(Chest. 1999;116:1762-1771.)
© 1999
American College of Chest Physicians
A Pilot Study of Expiratory Flow Limitation and Lung Volume Reduction Surgery*
Ron Dueck, MD;
Sheila Cooper, MD;
David Kapelanski, MD;
Henri Colt, MD, FCCP and
Jack Clausen, MD
*
From the Departments of Anesthesiology (Drs. Dueck and Cooper), Surgery (Dr. Kapelanski), and Medicine (Drs. Colt and Clausen), University of California, San Diego and Veterans Affairs Medical Center, San Diego, CA.
Correspondence to: Ron Dueck, MD, 3350 La Jolla Village Dr, San Diego, CA 92161-5085; e-mail: rdueck{at}ucsd.edu
 |
Abstract
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|---|
Study objectives: To examine the relationships between
changes in expiratory flow limitation (FL) during anesthesia and
postoperative responses to lung volume reduction surgery (LVRS).
Design: Prospective consecutive case comparison.
Setting: University medical center.
Patients: Eight patients with severe emphysema.
Interventions: General anesthesia with muscle paralysis and
thoracic epidural analgesia were provided for LVRS via median
sternotomy.
Measurements: FEV1, functional
residual capacity (FRC), and total lung capacity (TLC) were measured
preoperatively and 3 months postoperatively. Tidal volume
(VT) flow/volume (F/V) curves were obtained with a
Pitot-type spirometer. VT, expiratory flow rate at
0.25 x VT (V'VT,25% ), and peak expiratory
flow rate (V'VT,MAX) were obtained from VT F/V
curves to derive V'VT,25%/V'VT,MAX ratio as a
measure of FL.
Results: Closed chest VT
F/V curves during anesthesia pre-LVRS showed four
patients with FL (group A) whose
V'VT,25%/V'VT,MAX ratio was 0.38 ± 0.06
(mean ± SD) and four patients without FL (group B) whose
V'VT,25%/V'VT,MAX ratio was 0.82 ± 0.06
(p = 0.0001). Closed chest post-LVRS
V'VT,25%/V'VT,MAX ratio during anesthesia
increased by 0.48 ± 0.08 in group A, compared with a 0.19 ± 0.16
reduction in group B (p = 0.0001). Preoperative FEV1 was
0.57 ± 0.10 L for group A vs 0.82 ± 0.13 L for group B
(p = 0.02). Postoperative FEV1 increased
by 67 ± 40% for group A (p = 0.03) vs 29 ± 21% for group B
(not significant). FRC decreased by 33 ± 3% for group A vs
17 ± 5% for group B (p = 0.0007), and FRC/TLC decreased by
0.14 ± 0.05 for group A vs 0.01 ± 0.07 for group B (p = 0.026).
Post-LVRS V'VT,25%/V'VT,MAX ratio
change during anesthesia correlated with postoperative reduction in FRC
(r2 = 0.89, p = 0.0004) and FRC/TLC (r2
= 0.52, p = 0.045).
Conclusion: Post-LVRS change in
V'VT,25%/V'VT,MAX ratio during anesthesia
showed a linear relationship with 3-month postoperative improvement in
dynamic hyperinflation. Thus,
V'VT,25%/V'VT,MAX ratio may help provide
valuable insights into the interactions between chest wall recoil,
dynamic hyperinflation, and VT flow rates in patients with
severe COPD and LVRS.
Key Words: COPD • dynamic hyperinflation • emphysema • expiratory flow limitation • flow/volume curve • lung volume reduction surgery
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Introduction
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Lung
volume reduction surgery (LVRS) for
severe emphysema can significantly improve maximal expiratory
flow rates and ameliorate dyspnea on exertion, probably by reducing
airway resistance and by reducing hyperinflation with corresponding
improvement in inspiratory muscle function.1
2
3
4
The
benefit derives from increased lung elastic recoil (EL)
associated with reduced dynamic hyperinflation,1
2
3
outcomes that Hoppin5
proposed may be more dependent on
the quantity of lung resected than on the severity of distension of
these resected areas.
