Download Treatment of Congestive Heart Failure

Treatment
Its Effect
Simon
on Pleural
C. Chakko,
andPeterP
The
of Congestive
Fluid Chemistry
M.D.;t
Sforza,
Heart Failure*
Stephen
H.
Caldwell,
M.D.;1
M.D.*
classification
of pleural
effusions
into transuexudates
has great
clinical
significance.
It is
believed
that the treatment
of congestive
heart failure may
convert
an associated
transudative
pleural
effusion
into a
“pseudoexudate.”
We studied
eight patients
with congestive
heart failure during nine episodes
of decompensation
with
pleural
effusion,
which was bilateral
in five and right-sided
in three.
Thoracocentesis
was done on identification
of the
patient
and at 6 ± 2 days after
treatment
of heart failure
resulting
in diuresis
and a mean weight loss of 5.8 ± 3.2 kg.
The mean protein
level of the pleural
fluid was 2.2 ± 0.7 g/
dL at the initial
study and increased
to 3.2± 1.08 g/dL at
the final study (p<O.Ol).
The LDH level of the pleural
fluid
increased
from 116±69
to 183± 117 unitslL
(p<O.Ol).
The
proper
dates
and
P leural
effusions
may develop
as a complication
of
many
local
and
systemic
disease
processes.’
In
many cases the clinical
and roentgenographic
manifestations
associated
ease-specific,
invariably
will
centesis.2
pleural
with
so the
pleural
starting
be consideration
since
not disevaluation
are
of an
of diagnostic
The first diagnostic
fluid is to determine
exudate,
effusions
point
thoraco-
presence
process
always
requires
pleural
An exception
would
clinical
manifestations
failure.
In
this
elevate
such
that
the
it may
circumstance,
*From
prospectively
the Veterans
with clear
ventricular
studied
Administration
in the
criteria
of an
may
for
an
p<O.05).
congestive
heart
pleural
fluid’s
eight
Medical
patients
Center,
Salem,
con-
and
the
fluid
VA Medical
Center,
initial
to
to
fluid was
but met the
pleural
study
treatment
± 0.09
0.39±0.16
of heart
failure.
conclude
that
causes
the
treatment
significant
in some
of
changes
in the
cases,
a transudate
may
(Chest
1989; 95:798-802)
into a “pseudoexudate.”
from
Patients
Salem,
was
transudate
admitted
VA, with
bilateral
records
to exudate.
heart
pleural
not
chest
pain,
monia,
eligible
reviewed
failure
and
ratio
disease,
or renal
tissue
Patients
with
time
that
chest
was
determined
g/dL
M-mode
and
was
typical
clinical
failure
and
ular
function
the
and
Medical
The
cardiothorview’
All patients
Only
features
protocol
of congestive
was
of the
ventricapproved
Veterans
consented
done
patients
for depressed
Committee
The
ultrasonogwere
rmto
study
serum
posteroan-
echocardiograms
The
Center.
and
by real-time
evidence
Development
of pneu-
seconds,
done.
of
failure
pleuritic
Upright
roentgenographic
enrolled.
or hepatic
posteroanterior
confirmed
other
a history
sputum,
excluded.
echocardiographic
were
14
fraction
and
with
suggestive
were
from
ejection
heart
were
two-dimensional
ventricular
with
than
which
All patients’
no etiology
purulent
roentgenograms
effusion
was
infiltrates
greater
2.5
there
fever,
thrombosis,
lateral
the Research
Patients
venous
ofpleural
left
that
effusion.
Center,
effusion
study.
pleural
connective
less
for the
to ensure
for the
deep
Medical
and pleural
were
level
terior
Administration
or right-sided
prothrombin
acic
Veterans
failure
included.
albumin
METHODS
heart
disease,
were
to the
AND
congestive
were
than
part
to be
by
Adminof the
study.
Each
patient
within
36
study
after
failure
had clinically
6
were
±
hours
of the
2 days
improved
from
the
was
provided
and
the patient.
