methacholine
in FEY1
p>O.2).
asthmatic
challenge
in asthmatics
Rate
was
and con(p>0.2).
was 33
pc(0.001
0
C
I
with
studied
Challenge
Respiratory
challenge
15.8 ± 5.0
±
rate
than
the
p<O.OOl).
Methacholine
(18.0
patients
However,
with
any of
Y,
p>O.3).
patients
complaints
nonasthmatic
expiratory
line represents
following
therapy
L, p<O.00l),
res-
correlated
PEFR,
Y,
nonasthmatic
noncardiorespiratory
50
(breaths/mm)
Ficuax
1. Relation
between
respiratory
rate and
flow rate on admission
to emergency
room.
Solid
least squares
linear regression.
the
the emergency
patients,
while
calculated
patients
0
breaths/mm,
and had presented
ment
of asthma.
spirometry,
taken
value,
these
0
80 years).
The initial
respiratory
patients
was signfficantly
higher
10 percent.
Room
Forty-seven
tered
were
S
200
U-
termination
RESULTS
Emergency
S
S
an
a multichannel
was verified
volume
spirometry
conclusion
against
rejected
two
postures
calibration
by
300
Plethysmography
deflections
measured
0.02
p<
C
0.
equations.
of the
r0.42
or
and separate
compartmental
amplification
factors were
from simultaneous
spirometric
measures of tidal volume
usingsimultaneous
#{149}
S
early
challenge.
Inductance
of
400
.
of dyspnea
spirometer
serially
‘;
so that
predicted
by a wedge
(6to
speed
In studies 2 and 3, each subject had a suitably sized transducer
inductance
coil placed around the rib cage just below
the axilla,
and a second coil positioned
at the umbilicus
above the iliac crest.
The location of the coils was marked and checked
regularly
to
ensure
that their positions
did not change. Theleast
squares method
of calibration
for RIP was used. Following
the technique
specified
by the manufacturer,
calibration
of RIP (DC mode) was performed
with the subjects
in both standing
and supine
postures.
Rib cage
and abdominal
deflections
from at least three representative
breaths
in
500
for at
laboratory
treadmill
The
80 percent
longer
was
one-second
exercise
Respiratonj
performed
inclination
by the end
The
ofthe
was
achieved
patient
fatigue.
All medications
environmental
rates
if the
RIP.
to testing.
test
stable
8.5
heart
using
prior
ASTHMATICS
E
w
CONTROLS
25
20
I-.
1<
10
a.
0
w
0
AdmIssion
Ficuax
therapy
subjects.
2. Respiratory
in emergency
One-hour
rate on admission
and at one-hour
after
room for asthmatic
and non-asthmatic
control
Bars represent
±
1 SEM.
CHEST
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I 97 I 1 I JANUARY,
1990
59
gency
room
patients
environment.
One
exposed
might
also
to a similarly
stressful
the
postulate
hypoxe-
drive.
The
increase
in respipatients
have
noted
in the
that
mia is responsible
for the observed
ratory
rate. However,
most of our
increase
asthmatic
were
in the
given
supplemental
oxygen
room
and it is unlikely
that
the time of our assessments.
they were
Moreover,
emergency
hypoxemic
at
there
is evi-
alterations
in breathing
than
degree
room
of
for changes
the
oxygen
saturation
to 95
±
2 percent,
89 ± 5
mean
respiratory
rate
remained
unchanged
(22 ± 1 and 21 ± 1 breaths!min,
respectively).
Is respiratory
rate simply an indicator
ofthe
severity
of airflow
obstruction?
If this were so, the difference
in respiratory
rate between
asthmatic
patients
seen in
the emergency
room and asthmatics
studied
laboratory
would
simply
be a consequence
severe
airflow
obstruction
observed
in
in the
of more
the
former
setting.
Although
both emergency
room
and laboratory-studied
asthmatic
patients
were
symptomatic
with wheezing
and dyspnea,
mean FEY1 was lower in
the former
FEY1 of2.
(1.42±0.50
12 ± 0.53
L vs a mean postmethacholine
L). This explanation
is not entirely
satisfactory
for three
reasons.
