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* From the Pulmonary Division, Departments of Medicine (Dr. Gelb) and Radiology (Dr. Schein), Lakewood Regional Medical Center, University of California Los Angeles, Los Angeles, CA; the School of Medicine (Dr. Brenner), University of California, Irvine, Irvine, CA; the Faculty of Medicine (Dr. Zamel), University of Toronto, Toronto, Ontario, Canada; and the Department of Thoracic Surgery (Drs. McKenna and Fischel), Chapman Medical Center, Orange, CA.
Correspondence to: Arthur F. Gelb, MD, FCCP, 3650 E. South St, Suite 308, Lakewood, CA 90712; e-mail: afgelb{at}msn.com
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Abstract |
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 TOP Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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Intervention: Bilateral targeted upper lobe stapled LVRS using video thoracoscopy was performed in 26 symptomatic patients (18 men) aged 67 ± 6 years (mean ± SD) with severe and heterogenous distribution of emphysema on lung CT. Lung function studies were measured before and up to 4 years after LVRS unless death intervened.
Results: No patients were lost to follow-up. Baseline
FEV1 was 0.7 ± 0.2 L, 29 ± 10% predicted; FVC,
2.1 ± 0.6 L, 58 ± 14% predicted (mean ± SD); maximum oxygen
consumption, 5.7 ± 3.8 mL/min/kg (normal, > 18 mL/min/kg);
dyspneic class 
3 (able to walk 
100 yards) and oxygen dependence
part- or full-time in 18 patients. Following LVRS, mortality due to
respiratory failure at 1, 2, 3, and 4 years was 4%, 19%, 31%, and
46%, respectively. At 1, 2, 3, and 4 years after LVRS, an increase
above baseline for FEV1 > 200 mL and/or FVC > 400 mL
was noted in 73%, 46%, 35%, and 27% of patients, respectively; a
decrease in dyspnea grade 1 in 88%, 69%, 46%, and 27% of
patients, respectively; and elimination of oxygen dependence in 78%,
50%, 33%, and 22% of patients, respectively. The mechanism
for expiratory airflow improvement was accounted for by the increase in
both lung elastic recoil and small airway intraluminal caliber and
reduction in hyperinflation. Only FVC and vital capacity (VC) of all
preoperative lung function studies could identify the 9 patients with
significant physiologic improvement at > 3 years after LVRS,
respectively, from 10 patients who responded 2 years and died
within 4 years (p < 0.01).
Conclusions: Bilateral LVRS provides clinical and physiologic improvement for > 3 years in 9 of 26 patients with emphysema primarily due to both increased lung elastic recoil and small airway caliber and decreased hyperinflation. The 9 patients had VC and FVC greater at baseline (p < 0.01) when compared to 10 short-term responders who died < 4 years after LVRS.
Key Words: emphysema • lung elastic recoil • lung function • lung volume reduction surgery • transdiaphragmatic pressures
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Introduction |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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1-antitrypsin
deficiency, variable improvement in relief of dyspnea, exercise
tolerance, oxygen use and lung function, and mortality has been noted
for 2 years following surgery.1
2
3
4
5
6
Beyond 2 years after
LVRS, there is very limited experience. The 2-year post-LVRS results
are in contrast to the progressive deterioration in lung function in
similar patients originally accepted, but denied LVRS by Medicare and
followed for 2 years.6
Furthermore, historical data of
patients with severe expiratory airflow limitation due to emphysema and
FEV1 < 0.75 L or 30% predicted indicates
survival of 50 to 60% at 3 years.7
8
Additionally,
patients admitted to an ICU for exacerbation of COPD have a 1-year
mortality rate of 30% irrespective of the need for endotracheal
intubation and mechanical ventilation; in patients > 65 years old,
the mortality rate at 1 year doubles.9
The present study prospectively evaluates annual clinical as well as
physiologic changes in lung function, including mechanisms of
expiratory airflow limitation following LVRS for
non-1-antitrypsin emphysema. Results indicate
significant clinical and physiologic improvement in lung function in 9
of 26 patients and 7 of 26 patients at 3 years and at 4 years after
LVRS, respectively. However, of all preoperative lung function tests,
only vital capacity (VC) and FVC could identify these 9 long-term
patients from 10 others who only had improvement for 2 years and
died. The improvement in expiratory airflow and hyperinflation is
related to the increase in lung elastic recoil pressure and its
secondary effect on increasing small airways diameter.
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Materials and Methods |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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3 dyspnea10
(able to walk 100 yards), who had
exhausted all medical therapy including antibiotics, aerosol and
systemic bronchodilators (including ß2-agonists
and ipratropium bromide), aerosol and systemic corticosteroids, and
repeated attempts at physical conditioning. As previously noted,
high-resolution, thin-section CT of the lung demonstrated emphysema
severity scores11
60 with heterogenous distribution,
ie, severe emphysematous destruction predominantly in upper
and middle lung fields. Nuclear medicine perfusion scans demonstrated
similar heterogenous distribution. Smoking history was 52 ± 13
pack-years (mean ± SD).