Thoracocentesis
ultrasonic
and
guidance.
weight
when
by
the
primary
Treatment of Congestive
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21592/ on 05/05/2017
the
final
congestive
diuresis
achieved.
was performed
Approximately
and
patients’
significant
loss
an initial
identification
daily, and the effectiveness
weighed
estimated
thoracocenteses,
patient’s
of therapy
controlled
with
two diagnostic
underwent
study
was
27
We
failure
MATERIALS
Patients
September
patients,
at the
0.34
from
gestive
heart
failure
during
nine episodes
of decompensation
with
pleural
effusion.
We evaluated
the
changes
in the pleural
fluid’s chemistry
resulting
from
the treatment
of congestive
heart
failure
and
determined
if such changes
would
alter the classification
of
istration
with
from
LDH
after
chemistry;
be converted
raphy.
possibly
what,
in
increased
for
three
exudate
(r0.715;
and
effusion
and
Effectiveness
of diuresis
was measured
by weight
loss; a
significant
correlation
between
weight
loss per day and
change
in the protein
level of the pleural
fluid was noted
presence
exudate.357
dilemma
and
workup
for
effusion.8
University
ofVirginia,
Charlottesville,
VA.
tAssociate
Professor
of Internal
Medicine.
ChiefResident
in Internal
Medicine.
§Associate
Professor
of Radiology.
Manuscript
received
June 30; revision
accepted
Reprint
requests:
Dr Chakko,
111-A Cardiology,
Miami 3312.5
798
cause.
of diuresis
concentration
the
criteria
a
of thoracocentesis.”2
Neverthebelieve
that diuretic
therapy
protein
meet
a trial
This may lead to a diagnostic
an unnecessary
and expensive
reality,
was a simple
transudative
We
ofunknown
be a patient
presenting
of recurrent
left
precede
consideration
less, other
investigators
may
effusion
for protein
0.64 ± 0.28 (p<O.Ol).
In
classified
as a transudate
step in the evaluation
of
if it is a transudate
of an
an exudative
ofany
ratio
(p<O.0l)
the
more extensive
and invasive
diagnostic
workup.23
Congestive
heart
failure
is a common
cause
of
pleural
effusion.4
The health
and public
policy
committee
of the American
College
of Physicians
notes
that “the indication
for a diagnostic
thoracocentesis
is
the
fluid/serum
0.47±0.13
had
heart
occurred.
ofdiuretic
therapy
Therapy
physician
by the usual
50 ml offluid
Heart Failure (Chakko,
was
not
caring
for
technique”
was obtained
Caldwell,
Sfoiza)
Table
1 -Clinical,
Roentgenographic,
Echocardiographic
Age,
Etiology
Case
yr
ofCHF
1
49
Idiopathic
2
62
3
72
4
5
6
and
and
Findings*
Acute
receiving
C/T
Symptoms,
wk
JVP
S
3
+
-
Ischemic
2
+
Idiopathic
2
+
54
Ischemic
1
61
Idiopathic
1
49
Ischemic
2
+
0.27
0.60
+
+
0.36
0.64
+
+
0.30
0.55
+
+
+
0.29
0.70
mission
+
+
+
0.41
0.55
ceived
+
+
0.34
0.63
the
3
Adriamycin
+
+
0.28
+
50
*CHF,
Congestive
pressure;
53,
fraction;
at each
heart
third
count,
were
minutes
of thoracocentesis
protein
and
Values
and
failure,
LDH
of blood
for the
(normal
lost
were
obtained
estimation
range,
and
of the
1 12 to 237
within
serum
units/L).
of
tesis.
Long-term
chemistries
was used.
the
significant
SD.