First,
Chadha
et al8 have
monitored
respiratory
rate with inductive
plethysmography
in a group
of asthmatic
subjects
while
they
changes.
Methacholine
contraction.
However,
possibility
ulate irritant
the mucosa,
vating
that
methacholine
airway
smooth
receptors
muscle
irritant
receptors,
reflex secondary
inflated
of
may
be
rate.’2
predicted
percent.7
a mean
oxygen
saturation
of
supplemental
oxygen
increased
we
in the
process,
bronchospasm,
At first glance,
neither
methacholine
would
appear
to be responsible
for
and
While
that
presentation
in respiratory
dence
that the mild hypoxemia
of acute
asthma
has
little effect on ventilation
and no measurable
effect on
respiratory
rate. Freedman
studied
a group
of asthmatics
with
a mean
FEY1
of 43 ± 16 percent
of
inflammatory
smooth
muscle
respiratory
lack of any such
change
that the inflammatory
the
responsible
and
frequency
emergency
asthma
and the
laboratory
implies
rather
patterns
in breathing
nor exercise
inducing
acute
directly
induces
we acknowledge
could
possibly
by physical
contraction
stim-
irritation
of
in itself acti-
and stimulation
ofa
deflation
to compression
by contiguous
Similarly,
in asthmatic
patients,
hyperexer-
results
in thermal
changes
in the airways
leading
to sudden
increases
in blood
supply
to the bronchi,
hyperemia
and edema
ofthe
mucosa
with subsequent
airway
narrowing,’4
changes
which
could
arguably
be
cise
described
as inflammatory.
It remains
unclear
what
clinical
outcome
these
laboratory
findings
have on
irritant
airway
receptors.
Nevertheless,
the duration
and
degree
of
inflammation
in
the
airways
of
an
asthmatic
subject
presenting
to an emergency
and subsequent
stimulation
ofintrapulmonary
receptors
must
exceed
that which
accompanies
room
irritant
the
acute,
transient
airflow
laboratory
by methacholine
in
limitation
induced
or exercise.
the
provoked
more severe
airways
obstruction
with methacholine
than we did in the current
study.
Despite
a
mean FEY1, just 45 percent
of predicted
and compa-
Our
lowing
earlier
rable
to that
they observed
acholine
or histamine
challenge
in asthmatic
subjects.
Respiratory
rate appears
to be unchanged
when bron-
the
inverse
treatment
indices
statistical
correlations
observed
between
pre-
to control
subjects,
or
but
rate and
respiratory
any hint
of
PEFR
are not redundant
1:1 correlates.
the two asthmatic
patients
in our study
who
the most marked
response
to inhaled
metha-
et
al8
The airway obstruction
induced
in the laboratory
in
stable asthmatics
differed
from that in the emergency
room
in duration
of obstruction,
severity
of obstruction, and perhaps
most importantly,
in the degree
of
induced,
accompanying
jects,
sponse
and
release
of mediators
inflammatory
likely
contribute
in
to
in that
such
groups
include
re-
Tobin
et
alh8
this
noted
we
noted
manner,
but
that the relief
no change
and a significant
increase
mainly
from an increased
for
The
induced
various
of broncho-
constriction
in stable
asthmatic
subjects
was
not
accompanied
by any important
changes
in respiratory
rate or minute
ventilation.
Our findings
in laboratoryinduced
asthma
are more
similar
to those
of Chadha
choline
had a decline
in FEY1 of 49 percent
(similar
to pretreatment
values
we saw in the emergency
room)
but no change
in respiratory
rate.
inflammation.
is
lation.16,17
of correlation
airflow
measurements
rate and measures
chospasm
changes
in minute
ventilation
have
been
reported:
some
report
an increase,8”3
others
a decrease’5
and
still other
observers
report
unchanged
levels
of venti-
of subjects
involved.
Following
treatment,
rate remained
abnormally
high as com-
between
respiratory
disappeared.
Clearly,
FEY1
Finally,
showed
we
room patients,
rate. Second,
respiratory
rate and pretreatment
airflow
were little more than vague
trends
achieving
significance
by virtue
of the relatively
large
number
respiratory
pared
seen in our emergency
no increase
in respiratory
observation
of unchanged
respiratory
rate folmethacholine
inhalation
appears
to confirm
studies
of ventilatory
pattern
following
meth-
conflicting
may
the
the
in respiratory
rate
in minute
ventilation
tidal volume.