Operative Technique
From January to June 1995, after obtaining informed consent, 82
patients underwent sequential, bilateral stapled lung volume reduction
for emphysema using video-assisted thoracoscopic surgery at the same
sitting. The surgical technique and selection has been previously
reported.2
5
12
It was estimated that approximately 20 to
30% of each lung was excised, and the resected lung weighed 30 to
90 g. Twenty-six of the 82 patients agreed to undergo additional
studies, including lung elastic recoil, preoperatively and form the
basis of this prospective study.
Lung Function Studies
As previously reported,2
we obtained informed
consent and measured lung function, including maximum inspiratory and
maximum expiratory flow-volume (MEFV) curves, thoracic gas
volume, airway resistance, single-breath diffusing capacity of the lung
for carbon monoxide (DLCO), and static lung elastic recoil
when the patients were clinically stable, using a pressure-compensated
flow plethysmograph (Model 6200 Autobox; SensorMedics; Yorba Linda,
CA), and compared the results with predicted
values.2
During panting, the cheeks were supported and the
frequency was set at 1 Hz to avoid mouth pressure from spuriously
underestimating alveolar pressure13
and overestimating
thoracic gas volume. All studies were done after three inhalations of
aerosolized albuterol, 670 µg.
As previously noted,2 15 measurements of static lung elastic recoil pressures were obtained in the open plethysmograph with the patient in a sitting position after placement of a 10-cm-long balloon inflated with 0.5 mL of air, initially in the stomach and withdrawn into the lower third of the esophagus. After at least two inspirations to total lung capacity (TLC), static transpulmonary (mouth-esophageal) pressures were recorded following stepwise, 3-s interruptions of exhalation against a closed shutter at different lung volumes, and the expired volume was measured at the mouth. A minimum of five deflation curves were obtained for each patient, and a plot of best visual fit of the pooled data was drawn. Balloon position and volume were similar in each patient before and after LVRS.
Expiratory airflow limitation as seen in the MEFV curves does not distinguish whether the source is primarily due to loss of lung elastic recoil (emphysema),16 17 intrinsic small airway disease,16 17 or asthma,18 with no significant loss of elastic recoil or both. Therefore, to determine the mechanisms of expiratory airflow limitation in COPD before and after LVRS, we plotted the maximum expiratory airflow obtained from the MEFV curve against static lung elastic recoil pressure at corresponding lung volumes and constructed maximum expiratory airflow-static lung elastic recoil pressure (MFSR) curves2 15 16 17 19 20 . The slope of the MFSR curve between 50% and 25% of the FVC represents the conductance of the small airway S segment (Gs)19 and provides quantitative assessment of small airway caliber. Normal values were obtained previously in seven healthy subjects 61 to 74 years old in whom the Gs was 0.6 ± 0.1 L/s/cm H2O (mean ± SD) and static lung elastic recoil pressure at TLC was 25 ± 7 cm H2O.21
Exercise Studies
As previously described,2
progressive exercise
testing to symptom-limited maximum was obtained using electronically
braked cycle ergometry (Ergometrics 800; Sensor Medics; Yorba Linda,
CA) with increases of 10 to 20 W at 2-min intervals at a
pedaling cycle of 40 to 50 revolutions per minute. The patients
breathed room air or oxygen-enriched air through a mouthpiece with nose
clips using a low-resistance two-way nonrebreathing valve. Expired
gases were collected and analyzed using a pulmonary function analyzer
(Vmax 29; SensorMedics).
Follow-up
All patient were followed for up to 4 years after LVRS unless
death intervened. No patient was lost to follow-up.
Statistical Methods
Comparison of differences between patient groups included paired
and unpaired t tests, and analysis of variance was tested
using a statistical software package (Systat 7.0 for Windows; SPSS;
Chicago, IL). Values were considered significant at p < 0.05.
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Results |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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100 yards; mean ± SD). Actual survival at 0.5, 1, 2, 3, and 4 years after LVRS was 96%, 96%, 81%, 69% and 54%, respectively (See Fig 1 ). All deaths were related to respiratory failure, although concomitant lung malignancy was noted in two of four patients autopsied. Improvement in FEV1 > 0.2 L, FVC > 0.4 L, or both was 88%, 73%, 46%, 35%, and 27% respectively, and these patients are considered responders (See Fig 1 ). Six of nine patients at 3 years and five of seven patients who demonstrated this physiologic improvement at 4 years after LVRS had both FEV1 > 0.2 L as well as FVC > 0.4 L when compared to baseline values.