±
and
In comparing
after
the
Correlation
regression
at the
0.05
the
treatment
between
in pleural
equation.
pleural
All eight
patients
and
of heart
the amounts
fluid
chemistry
Probabilities
in the
roentgenographic
study
findings
had
effusion
Pleural
resolved
effusion
Table
prior to the
was bilateral
2-Pleural
Fluid
Protein
Fluid
Case
typical
were
5 had
At the time
for yenpatient
since
his
Serum Levels
before and after
Level,
patients
re-
mean
Digoxin
brisk
and
therapy.
and
weight
oral
doses
patients
who
one received
on vasodilator
to treatment,
unusually
Between
loss
before
the
5.8
± 3.2
was
diuresis
in response
given on admission
and had
prior to the initial
thoracocen-
ofthe
second
throacocentesis,
in all cases
persisted,
pleural
except
patient
4, in
and 600 ml of fluid
removed.
hospitalized
twice
exacerbation
ofcongestive
heart
failure
One patient
during
the
heart
range,
3
Three
with no
and no recur(patient
4) was
follow-up
failure
patient
(case 3) returned
of heart
failure
and
revealed
a transudative
of 0.44.
Two
intractable
ofProtein
Treatment
patients
heart
and LDH
of Heart
(patients
failure,
and Pleural
Failure
g/dl
one
period,
without
for
pleural
to the hospital
pleural
effusion.
effusion
with
Ratio
2 and
three
Fluid/Serum
LDH
Serum
ad-
patients
received
and intermittent
in the four
in addition,
or
between
an LDH
level of 153 units!L
in the fluid, a fluid/serum
ratio ofLDH
ofO.54,
and a fluid/serum
ratio of protein
second
thoracoin five patients
and
period
all
started
thoracocentesis,
effusion.
One
for exacerbation
Thoracocentesis
of congestive
heart
failure
and echocardiographic
evidence
tricular
dysfunction
(Table
1). One additional
was dropped
after
enrollment
in the study,
pleural
centesis.
three
responded
digoxin,
captopril
(20 to 40 mg).
exacerbation
of congestive
rence
of pleural
effusion.
were
level.
enrolled
furosemide
and
receiving
(20 to 40 mg).
all
mg) daily
160
not
was stopped.
with
thoracocentesis,
were continued
receiving
them;
patients
was
Long-term
follow-up
(mean,
7.4 months;
to 12 months)
was available
in all patients.
patients
(cases
5, 6, and 8) were doing
well,
RESULTS
clinical
(40 to
were
receiving
the
furosemide
effusions
were smaller
whom
the large effusion
and changes
diuresis
by
mean
before
t-test
evaluated
considered
as the
were
During
initial
patients
therapy
to intravenous
furosemide
lost 4 kg in body weight
ten
levels
patients
vasodilator
thoracocenteses,
kg. Patient
a
bacterial
was
with
two
second
in all patients.
expressed
blood
and
digitalis,
All
ejection
Analysis
are
the paired
of weight
were
Samples
was available
Statistical
fluid
done.
stain,
four
intravenous
0.68
and LDH;
protein,
which
dinitrate.
vasodilators
were already
by roentgenogram.
Gram’s
one
only,
isosorbide
of intravenous
venous
jugular
ventricular
glucose,
count,
0.23
+
left
ratio
for
cell
+
elevated
LVEF,
cardiothoracic
differential
culture
follow-up
JVP,
sound;
and examined
aspiration
WBC
failure;
heart
C/T ratio,
and
-
2
Idiopathic
and
therapy
and
0.70
toxicity
8
medications,
blocker
furosemide,
furosemide
tension
68
three
The remaining
+
and hyper.
7
in three.
of admission,
any
3-adrenergic
LVE F Ratio
Rales
right-sided
At the time
Level
Fluid
7)
months
died
and
from
the
Ratios
(units/L)
Serum
Ratio
Before
After
Before
After
Before
After
Before
After
Before
After
Before
After
1
2
1.7
2.7
2.7
3.8
5.5
7.2
5.6
8.1
0.30
0.37
0.48
0.47
282
100
794
489
0.35
0.94
487
295
0.20
0.55
3
3.0
4.6
6.9
7.4
0.43
0.62
114
214
212
0.53
0.75
4
1.2
1.4
5.7
5.4
0.26
0.26
4.4
6.4
7.1
206
226
0.18
3.2
222
0.64
1.03
6
2.7
3.5
5.9
6.3
0.45
0.55
38
145
109
138
5
0.21
0.50
462
164
160
53
229
157
212
176
0.51
0.89
7a
2.0
1.8
6.7
6.2
0.30
0.29
111
82
458
318
0.24
0.25
Th
1.8
3.3
6.2
6.5
0.29
0.51
82
178
318
342
0.25
0.52
8
1.5
3.0
5.9
6.4
0.47
68
161
240
286
0.42
0.56
Mean
SD
2.2*
3.2*
6.3
6.5
0.47*
116*
183*
380
274
039*
064*
0.7
1.1
0.6
0.9
0.25
0.34*
0.09
0.13
69
117
198
106
0.16
0.28
I 95
I 4 I APRIL
*p<0.01
for before
0.61
vs after.