Limitation of tidal volume (VT) increases during exercise
because of expiratory flow limitation (FL) during tidal breathing is an
important factor for exercise limitation in cases of
COPD.6
LVRS enables increased exercise VT as
well as work capacity and maximal expiratory flow rates and decreased
dynamic hyperinflation and dyspnea during exercise.7
Based
on the increased VT flow rates during exercise after
LVRS8
and other observations, we suggest that improvement
in expiratory FL during tidal breathing is an important outcome of
LVRS. Reduced dynamic hyperinflation plays a major role in improving
dyspnea after LVRS because of the recognized relationship between
dynamic airway compression and sensations of dyspnea. However, we
believe that reduced dynamic airway compression during exercise after
LVRS may also contribute to reduced dyspnea. The importance of the
interrelationships between hyperinflation and limitation of tidal flow
has also been demonstrated during methacholine-induced
bronchoconstriction9
and in the response to
bronchodilators.10
11
Expiratory FL has also been recognized as an important determinant of
dynamic hyperinflation during assisted ventilation for patients with
COPD and helps identify patients who will be difficult to
wean.12
Chest wall recoil is substantially elevated in
such patients.13
Because of these interrelationships
between the positive pressures exerted by the chest wall during
expiration, dynamic hyperinflation, and limitations in tidal flow
during rest and exercise, we reasoned that the study of flow/volume
(F/V) curves during anesthesia may provide important insights into
changes in FL after LVRS. We sought to determine whether the post-LVRS
changes in severity of FL during tidal breathing, anesthesia, and
muscle paralysis would correlate with postoperative improvement in lung
function. Pre- and post-LVRS closed chest VT F/V curves
during anesthesia were analyzed for the presence and severity of FL.
Anesthesia post-LVRS expiratory flow rate and FL changes were then
compared with 3-month postoperative static lung volumes (functional
residual capacity [FRC], total lung capacity [TLC]) and maximum
FEV1 changes. These findings were used for a
preliminary test of the hypothesis that post-LVRS FL improvement during
anesthesia with muscle paralysis correlated with 3-month postoperative
improvement in dynamic hyperinflation.
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Materials and Methods
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Participants
Informed consent was obtained according to University of
California, San Diego Internal Review Board guidelines. Eight
consecutive patients selected for bilateral LVRS and available for
3-month postoperative pulmonary function tests (PFTs) were included in
this pilot study (see Table 1
for anthropometric data). All had severe emphysema (as determined by
history, physical examination, radiographic imaging, and PFTs) and
severely emphysematous lung regions identifiable on chest radiographs,
CT scans, and pulmonary ventilation-perfusion images. PFTs included FVC
and static lung volume measurements before and 3 months after bilateral
LVRS.
Anesthesia and Surgery
A thoracic epidural catheter was placed for intraoperative
analgesia with lidocaine and postoperative analgesia with Dilaudid and
bupivacaine. A ß2-agonist bronchodilator aerosol was
administered to reduce the bronchomotor response to tracheal
intubation. General anesthesia was induced and maintained with IV
propofol infusion and was accompanied by neuromuscular blockade with
vecuronium. Airway secretions were removed by fiberoptic bronchoscopy
before VT F/V spirometry pre- and post-LVRS. VT
measurements of approximately 10 mL/kg with 100% O2 were
provided at a rate of eight breaths per minute. The
inspiratory/expiratory ratio was set at 1:4.5, the longest expiratory
time setting available for the anesthesia ventilator (model 2.B; North
American Dräger; Telford, PA).