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There was a decrease in dyspnea grade 1 in 88%, 69%, 46% and
27% of the 26 patients at 1, 2, 3, and 4 years after LVRS. Oxygen
dependence (part- or full-time) initially present in 18 patients was
eliminated in 78%, 50%, 33% and 22% of patients at 1, 2, 3, and 4
years after LVRS.
Maximum Expiratory Airflow
At > 3 years after LVRS, we analyzed the mechanism of
improvement in expiratory airflow in the nine long-term responder
patients who increased FEV1 > 0.2 L, FVC
> 0.4 L, or both following LVRS. Compared to the preoperative
baseline, the MEFV demonstrated a reduction in both TLC and residual
volume (RV), but more so in the latter, such that FVC increased (See
Table 1
and Fig 2 ). Furthermore, maximum expiratory airflow at any lung volume was
increased when compared to the same lung volume prior to LVRS, but was
still far below normal values. FEV1 increased
0.30 ± 0.1 L compared to baseline (mean ± SD). FVC increased
0.48 ± 0.25 L.
|
|
3
years after LVRS), maximum expiratory airflow increased, both to
greater lung elastic recoil as well as increased conductance of the
S-segment slope, reflecting better airway stability with less
collapse/obstruction of flow-limiting segments.
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0.2 L, FVC 0.4 L, or
both from baseline and 10 short-term responders who died within 4 years
of LVRS (See Table 1
). Short-term responders had increase in
FEV1 0.2 L, FVC 0.4 L, or both 2
years after LVRS. |
Discussion |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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These observations, based on very strict outcome criteria, are impressive in elderly patients with end-stage emphysema with a high mortality rate from respiratory failure. Preoperatively, they had very severe airflow limitation, hyperinflation, markedly impaired lifestyle with dyspnea limiting walking < 100 yards, and 18 of 26 patients required part- or full-time oxygen administration.
The mortality rate due to respiratory failure in 4%, 19%, 31%, and 46% of patients following LVRS at 1, 2, 3, and 4 years, respectively, is consistent or lower than previous nonsurgical data in similarly impaired patients with emphysema.6 7 8 9 The improvement in expiratory airflow limitation and decrease in hyperinflation is predominantly due to increased lung elastic recoil following LVRS2 15 with expansion of remaining lung.
Only VC and FVC of all preoperative clinical, physiologic, perfusion, and lung CT emphysema heterogeneity tests could identify the 9 individual patients who achieved significant improvement at > 3 years after -LVRS from the 10 patients whose physiologic improvement was < 2 years and who died within 4 years of LVRS.
Lung Elastic Recoil and Mechanisms of Airflow Limitation
Expiratory airflow at any given lung volume is directly
proportional to the alveolar driving pressure (ie, elastic
recoil) and inversely proportional to resistance offered by small
airways < 2 mm in diameter.19
20
Elastic recoil also
provides tethering support to small airways to reduce collapse during
forced exhalation.
Emphysema destroys the alveolar-capillary surface area of the lung, which results in decreased DLCO and mechanical loss of lung elastic recoil, with increased collapse of small airways during exhalation even in early disease.16 17 This causes expiratory airflow limitation often best visualized on MEFV curves.16 17 However, there may be concomitant, independent, intrinsic small airway disease,16 17 22 especially in chronic cigarette smokers causing similar airflow limitation on MEFV11 16 17 curves. We have shown previously in clinically unsuspected emphysema, when the FEV1 is normal or borderline16 17 despite significant parenchymal destruction, the reduction in expiratory airflow was predominantly accounted for by the loss of lung elastic recoil, implying small airway disease did not contribute significantly to airflow limitation. This is in contrast to results in the present study where severe expiratory airflow limitation is due to both loss of lung elastic recoil as well as suspected severe intrinsic small airway disease (reduced Gs). These results are consistent with the pathophysiologic studies by Hogg et al11 22 23 in chronic cigarette smokers with far-advanced emphysema.
Elastic Recoil Following Lobectomy and Pneumonectomy
Following lobectomy and pneumonectomy, previous
studies24
25
26
have emphasized the reduction in both RV and
TLC, but more so in the latter, causing a reduction in both VC and
FEV1. The lungs become stiffer with decreased
compliance over the tidal volume range, and lung elastic recoil at TLC
is increased, especially following pneumonectomy. Because of the
reduced lung volume, airway resistance increases despite the stiffer
lungs. DLCO is maintained after lobectomy, but decreases
following pneumonectomy.
Elastic Recoil Following Bullectomy and LVRS
Large lung bullae may occur in the presence or absence of
emphysema. Rogers et al27
initially showed long-term
improvement in airway conductance as measured by plethysmography,
following bullectomy in isolated bullous lung disease without
emphysema, and short-term improvement in bullous emphysema.