The
results
among
different
derived
reasons
research
be related
to a variety
of factors
differing
degrees
of bronchoconstriction
use
of mouthpieces
and
nose
that
clips
by
some investigators,’9’2#{176} small sample
size, or different
populations
(healthy
volunteers,
COPD
or asthmatic
patients).
several
Our protocol
was limited
to asthmatic
subhad a sample
size larger
than that reported
in
of the other
studies,
and measured
respiratory
CHEST
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I 97 I I I JANUARY,
1990
61
gency
room
patients
environment.
One
exposed
might
also
to a similarly
stressful
the
postulate
hypoxe-
drive.
The
increase
in respipatients
have
noted
in the
that
mia is responsible
for the observed
ratory
rate. However,
most of our
increase
asthmatic
were
in the
given
supplemental
oxygen
room
and it is unlikely
that
the time of our assessments.
they were
Moreover,
emergency
hypoxemic
at
there
is evi-
alterations
in breathing
than
degree
room
of
for changes
the
oxygen
saturation
to 95
±
2 percent,
89 ± 5
mean
respiratory
rate
remained
unchanged
(22 ± 1 and 21 ± 1 breaths!min,
respectively).
Is respiratory
rate simply an indicator
ofthe
severity
of airflow
obstruction?
If this were so, the difference
in respiratory
rate between
asthmatic
patients
seen in
the emergency
room and asthmatics
studied
laboratory
would
simply
be a consequence
severe
airflow
obstruction
observed
in
in the
of more
the
former
setting.
Although
both emergency
room
and laboratory-studied
asthmatic
patients
were
symptomatic
with wheezing
and dyspnea,
mean FEY1 was lower in
the former
FEY1 of2.
(1.42±0.50
12 ± 0.53
L vs a mean postmethacholine
L). This explanation
is not entirely
satisfactory
for three
reasons.
First,
Chadha
et al8 have
monitored
respiratory
rate with inductive
plethysmography
in a group
of asthmatic
subjects
while
they
changes.
Methacholine
contraction.
However,
possibility
ulate irritant
the mucosa,
vating
that
methacholine
airway
smooth
receptors
muscle
irritant
receptors,
reflex secondary
inflated
of
may
be
rate.’2
predicted
percent.7
a mean
oxygen
saturation
of
supplemental
oxygen
increased
we
in the
process,
bronchospasm,
At first glance,
neither
methacholine
would
appear
to be responsible
for
and
While
that
presentation
in respiratory
dence
that the mild hypoxemia
of acute
asthma
has
little effect on ventilation
and no measurable
effect on
respiratory
rate. Freedman
studied
a group
of asthmatics
with
a mean
FEY1
of 43 ± 16 percent
of
inflammatory
smooth
muscle
respiratory
lack of any such
change
that the inflammatory
the
responsible
and
frequency
emergency
asthma
and the
laboratory
implies
rather
patterns
in breathing
nor exercise
inducing
acute
directly
induces
we acknowledge
could
possibly
by physical
contraction
stim-
irritation
of
in itself acti-
and stimulation
ofa
deflation
to compression
by contiguous
Similarly,
in asthmatic
patients,
hyperexer-
results
in thermal
changes
in the airways
leading
to sudden
increases
in blood
supply
to the bronchi,
hyperemia
and edema
ofthe
mucosa
with subsequent
airway
narrowing,’4
changes
which
could
arguably
be
cise
described
as inflammatory.
It remains
unclear
what
clinical
outcome
these
laboratory
findings
have on
irritant
airway
receptors.
Nevertheless,
the duration
and
degree
of
inflammation
in
the
airways
of
an
asthmatic
subject
presenting
to an emergency
and subsequent
stimulation
ofintrapulmonary
receptors
must
exceed
that which
accompanies
room
irritant
the
acute,
transient
airflow
laboratory
by methacholine
in
limitation
induced
or exercise.
the
provoked
more severe
airways
obstruction
with methacholine
than we did in the current
study.