Bilateral LVRS was performed through a median sternotomy. During
one-lung ventilation via double lumen left endobronchial tube (see
Table 1 for tube sizes), the most severely hyperinflated emphysematous
lung tissue identified during each surgical side deflation was removed
using a surgical stapling device. Bovine pericardium was used to
buttress the suture line in an attempt to limit postoperative air
leaks.14
When no further overdistended lung regions
were identifiable, the lung was reinflated and ventilated while surgery
was performed on the opposite lung. Checks for air leaks were made with
gradual sustained manual inflation to 20 cm H2O
after lung immersion in normal saline solution and with comparison of
inspired vs expired VT on VT F/V curves.
All patients were extubated after post-LVRS anesthesia VT
F/V measurements were obtained, after neuromuscular blockade reversal
was achieved with the IV administration of glycopyrrolate (0.8 to 1.0
mg) and neostigmine (4.0 to 5.0 mg), and after recovery of upper airway
reflexes was achieved.
PFTs
Preoperative and 3-month postoperative FVC and FEV1
were obtained by pneumotach-based spirometry following standards
recommended by the American Thoracic Society.15
FRC and
TLC measurements were obtained by variable pressure body
plethysmography (E. Jaeger, Inc; Warzburg, Germany) following the
guidelines of the California Thoracic Society,16
except
that panting/breathing frequency was approximately one cycle/s to avoid
spurious overestimates of plethysmographic volumes.17
Anesthesia VT F/V Curves
A Pitot-type (D-lite sensor; Datex-Ohmeda; Helsinki, Finland)
flowmeter was used to measure anesthesia VT, VT
F/V curves, percent of VT exhaled in 1.0 s
(VT1.0/VT,%), and inspiratory pressure.
Calibration procedures were performed using a 1-L syringe (Hans
Rudolph; Kansas City, MO) pumping through an identical size
double-lumen endobronchial tube, adaptors, and connectors. When water
vapor condensation produced visibly apparent water droplets, the D-lite
sensor was removed, cleaned, and recalibrated and was then reinserted
into the patient’s endotracheal tube adaptor.
Serial breath VT F/V curves were recorded during periods in
which neither lung nor chest wall surgical manipulation was present,
first during general anesthesia with muscle paralysis before sternotomy
(pre-LVRS) and then after completion of LVRS, lung reexpansion, and
sternotomy closure (post-LVRS). Any VT F/V loops with
artifacts such as an irregular F/V pattern, VT,
VT1.0/VT,%, or airway pressure variation were
rejected. The measured parameters for each study condition were then
averaged from a minimum of three VT F/V loops.
The VT F/V curves were reviewed for evidence of FL, as
described by Gottfried et al.18
Their criteria for
evidence of FL included a sharp initial expiratory flow peak followed
by a slow expiratory flow pattern with convexity toward the volume axis
(Fig 1)
. Participants whose closed chest anesthesia pre-LVRS
VT F/V curves satisfied these FL criteria constituted group
A, whereas those whose closed chest pre-LVRS VT F/V curves
did not satisfy these FL criteria constituted group B (Fig 2
, 3)
. In
addition, we identified "overt auto-positive end-expiratory pressure
(PEEP)" as an abrupt interruption of prolonged expiratory flow by
onset of inspiratory flow for the next breath (Fig 2
, participant 2,
pre-LVRS). Post-LVRS disappearance of overt auto-PEEP was defined as a
complete fall to zero expiratory flow before the onset of inspiratory
flow for the next breath.
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Figure 1.. V'VT,MAX and
V'VT,25% were derived with the aid of coordinate scales
(Photoshop 3.0) using scanned expiratory VT F/V curves pre-
and post-LVRS. The V'VT,25%/V'VT,MAX ratio
was, thus, a measure of the convexity of the F/V curve toward the
x-axis, where lower
V'VT,25%/V'VT,MAX values represent greater
convexity and, thus, more a severe expiratory FL.
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Figure 2.. Left panels: representative anesthesia
closed chest pre-LVRS VTF/V curves from the four subjects
in group A show inspiratory (negative) and expiratory (positive) flow
on the ordinate, plotted clockwise from zero volume on the abscissa.
