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ABSTRACT |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Early experience suggests that lung volume reduction surgery improves exercise tolerance as measured by the 6-min walk distance in patients with emphysema. To identify the physiologic mechanism(s) by which lung volume reduction surgery improved exercise, we performed progressive cardiopulmonary exercise testing, including rest and peak exercise blood gas determinations, on 21 consecutive patients before and 3 mo after lung volume reduction surgery. Maximal work (median,
range, % change) increased 17.5 watts (
13 to +44 watts, 46%, p < 0.05), maximal oxygen consumption increased 0.16 L/min (0.17 to +0.48, 25%, p < 0.05), maximal ventilation increased 6.6 L/min
(7 to +26 L/min, 27%, p < 0.05), and the dead space/tidal volume ratio at peak exercise decreased
0.07 (0.22 to +0.09, 12%, p < 0.05), exclusively as a result of an increase in the tidal volume. After
lung volume reduction surgery heart rate decreased at the point of isowatt exercise, from 115 to 111 beats/min (p < 0.05). No difference was observed in the other physiologic variables measured at isowatt exercise. In 13 patients exercised while breathing room air, the alveolar-to-arterial O2 difference
increased, and the arterial O2 tension decreased from rest to peak exercise both before and after the
operation, but significant changes in this response were not observed after surgery. The primary problem limiting exercise performance in these patients was the limited ventilatory capacity as 16 and 13 of the 21 subjects developed acute respiratory acidemia at peak exercise before and after surgery, respectively. Lung volume reduction surgery in patients with severe emphysema improved maximal
ventilation, thereby improving maximal exercise performance.
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Patients with emphysema often have severely limited exercise performance as a result of (1) airflow limitation reducing their ventilatory reserve, (2) hyperinflation-associated respiratory muscle dysfunction, (3) exercise-induced hypoxemia, (4) cardiac dysfunction, (5) dyspnea, and/or (6) deconditioning. Both unilateral and bilateral lung volume reduction surgery (LVRS) have been reported to improve exercise capacity as measured by the 6-min walk test (1).
Although the 6-min walk test is considered to be an excellent measure of functional capacity, it is limited in its ability to assess the physiologic cause(s) of exercise limitation. In contrast, incremental symptom-limited cardiopulmonary exercise testing allows quantitative and qualitative assessment of the physiologic determinants of maximal exercise performance. Although there are numerous physiologic effects of LVRS that might result in improved exercise capacity (e.g., augmented elastic recoil and expiratory airflow, improved patterns of breathing and respiratory muscle recruitment associated with reduced lung volumes, improved gas exchange, and increased right heart filling) (5, 6), the mechanism(s) by which the improvement might occur has not been determined. Accordingly, we evaluated a consecutive series of consenting patients with a progressive work cardiopulmonary exercise test in patients with emphysema before and 3 mo after LVRS.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Between October 1994 and November 1995, 47 patients with severe airflow limitation, air-trapping, and roentgenographic evidence of emphysema underwent LVRS at our institution. Screening criteria for entry into our LVRS program included: (1) evidence of severe airflow obstruction (15% < FEV1 < 35%), (2) evidence of severe hyperinflation (TLC > 120% or RV > 150%), (3) age < 75, (4) smoking cessation for at least 3 mo, (5) lack of significant daily sputum production; (6) CT evidence of emphysema, and (7) lack of other comorbid diseases. Any patient with EKG or roentgenographic evidence of pulmonary hypertension underwent echocardiography to evaluate pulmonary artery pressures; if the echocardiogram revealed pulmonary hypertension or was equivocal, the right half of the heart was subsequently evaluated. Twenty-one consecutive subjects who agreed to undergo preoperative and 3-mo postoperative cardiopulmonary exercise testing were enrolled in this study, which was approved by our institutional review board. Each patient underwent bilateral lung reduction via median sternotomy with resection of approximately 25% of the volume of each lung, as described by Cooper and colleagues (1).
Spirometry was performed utilizing a pneumotachograph attached to a microprocessor (Jaeger Masterlab, Wurtzburg, Germany). Lung volumes were measured in a body plethysmograph (Sensormedics, Yorba Linda, CA). Spirometry, plethysmographic lung volume, and maximal voluntary ventilation measurements were performed according to American Thoracic Society guidelines (7).