CHEST
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21592/ on 05/05/2017
1989
799
effectiveness
of diuretic
therapy
and changes
in the
pleural
fluid’s chemistry,
weight
loss was used
as a
measure
of diuresis
(Table
3). There
was a significant
correlation
and
the
(r = 0.715;
0.9
0
0.8
w
0.7
was weak
(r=O.642;
relationship
0.6
and
and did
p<O.l).
between
0.5
-j
U-
not reach
statistical
significance
We did not find any significant
the size of the pleural
effusion
0.3
LDH
ratio was normal.
level and the fluid/serum
thoracocentesis.
Another
0.2
protein
0.4
study
had
PRE
POST
PRE
POT
PROTEIN
#{149}
LDH .
1 . Pleural
and after
treatment
transudate.
fluid/serum
of heart
FIGURE
ratios
failure.
and
area
of protein
Shaded
other five months
after the study; no evidence
disease
was found.
One
patient
(case
repeated
thoracocentesis
and eventually
empyema
tesis done
and congestive
heart
failure.
a few weeks
after participation
LDH
before
is range
for
for pleural
1) required
died
from
showed
sterile
fluid with no evidence
of infection.
Pleural
fluid levels
and simultaneous
serum
levels
of protein
and LDH
and fluid/serum
ratios during
the
two thoracocenteses
are shown
in Table 2. The mean
level
in the
pleural
fluid
increased
(p<O.Ol).
The
0.34
±
fluid
was
from
116±69
fluid/serum
ratio
0.09
2.2±0.71
g/dl
to 0.47
±
and
level
and
was
a fluid/serum
range,
0.64.
This
ratio
of
but
his fluid/serum
patient,
as described
had marked
diuretic
response
to intravenous
with furosemide
started
on admission
and had
lost 4 kg
tesis.
A
revealed
was low
When
of body weight
before
the initial
thoracocenpulmonary
ventilation
and
perfusion
scan
that the probability
of pulmonary
embolism
applying
the
et al,’2 the sensitivity
ing upon
how many
pairs
three
criteria
proposed
and specificity
of the criteria
of throacocenteses,
we
applied
range
in two
to 10 criteria
the
three
there
group.
were
(7
exudative
increased
by Light
will vary dependare met.3”3
In the
criteria
to each
thoracocentesis.
Thus,
total of 27 pairs of criteria
for the whole
initial
study,
two
criteria
percent)
were
a
In the
in the
patients.
After treatment,
(37 percent)
in five patients.
this
DISCUSSION
The
and
to 183±
117 units/L
for protein
increased
0. 13 (p<O.Ol)
LDH
at
increased
to 3.2 ± 1.08 g/dl at the
The
LDH
level of the pleural
the initial
study and
final study
(p<O.Ol).
Both the pleural
fluid LDH
ratio increased
at the second
patient
(case 5) at the initial
transudative
of LDH
earlier,
therapy
nine
A thoracocenin this study
a fluid
in the
ratio
‘f’
protein
weight
loss per day
fluid
protein
level
with
the LDH
level
changes
in pleural
fluid chemistry.
One patient
(case 1) had an initial
LDH
level in the
pleural
fluid of 282 units/L,
with a markedly
elevated
serum
LDH
level
of 794 units/L.
The
fluid/serum
U)
from
between
the average
change
in the pleural
p<O.O5);
correlation
classification
exudates
ofpleural
has
great
Table 3-Correlation
Day and Percentage
and LDH Level
for LDH
effusion
clinical
between
into
transudates
significance.