Subsequently, we28
as well as other
investigators29
30
31
reported that bullectomy in the
presence (LVRS equivalent) or absence32
of emphysema
reduced hyperinflation and increased expiratory airflow and airway
conductance by increasing lung elastic recoil.
By removing nonfunctioning lung, TLC and RV would be similarly reduced, and the lung pressure-volume curve would have a nearly parallel shift to lower lung volumes. The lung elastic recoil pressure at TLC would be relatively increased. Alternatively, expansion of remaining near-normal functioning lung would result in increased VC, FEV1, airway conductance, DLCO, and lung elastic recoil at TLC, such that RV would be decreased more than TLC.
Similar mechanisms, but to a lesser extent, were observed following LVRS for severe emphysema with heterogenous distribution, such that the upper half of the lungs were more adversely affected. Sciurba et al33 reported increases in lung elastic recoil at 4 months after unilateral LVRS.
We have previously demonstrated2 15 34 that bilateral upper lobe LVRS for generalized nonbullous emphysema increases forced total capacity, FEV1, expiratory airflow, and airway conductance, and reduces hyperinflation at TLC, all due to real increases in lung elastic recoil. The maximal increase in elastic recoil occurred 6 to 12 months after LVRS with subsequent loss to near baseline levels by 2 years after LVRS.2 Furthermore, analysis of the mechanism of airflow limitation using MFSR curves prior to LVRS demonstrated, in addition to the severe loss of lung elastic recoil, suspected independent intrinsic small airway involvement (ie, reduced Gs),2 similar to the present study.
Following LVRS, we noted an increase in lung elastic recoil that was probably due to improved functioning of the remaining lung with less-extensive emphysema. The increase in Gs was attributed to reduced extrinsic compression and more effective tethering of small airways, thereby reducing collapse during forced exhalation and allowing for overall increased airway conductance.2 15 Subsequently, Martinez et al35 and Jubran et al36 also reported short-term increase in lung elastic recoil following bilateral LVRS.
Dyspnea and Exercise Tolerance After LVRS
Numerous investigators have reported improvement in dyspnea and
exercise tolerance after LVRS.1
2
3
4
5
6
17
35
37
38
39
40
41
42
43
44
This best
correlated with the reduction in hyperinflation and increase in
transdiaphragmatic pressure due to recruitment of inspiratory
respiratory muscles1
17
35
37
38
39
40
41
42
43
44
and subsequent increased
neuromechanical coupling,45
often irrespective of changes
in FEV1. However, we believe the reduction in
hyperinflation and increased transdiaphragmatic pressure is consequent
to the increase in lung elastic recoil following LVRS and repositioning
of the diaphragm.
Selection Criteria
The results of this study identified preoperative significant VC
and FVC differences between nine patient responders with > 3-year
increase in FEV1 > 0.2 L and/or FVC > 0.4 L
from short-term responders with physiologic improvement 2 years who
died within 4 years of LVRS. This difference may reflect a global
estimate of functioning lung tissue. Additional evaluation will be
required to test the reliability of this observation.
A previous study by Ingenito et al46 correlated 6-month increase in FEV1 following LVRS with baseline lung elastic recoil at TLC and inspiratory total lung resistance. However, their range of lung resistance was much higher than what was measured in our patients. Furthermore, a review of the data of Ingenito et al46 over the range of inspiratory airway resistance similar to our patients (< 9 cm H2O/L/s) revealed no significant correlation with short-term increase in FEV1. Inspiratory airway resistance in the present study was obtained using noninvasive plethysmography. This technique does not measure lung tissue resistance, which would not be expected to be significantly increased, and is a small component of total lung resistance. We found no significant correlation (r = 0.3) between preoperative airway conductance and subsequent long-term improvement in FEV1 > 0.2 L and FVC > 0.4 L.
With the exception of one study,47 most investigators48 49 have found preoperative mild pulmonary hypertension that improved following LVRS. Mild changes in gas exchange after LVRS have been reported, presumably from alternations in ventilation-perfusion heterogeneity.50
In summary, LVRS provides significant clinical and physiologic
improvement to a subset of patients with severe emphysema for up to 4
years. Baseline differences for VC and FVC separated these patients
preoperatively from short-term responders who had physiologic
improvement 2 years after LVRS and who died during the study.
However, the importance of heterogenous distribution of emphysema on
lung CT and perfusion scans in choosing potential LVRS candidates must
still be emphasized.51
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Footnotes |
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Supported by Department of Energy Grant No. DE-FG03–91ER61227, American Lung Association Grant No. CI-030-N, and California Tobacco Related Disease Research Program Grant No. 6RT-0158.
Received for publication June 25, 1999. Accepted for publication September 9, 1999.
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References |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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1-antitrypsin deficiency versus smoker’s emphysema. Eur Respir J 12,1028-1032[Abstract]
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max = maximum
oxygen consumption; lps = liters per second.