Expiratory flow starts with a sharp upward peak, then falls immediately
to a low flow rate with convexity toward the volume axis, suggesting FL
and, thus, a low V'VT,25%/V'VT,MAX ratio (see
Table 3
, group A). Expiratory flow is eventually interrupted by
inspiratory flow for the next breath before it falls to zero,
suggesting "overt auto-PEEP." Right panels: Anesthesia
closed chest post-LVRS VTF/V curves show an improved
expiratory flow rate with less convexity toward the volume axis and a
higher V'VT,25%/V'VT,MAX ratio, with no FL and
no "overt auto-PEEP."
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Figure 3.. Left panels: anesthesia closed chest
pre-LVRS VTF/V curves from the four subjects in group B
showed higher expiratory flow rates and, thus, a higher
V'VT,25%/V'VT,MAX ratio and no FL (see Table 3
, group B), while the expiratory flow rate fell to zero before the
next breath started (ie, no "overt auto-PEEP").
Right panels: anesthesia closed chest post-LVRS expiratory
VTF/V curves showed a reduced
V'VT,25%/V'VT,MAX ratio compared to pre-LVRS,
while the post-LVRS VTF/V curve for subject 6 shows both FL
and "overt auto-PEEP."
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|
Inspiratory and expiratory anesthesia VT flow rates were
derived off-line using computer software (Photoshop, version 3.0;
Adobe; Mountain View, CA) from scanned VT F/V curves. More
specifically, X and Y gradations in Photoshop were used to derive the
expiratory flow rate at 25% of VT (V'VT,25%)
and the peak expiratory flow rate (V'VT,MAX) (Fig 1
); thus, the V'VT,25%/V'VT,MAX ratio is a
measure of FL pre-LVRS and post-LVRS.
Statistical analysis was performed with linear regression, repeated
measures analysis of variance for a treatment effect, and factorial
analysis of variance for group A vs group B differences, using computer
software (Statview SE; SAS Institute; Cary, NC).
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Results
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Preoperative PFTs
Preoperative FEV1 for all eight participants was
severely reduced at (mean ± SD) 0.70 ± 0.18 L (29.4 ± 8.5% of
predicted FEV1). Plethysmographic FRC showed severe
hyperinflation at 5.99 ± 0.93 L (207 ± 28% of predicted FRC).
Individual data are shown in Table 2
. Participants whose anesthesia pre-LVRS VT F/V curves
showed expiratory FL (group A, see below) had an average 0.26 L lower
FEV1 (p = 0.019) and an average 0.13 higher FRC/TLC ratio
(p = 0.047) compared with those whose anesthesia VT F/V
curves did not show FL (group B). Preoperative FVC F/V curves did not
show consistent shape or pattern differences between groups A and B.
Anesthesia Closed Chest Pre-LVRS VT F/V Curves
Four participants from group A (participants 2, 4, 5, and 8)
showed a pre-LVRS FL pattern during anesthesia (Fig 2
, left) and failure to reach zero expiratory flow before
interruption by the next breath’s inspiratory flow or overt auto-PEEP.
Four participants from group B (participants 1, 3, 6, and 7) did not
show an FL pattern pre-LVRS and clearly showed expiratory flow falling
to zero before the onset of the next breath (no overt auto-PEEP, Fig 3
, left).
Peak VT inspiratory flow rate was 38 ± 5 L/min for group
A vs 40 ± 8 L/min for group B, a difference that was not significant
(NS). Pre-LVRS VT1.0/VT,% was
< 40% of VT for all group A participants, whereas all
group B VT1.0/VT,% values were > 40%
of VT (Table 3
). The difference in peak expiratory flow rate (V'VT,MAX)
for group A vs group B was NS, whereas the V'VT,25% was an
average 2.6-fold higher for group B vs group A. Lower pre-LVRS
V'VT,25%/V'VT,MAX ratios were thus consistent
with greater expiratory F/V convexity toward the volume axis in group A
(more severe FL; Fig 2
, 3
, Table 3
).