Despite
a
mean FEY1, just 45 percent
of predicted
and compa-
Our
lowing
earlier
rable
to that
they observed
acholine
or histamine
challenge
in asthmatic
subjects.
Respiratory
rate appears
to be unchanged
when bron-
the
inverse
treatment
indices
statistical
correlations
observed
between
pre-
to control
subjects,
or
but
rate and
respiratory
any hint
of
PEFR
are not redundant
1:1 correlates.
the two asthmatic
patients
in our study
who
the most marked
response
to inhaled
metha-
et
al8
The airway obstruction
induced
in the laboratory
in
stable asthmatics
differed
from that in the emergency
room
in duration
of obstruction,
severity
of obstruction, and perhaps
most importantly,
in the degree
of
induced,
accompanying
jects,
sponse
and
release
of mediators
inflammatory
likely
contribute
in
to
in that
such
groups
include
re-
Tobin
et
alh8
this
noted
we
noted
manner,
but
that the relief
no change
and a significant
increase
mainly
from an increased
for
The
induced
various
of broncho-
constriction
in stable
asthmatic
subjects
was
not
accompanied
by any important
changes
in respiratory
rate or minute
ventilation.
Our findings
in laboratoryinduced
asthma
are more
similar
to those
of Chadha
choline
had a decline
in FEY1 of 49 percent
(similar
to pretreatment
values
we saw in the emergency
room)
but no change
in respiratory
rate.
inflammation.
is
lation.16,17
of correlation
airflow
measurements
rate and measures
chospasm
changes
in minute
ventilation
have
been
reported:
some
report
an increase,8”3
others
a decrease’5
and
still other
observers
report
unchanged
levels
of venti-
of subjects
involved.
Following
treatment,
rate remained
abnormally
high as com-
between
respiratory
disappeared.
Clearly,
FEY1
Finally,
showed
we
room patients,
rate. Second,
respiratory
rate and pretreatment
airflow
were little more than vague
trends
achieving
significance
by virtue
of the relatively
large
number
respiratory
pared
seen in our emergency
no increase
in respiratory
observation
of unchanged
respiratory
rate folmethacholine
inhalation
appears
to confirm
studies
of ventilatory
pattern
following
meth-
conflicting
may
the
the
in respiratory
rate
in minute
ventilation
tidal volume.
The
results
among
different
derived
reasons
research
be related
to a variety
of factors
differing
degrees
of bronchoconstriction
use
of mouthpieces
and
nose
that
clips
by
some investigators,’9’2#{176} small sample
size, or different
populations
(healthy
volunteers,
COPD
or asthmatic
patients).
several
Our protocol
was limited
to asthmatic
subhad a sample
size larger
than that reported
in
of the other
studies,
and measured
respiratory
CHEST
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21605/ on 06/18/2017
I 97 I I I JANUARY,
1990
61
rate
by a technique
the face
We
would
that
did
not
require
contact
6 Roussos C, Macklem
FT The respiratory
muscles.
Med 1982; 307:786-97
7 Freedman
AR, Mangura
BT, Lavietes
MH. Minute
with
or mouth.
thought
that exercise,
unlike
methacholine,
be a more natural
stimulant
of bronchospasm
in
oxygen
in asthmatic
subjects
and might induce
changes
similar
to those
in spontaneously
occurring
asthma
attacks.
However,
the pattern
of changes
in respiratory
rate
and minute
ventilation
following
exercise
were
similar
that is,
minute
ventilation
in tidal
naturally
secondary
that
occurring
respiratory
asthma
obstruction
is induced
In the former
setting,
correlated
struction,
allow
to an increase
8 Chadha
TS,
Breathing
but
rate
not
is increased
when
transiently
respiratory
with
spirometric
but the weakness
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acute
in the
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Physiol
Schneider
1984;
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White
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Asthma-what
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5 Knudson
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alone
pattern
the
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loading
and
TF,
ofthe
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DF,
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1978;
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1983;
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1982;
and
of the
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Effect
adult
of the
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1980;
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Chester
EH,
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responses
to external
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1978;
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MJ, Birch
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Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21605/ on 06/18/2017
Rate
during
Acute
Asthma
(Kesten
eta!)