Average
Transu-
Weight
froni 0.39±0.16
to 0.64±0.28
(p<O.Ol)
(Fig 1). The
mean
WBC
count
in the pleural
fluid increased
from
1,137/cu
mm±1,085/cu
mm to 2,734/cu
mm±2,381/
Percen
Weigh
kg
t LoSS,
per
Loss
ofChange
in Phural
Fluid
between
Two Thoracocenteses*
Protein
tage
of
Cha nge
cu mm (p<O.O5)
(Fig 1). Gram
stains
and cultures
of
all specimens
were
done,
and no evidence
for an
infectious
process
was found.
The following
criteria
described
by Light
et al’2 are commonly
used
to
1
9
7.2
0.80
59
64
2
3
4
5.5
1.37
41
64
1.57
53
40
differentiate
transudates
(1) a pleural
4
8
6.6
0.82
17
39
fluid-to-serum
pleural
fluid
protein
LDH
level
0.5;
units/L;
5
4
2.5
0.63
37
58
6
4
2
0.50
30
7a
6
1.6
0.27
7b
9
7.5
0.83
8
3
6.4
2.13
(3) a pleural
0.6.
Using
and
7b)
initially.
the
800
were
The
order
LDH
criteria,
found
fluid
exudates:
ratio
greater
greater
than
fluid-to-serum
these
criteria
In
from
three
to
at the
have
than
200
ratio
greater
patients
(cases
transudative
second
(2) a
and
than
3, 6,
effusion
thoracocentesis
evaluate
Days
niet
day
was
and
correlation
the
correlation
between
the
Total
7
*There
for exudate.
to
Case
11
significant
change
with
Per
correlation
in pleural
LDH
significance (r=0.642;
Treatment
level
fluid
was
Day
Protein
LDH
44
-10
-26
83
117
100
between
protein
average
level
weak
and
Heart
Failure
did
(r
not
137
weight
loss
0.715;
p<O.05);
reach
statistical
per
p<O.l).
of Congestive
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21592/ on 05/05/2017
(Chakko,
Ca/dwell,
Sforza)
dative
effusions
systemic
develop
factors
hydrostatic
when
such
as
pressure
or
there
an
is a change
increase
a decrease
in
in
capillary
in colloid
oncotic
Exudates
are the result
of pleural
inflaminjury,
or lymphatic
obstruction.
An exudative
process
always
requires
workup
of the
a more
extensive
pleural
space
search
for more
life-threatening
occult
malignancy.2
Transudative
common
finding
in patients
14
It is believed
that
elevate
convert
the
protein
content
it into a “pseudoexudate
More
than
50 years
ago,
effect
of diuresis,
using
concentration
of protein
with decompensated
volume
of fluid
and
concentration
investigators7
diuresis
and
an
a
effusion
and
et a17 studied
the
on the
patients
cardiac
failure.
A decrease
a small
increase
in the
in the
protein
by digitalis
were
similar
and
reported.
changes
rest
in bed.
About
To the
in
and the
three
transudates
in the
pleural
was ofthe
the more
while
the
more
fluid
opinion
in effusions
rapid
protein
Some
The
the
exudate
at the
level
may
One
in this
serum
protein
levels
believe
ratio
study
hypoalbuminemia.
of
that
protein
the
would
were
use
to
that
the
than
study,
ago.5’7
This
diuretics
the
an
fluid
our
years
that
were
for
pleural
in
many
would
these
criteria
impressive
potent
ratio
was
0.64.
used
ones
used
in the
fluid
LDH
level
treatment
this
and
took
a pleural
range
In this
ofheart
failure,
pleural
ofLDH
level
rose
of LDH
38
LDH
ratio
5) had a pleural
also
fluid
his
patient,
and
failure,
all three
resolved
the
protein
pulmonary
LDH
embolism
scan.
fluid
With
well
after
the
chemistries
for exudate
the treatment
is doing
ratio
fluid/serum
the pleural
criteria
with
patient
64 percent,
fluid/serum
but
that this
of LDH
of heart
decreased
by ventilation-perfusion
simulta-
permitted
and
excluded
data
presented.
a pleural
level
serum
transudative
had
proper
classification
of these
patients;’5
however,
contention
has not been
tested
so far.