Anesthesia Closed Chest Post-LVRS
VT F/V curves showed improved
VT1.0/VT,%, disappearance of the FL pattern,
and disappearance of overt auto-PEEP post-LVRS for all four
participants in group A (Fig 2
, right). One participant in
group B (participant 6) did show an FL pattern post-LVRS (Fig 3
,
right), whereas his pre-LVRS VT F/V pattern did
not show FL. This participant’s post-LVRS
VT1.0/VT,% was reduced to the group A pre-LVRS
VT1.0/VT,% range (< 40% of VT).
Thus, our eight participants showed an anesthesia FL pattern
only when VT1.0/VT,% was < 40% of
VT.
Peak VT inspiratory flow rate post-LVRS was 32 ± 2
L/min for group A vs 36 ± 1 L/min for group B (p = 0.02), although
pre- and post-LVRS inspiratory flow rate differences were NS for either
group. Expiratory flow rates showed substantial improvement for group A
participants. Post-LVRS VT1.0/VT,% was
100 ± 43% higher than pre-LVRS for group A, whereas group B showed
an average 20 ± 19% reduction in post-LVRS
VT1.0/VT,% (p = 0.0023).
V'VT,25% improved by 176% post-LVRS for group A (Table 3) , whereas V'VT,MAX showed a modest NS increase. In
contrast, Group B showed a 32% V'VT,25% reduction
(significant difference, p = 0.0156) and NS V'VT,MAX
change. Thus, the V'VT,25%/V'VT,MAX ratio
improved by 128% for group A vs a 25% reduction for group B
(p = 0.0001) (ie, significantly different FL changes).
Assessment of the reproducibility of our VT F/V
measurements showed breath-to-breath VT variation of
2.1 ± 0.9% of VT pre-LVRS, and 1.8 ± 0.7% of
VT post-LVRS (NS difference).
VT1.0/VT,% showed an average
2.3 ± 1.2% breath-to-breath variation pre-LVRS vs 2.5 ± 3.2%
post-LVRS (NS difference). Inspired VT was an average
6 ± 2 mL higher than expired VT pre-LVRS (p = 0.25),
vs 9 ± 4 mL higher than expired VT post-LVRS, suggesting
that post-LVRS staple line leaks were NS.
3-Month Postoperative PFTs
The post-LVRS increase in FEV1 was significant only
for group A (p = 0.03). Group A had an average 33 ± 3% FRC
reduction, compared with a 16 ± 4% FRC reduction for group B
(p = 0.0002, Table 2
), whereas post-LVRS change in FEV1
and FRC showed modest correlation (r2 = 0.56, p = 0.03).
In addition, group A showed an average 0.14 ± 0.05 FRC/TLC reduction
vs a 0.01 ± 0.07 FRC/TLC reduction for group B (p = 0.026).
Anesthesia VT F/V and Postoperative PFT Relationships
Change in VT1.0/VT,% during
anesthesia with muscle paralysis did not correlate with 3-month
postoperative change in FEV1 (r2 = 0.45,
p = 0.07). Similarly, V'VT,25%/V'VT,MAX
ratio change during anesthesia did not correlate with 3-month
postoperative change in FEV1 (r2 = 0.16,
p = 0.32). However, post-LVRS change in
VT1.0/VT,% during anesthesia showed excellent
correlation with 3-month postoperative percent FRC reduction
(r2 = 0.94, p = 0.0001; Fig 4
) and with FRC/TLC reduction (r2 = 0.80, p = 0.003; Fig 5
). Failure to show improved post-LVRS
VT1.0/VT,% during anesthesia was associated
with < 15% postoperative FRC reduction. Likewise,
V'VT,25% change during anesthesia showed high correlation
with postoperative percent FRC reduction (r2 = 0.96,
p = 0.0001) and with change in FRC/TLC (r2 = 0.52,
p = 0.045). Finally, V'VT,25%/V'VT,MAX ratio
change during anesthesia also showed significant correlation with FRC
and FRC/TLC reduction (Fig 6
,
7
).