We studied
eight
patients
with typical
clinical
roentgenographic
findings
of heart
failure.
We
in the
The
pleural
fluid/serum
Another
patient
(case
No
have
rise
fact
fluid
the
changed,
and
The
effusion
of the
The
1) had
the pleural
electrolytes,
larger,
move
for
(case
of LDH
was
related
of water
and
being
much
patients
He
concentration
probably
met
the
more
effusions
at the initial
study. We believe
markedly
elevated
serum
level
In this patient,
after treatment
though
in the
was
and
transudates.
criteria
Using
but
more
by
patient
even
2.0
1.3
g/dl).
pleural
reported
explained
failure,
level
(3.8
such
and
for LDH
study
study.
was
are much
with
high
is no
past.
level
remarkably
had
to those
be
mean
protein
there
ratios
exudates
initial
final
of protein
compared
in five patients
the rise in protein
diuresis
and
investigators
fluid/serum
that
clearance
molecules,
ascites
simultaneous
noted
failure,
was
that
following
slowly.
neous
also
cardiac
fluid/serum
patients
at the
percent.
increased.
Pillay
knowledge,
and
LDH
which
has done
fluid levels
of protein
to differentiate
total
g/dL
long-standing
pleural
for
from
used
of 282 unitslL
was from
the
of794
unitsfL.
to 3. 1 g/dL.
ofour
literature
pleural
of LDH
ratios
monly
20
and
from
best
the
The
levels
The presence
of any one of the three
classify
the pleural
fluid as an exudate.2”2
years
ago,
Pillay
studied
six patients
with
cardiac
failure
and pleural
effusions.
The protein
concentration of the pleural
fluid was estimated
on admission
and
after
a period
of treatment
for cardiac
failure
when
substantial
diuresis
had occurred.
The
mean
protein
level was 1.5 g/dL on admission
after treatment.
In one patient,
it rose
fluid
fluid/serum
the treatment
of
of Light
et al,12
section,
are com-
today
These
during
pleural
pleural
protein
increased
significantly
with
congestive
heart
failure.
The criteria
which
are described
in the results
criteria,
mercurial
diuretics,
in chest fluid in four
the
the
protein.
LDH
often
entails
#{149}“3,6
Gilligan
and
other
study
measurements.
disease,
especially
pleural
effusion
is a
with
congestive
heart
diuretic
therapy
may
of such
of the fluid
had observed
caused
and
and
using
protein
pressure.
mation,
invasive
evaluated
were
of
four
met.
heart
months
offollow-up.
to furosemide
the elevated
This patient
had a brisk diuretic
response
before
thoracocentesis.
We believe
that
pleural
fluid/serum
ratio is explained
by
this.
investigators
Other
stances
where
pleural
tive heart
failure
met
and Speicher’7
whether
the
studied
criteria
have
effusions
criteria
reported
similar
secondary
for exudates.
495 pleural
of Light
et
in-
to congesPeterman
effusions
would
to evaluate
be highly
alh2
care not to include
patients
in whom
another
etiology
for pleural
effusion
might
coexist.
Patients
with isolated
left-sided
pleural
effusion
were excluded,
since
discriminating
this
percent)
had exudative
effusions.
These
investigators’7
did not address
the issue of treatment
of heart
failure
or timing
of thoracocentesis.
It is possible
that such a
is an uncommon
effusions
responded
Long-term
did
The
similar
finding
to the
follow-up
was
in heart
treatment
available
the
ones
used
by
of heart
Pleural
failure.
in all patients
not reveal
any other
coexistent
criteria
we used for selecting
to
16
Light
and
pleural
disease.
patients
were
very
et
al’2
for
the
diagnosis
of congestive
heart
failure
in their
study
of
pleural
effusions.
Treatment
ofcongestive
heart failure
and its effect
on pleural
chemistry
was prospectively
Of
no
high
incidence
ofheart
The
et
to separate
transudates
and
the 57 patients
with congestive
other
cause
for pleural
effusion,
alh2
depending
example,
of exudates
failure.
sensitivity
for
and
diagnosing
was
specificity
exudative
the
exudates.
heart
failure
19 patients
result
ofthe
and
(33
of treatment
criteria
effusion
of Light
will
vary
on how many
of the criteria
are met;
for
if an exudate
is diagnosed
when
only one of
CHEST
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21592/ on 05/05/2017
I 95 I 4 I APRIL,
1989
801
the criteria
is abnormal,
would
be 99 percent
and
an exudate
sensitivity
98 percent
is diagnosed
are abnormal,
the
54 percent
and
that
range
to the
demonstrated
when
sensitivity
all three
specificity
and
100 percent
is of interest
exudative
compared
only
and specificity
respectively.
many
that
in
criteria
would
respectively.3”2”3
more
criteria
during
the second
initial thoracocentesis.
pleural
be
were
in
failure.
that the
may
later
The
In some
patients,
fluid which
was
be
classified
as an
mechanism
which
pleural
fluid
is not well
to the
visceral
pleura
and
its capillaries
sure
than
the
receives
Pleural
lymphatic
in the reabsorption
molecules
are
capillaries,
removed
molecules
There
and
has
while
mainly
has
however,
is a dynamic
The
much
lower
of the
blood
congestive
hydrostatic
between
bein the
that
water
rapidly
ofprotein
other
LDH
reasonable
would
than
the
to assume
be
large
more
that
likely
effusion,
a relatively
where
the
concen-
with
a larger
such an effect.
relieves
hepatic
number
of patients
may demonstrate
Treatment
of congestive
heart
failure
congestion
and may reduce
the serum
level
ratio.
which
ofLDH,
alter
of the
studied.
study
Due
therapy
was given.
Four
ing treatment
for heart
which
may have altered
802
results
have
great
include
to ethical
we were
unable
to perform
ately
up on identification
Our
the
pleural
the
and
small
number
reasons,
thoracocentesis
of a patient
clinical
significance
in the
American
and
Med
1985;
pleural
Lea and
Febiger,
College
of Physicians.
biopsy
1983
in pleural
effu-
103:799-802
procedures
Pleural
VKG.
space
Total
KG.
and
proteins
for
pleural
pleural
fluid.
in serous
Transudative
7 Gilligan
DR,
Volk
chemical
and
physical
body
J
fluids.
8 Kupfer
pleural
Ann
9 Baron
disease.
Clin
Mayo
Clin
fluids
in cardiac
effusions.
Clin
In:
Co,
Chest
Proc
1972;
failure.
S
Chest
Med
Lea
12
eds.
Co.
1982:325-31
Light
RW,
13
Intern
14 Vladutiu
AD,
thoracentesis
examination
of
the
Philadelphia:
evaluation
ed.
WB
of cardiac
Echocardiography.
cham-
Philadelphia:
I,
1972;
In: Suratt
procedures.
St.
Luchsinger
PM,
Louis:
PC,
separation
Gibson
CV
Ball
Mosby
WC.
oftransudates
Pleural
and
exudates.
77:507-13
Mayewski
1981,
and
disease.
C. Thoracentesis.
diagnostic
and interpretation
Med
Heart
of medical
Med
PF,
and
1981:119-79
MacGregor
the
Griner
failure
angiographic
ed.
H,
Manual
effusions:
heart
and
Fishburne
RS,
the
serum
104:584-85
Echocardiographic
Febiger,
PM,
of
blood
13:365-81
1986;
E,
Feigenbaum
and
Suratt
1934;
Med
Observations
1984:146-94
H.
In:
HS.
between
Congestive
.
Radiologic
Feigenbaum
bers.
11
Invest
S
Braunwald
Saunders
10
Blumgart
relationship
Intern
MG.
heart.
MC,
Clin
Y, Tessler
(letter).
RJ,
Mushlin
ofdiagnostic
tests
Al,
Greenland
and
procedures.
P Selection
Ann Intern
94:553-600
AO. Cardiac
ed.