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Figure 6.. Anesthesia post-LVRS change in FL
(V'VT,25%/V'VT,MAX ratio) showed excellent
correlation with 3-month postoperative percentage of FRC reduction
(y = 0.037 x -0.759; r2
= 0.889; p = 0.0004).
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Discussion
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VT F/V curves during anesthesia with muscle paralysis
showed that four of eight emphysema LVRS patients had an expiratory FL
pattern pre-LVRS (group A), whereas four participants did not show an
FL pattern (group B). Group A participants had significantly lower
V'VT,25% and
V'VT,25%/V'VT,MAX ratio pre-LVRS
(Table 3)
. The finding that an FL pattern was seen only in participants
with VT1.0/VT,% < 40% was consistent
with our observation that pre-LVRS FEV1 was lower
and FRC/TLC was higher in group A. FL on pre-LVRS anesthesia
VT F/V curves was therefore consistent with more severe
dynamic hyperinflation.10
22
The severity of FL appeared appropriately quantified with the
V'VT,25%/V'VT,MAX ratio (Table 3)
to enable
regression of post-LVRS FL changes during anesthesia with muscle
paralysis and 3-month postoperative static lung volume changes. LVRS
provided significantly greater anesthesia expiratory flow rate
improvement, as well as significantly greater FRC and FRC/TLC reduction
3 months after LVRS in group A compared with group B participants.
Linear regression suggested that
V'VT,25%/V'VT,MAX ratio changes during
anesthesia showed a continuous function related to postoperative
FRC and FRC/TLC reduction. We therefore suggest that the distinction
between group A vs group B participants as FL vs non-FL based on visual
inspection of the expiratory VT F/V curve may be arbitrary,
whereas the V'VT,25%/V'VT,MAX ratio may
provide a more reproducible measure of FL.
Selection of patients for this study was not based on their
likelihood of having FL vs not being FL. Patients were recruited in a
consecutive manner after the decision was made to provide LVRS based on
the presence of severe chronic dyspnea symptoms, severe expiratory
obstruction, and severe hyperinflation.1
Possible concerns
regarding participant selection bias might be raised in that all
four participants in group A were female participants. However, there
were also two female participants in group B, and we are not aware of a
male/female difference in either FL or efficacy of LVRS. We were
surprised to note that the four group B participants did not show FL on
their anesthetized-paralyzed supine position pre-LVRS VT
F/V curves and that these four participants did not show
significant improvement during anesthesia post-LVRS.
The assessment of greater severity of expiratory obstruction
in group A was supported by the presence of overt auto-PEEP or
interruption of prolonged expiratory flow by inspiratory flow for the
next breath, despite a ventilator inspiratory:expiratory setting of
1:4.5. Bardoczky et al.19
recently showed that overt
auto-PEEP had 78% sensitivity and 91% specificity for intrinsic PEEP
(PEEPi). We note that these authors did not find a size of
double-lumen endotracheal tube effect on presence or absence of overt
auto-PEEP, even though they used the same VT, frequency,
and inspiratory flow rates for one-lung vs two-lung ventilation. This
observation was consistent with our present findings; female
participants who were intubated with a 37-French double lumen
endotracheal tube were present in both groups A and B, suggesting that
there was not a sufficient extrinsic PEEP effect to prevent showing FL
vs non-FL differences.