Pleural
failure
with
effusion.
pleural
New
effusion.
York:
In: Vladutiu
Futura
Publishing
Co,
1986:173-74
15
16
Hall
WJ,
tesis
(letter).
McPeak
rax
Mayewski
RJ. Congestive
Ann
EM,
Intern
Levine
in congestive
SA.
heart
heart
Med
1986;
The
preponderance
failure.
failure
and
thoracen-
104:584-85
Ann
ofright
Intern
Med
hydrotho1946;
25:916-
27
17
Peterman
TA,
stage
laboratory
Pierce
AK.
Speicher
CE.
approach.
Pleural
Pulmonary
Evaluating
JAMA
disease.
medicine.
pleural
1984;
In:
Guenter
Philadelphia:
effusions:
a two-
252:1051-53
CH,
Welch
JB Lippincott
MH,
Co,
eds.
1982:555-
605
19
immedibefore
any
patients
were already
receivfailure
before
hospitalization,
the pleural
fluid chemistry.
of
1985; 6:49-54
fluid/serum
logistic
a trial
6:33-48
LF.
6 Chetty
18
Limitations
ofpatients
may
thora-
not after
Med J 1965; 39:142-43
Mr
to demonstrate
trating
effects
of diuresis
will be weak;
however,
we
did not find a significant
relationship
between
the size
of the effusion
and the change
in the pleural
fluid
levels
of protein
or LDH
. It is possible
that a study
and
Philadelphia:
Committee,
Diagnostic
5 Pillay
Ann
be
and
seen
47:493-506
from
than
and
into
is suspected,
early
diseases.
Intern
1985;
4 Black
the formation
is treated,
condition
thoracocentesis
SJ.
Med
which
effusions
hour.#{176}’2’
of
effusion
help to avoid unnecessary
effusions
are commonly
be done
Policy
Ann
3 Jay
arteries.4’8
fluid; the water
in the
of 30 to 75 percent
per
failure
and
sions.
pres-
pleura,
parietal
congestive
treatment
REFERENCES
artery,
the systemic
relationship
heart
effusion
effect
RW. Pleural
supply
pulmonary
the effusion
is reabsorbed
more
molecules,
and the concentrations
this
1 Light
to
that
failure,
and we do not believe
should
be performed
routinely;
be
in the
We have
demonstrated
a significant
correlation
tween
the amount
of diuresis
and the change
pleural
fluid
level
of protein.
We hypothesize
smaller
should
therapy.
due
fact
a transudative
if a comorbid
cocentesis
diuretic
Diagnostic
changes
convert
heart
complicating
such
the
from
may
in patients
with
that thoracocentesis
particulate
matter
and protein
are
by lymphatic
vessels.’8”9
Smaller
cleared
more
rapidly
than
protein.4
are
rise.
It would
failure
vessels
also play an important
role
of fluid.
Pleural
fluid and smaller
reabsorbed
by the
visceral
pleural
removal
ofpleural
a turnover
rate
when
heart
exudate.
understood.
supply
of the
2 Health
is from
capillaries
its blood
effusions
Knowledge
the
the changes
may
initially
a transudate
causes
have
of pleural
failure.
may
Pleural
it
congestive
heart failure,
significant
changes
in pleural
fluid chemistry
occur with the treatment
of congestive
heart
such
management
heart
a “pseudoexudate”
invasive
studies.
Thus,
thoracocentesis,
This study
effusions
If
Burke
between
HE.
The
the
lymphatics
which
visceral
and
the
Stewart
PB.
A method
pleural
and
other
drain
parietal
the
pleura.
potential
Am
space
Rev
Tuberc
1965; 79:52-65
20
21
Bergen
ASV,
of fluid
in the
1958;
52:118-21
Clauss
RH,
effusions.
Surg
Yacoubian
H,
Forum
1956;
Treatment of Congestive
Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21592/ on 05/05/2017
for measuring
serous
Barker
cavities.
HG.
the
J
Dynamics
Lab
turnover
Clin
Med
of pleural
7:201-04
Heart Failure (Chakko,
Ca!dwell,
Sltwza)