The disappearance of FL and overt auto-PEEP post-LVRS in group
A participants was consistent with increased EL post-LVRS
providing increased traction on the intrapulmonary airways to improve
airway caliber and conductance and increased driving pressure to
improve expiratory flow rate,
VT1.0/VT,%.3
In addition,
reduced thoracic cage volume, and thus reduced chest wall recoil, may
have contributed to reduced dynamic airway compression.3
Thus, the significantly greater post-LVRS
V'VT,25%/V'VT,MAX ratio improvement with the
disappearance of FL in group A may also reflect a difference in the
role of the chest wall, compared with group B, because of the
significantly greater FRC reduction in group A. This difference should
also be relevant to the loss of overt auto-PEEP post-LVRS in group A,
which was consistent with the report presented by Tschernko et
al.20
of reduced PEEPi, from 8.4 ± 1.1 cm
H2O to 1.1 ± 0.4 cm H2O.
However, the disappearance of overt auto-PEEP in our group A
participants did not imply complete loss of PEEPi, because
Bardoczky et al.21
showed that a small amount of
PEEPi may be present even in the absence of visible auto-PEEP on
the expiratory VT F/V curve.
The absence of FL and overt auto-PEEP during anesthesia in group B
participants suggests that their pre-LVRS expiratory obstruction was
less severe, even though their preoperative forced maximum F/V curves
showed no qualitative differences from group A participants.
FL might have been more readily revealed in group B with application of
negative airway pressure during VT
exhalation.12
22
However, the excellent correlation
between anesthesia VT1.0/VT,% and
V'VT,25%/V'VT,MAX ratio changes with
postoperative FRC and FRC/TLC reduction suggests that our measurements
of FL during muscle paralysis provided a valid reflection of the
mechanisms involved in the improvement of dynamic hyperinflation.
Because expiratory obstruction and hyperinflation with emphysema are
caused by severely reduced EL, we presume that pre-LVRS
EL was higher in group B than in group A. This is
consistent with the recent report by Barnas et al.,23
who
observed the greatest increases in EL and lung
resistance post-LVRS for participants with the highest
preoperative FEV1, maximum voluntary ventilation,
and lowest residual volume. Furthermore, because general anesthesia
with muscle paralysis is associated with increased
EL,24
we speculate that the increased
EL during anesthesia with muscle paralysis may have been
sufficient to enhance expiratory flow rate and thereby prevent FL on
pre-LVRS anesthesia VT F/V curves for group B.
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Conclusion
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We herein introduce a new measure of expiratory FL during
VT spirometry, the
V'VT,25%/V'VT,MAX ratio. The eight
participants in this pilot study showed a continuous relationship
between their anesthesia post-LVRS change in
V'VT,25%/V'VT,MAX ratio and
postoperative improvement in dynamic hyperinflation. Our
preliminary findings suggest that the
V'VT,25%/V'VT,MAX ratio may help provide
valuable insights into the mechanisms of improved lung function after
LVRS. Further studies are warranted to confirm these observations and
to examine their relationship to PEEPi, as well as pre- and
postoperative measures of chronic dyspnea.
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Figure 7.. Anesthesia post-LVRS change in
V'VT,25%/V'VT,MAX ratio showed significant
correlation with the 3-month postoperative change in the FRC/TLC ratio
(y = 3.077 x -0.088; r2
= 0.515; p = 0.0449).
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Footnotes
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Abbreviations:
V'VT,25% = expiratory flow rate when 25% of tidal
volume is exhaled; EL = lung elastic recoil; FL = flow
limitation; FRC = functional residual capacity; F/V = flow/volume;
PEEP = positive end-expiratory pressure; PEEPi = intrinsic PEEP;
V'VT,MAX = peak expiratory flow rate; LVRS = lung
volume reduction surgery; NS = not significant; PFT = pulmonary
function test; TLC = total lung capacity; VT = tidal
volume; VT1.0/VT,% = percent of tidal volume
exhaled in 1 s
Equipment and supplies for tidal volume spirometry were provided by
Datex Medical Instrumentation, Inc.
Received for publication October 13, 1998.
Accepted for publication May 21, 1999.
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Abstract
Introduction