Each patient performed a symptom-limited maximal exercise test
on an electronically braked cycle ergometer (Quinton Instruments, Bothell, WA) utilizing a smooth ramp protocol consisting of 3 min of
rest followed by 2 min of unloaded pedaling, and then by a work load
that progressively increased in increments of 10 watts/min until symptom limitation was reached. Breath-by-breath analysis was performed
with the patients breathing through a mouthpiece attached to a pneumotachograph that measured expiratory flow (Quinton Instruments).
The flow signal was integrated to obtain tidal volume (VT) and minute
ventilationV (
E). Breathing frequency (f) was averaged over 15 s.
Oxygen consumption (O2) was measured on a breath-by-breath basis using a zirconium oxygen analyzer; carbon dioxide production
(CO2) was measured with an infrared analyzer. Heart rate was measured continuously with a pulse oximeter (Ohmeda, Louisville, CO)
and 12-lead electrocardiographic tracings were obtained each minute.
Arterial blood gas samples were obtained from the radial artery at rest and at peak exercise. Seven patients who required O2 supplementation prior to LVRS were exercised while breathing approximately 35% O2 both before and after the operation. Blood gas determinations were obtained on the other 14 patients breathing air. The physiologic dead space to tidal volume ratio (VD/VT) was calculated at rest and at peak exercise utilizing the Inghoff modification of the Bohr equation. Hemoglobin saturation was monitored continuously with a pulse oximeter.
Measurements of f, VT, E, O2, CO2, heart rate (HR), and O2
pulse were made at rest and at maximal exercise no more than 7 d before LVRS. The values reported for these variables are averages obtained during the last 30 s of the rest period, denoted "rest," and during the 30 s preceding the maximal level of exercise attained, denoted
"peak exercise pre-LVRS." Three months after LVRS the same variables were measured at rest, at the maximal level of work attained
pre-LVRS (denoted "isowatt exercise post-LVRS"), and at the maximal exercise achieved (denoted "peak exercise post-LVRS").
Patients indicated their level of dyspnea at rest and at peak exercise using a 100 mm visual analog scale (VAS) (8).
Because the data were not normally distributed, results are presented as medians with ranges, and preoperative and postoperative comparisons were performed using Wilcoxon's signed rank test; p < 0.05 was taken to represent statistical significance.
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RESULTS |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Pulmonary Function Tests
Median values, ranges, and the percent of the predicted values
for the 15 male and six female patients are listed in Table 1. No
significant difference was observed in the age or any of the preoperative pulmonary function testing or arterial blood gas values for the entire population of subjects operated on at our institution versus the 21 subjects who agreed to participate in this
study. One patient (not enrolled in the study) died during the
period of data collection. The FEV1 increased in the study subjects a median of 29% (range, 16 to +88%, p < 0.05) and the FVC by 16% (range, 20 to +101%, p < 0.05). The TLC decreased a median of 8% (range, 24 to +21%, p < 0.05) and
the RV decreased by 22% (range, 45 to +21%, p < 0.05).
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Exercise Tests
Rest. No differences were observed in f, VT, E, O2, CO2,
HR, or O2 pulse (Table 2) before versus after LVRS. Small decreases in the PaCO2 and HCO3
were noted (Table 3). No statistical differences were noted in the PaO2 or the AaPO2 in the 14 patients exercised while breathing air after surgery. The VD/
VT decreased slightly but significantly (0.50 to 0.48, p < 0.05).
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Peak exercise. WORK. The maximal work performed after
LVRS increased a median of 17.5 watts (range, 13 to +44
watts, p < 0.05), a 46% improvement (range, 17 to +144%)
(Figure 1A). The maximal O2 (VO2max) increased 0.16 L/min
(range, 0.17 to +0.48 L/min, p < 0.05), or 25% (range, 15
to +81%) (Figure 1B).
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VENTILATORY PERFORMANCE. The E measured at peak exercise (Emax) after surgery increased 6.6 L/min (range, 7 to
+26 L/min, p < 0.05), or 27% (range, 14 to +167%) (Figure
2A). This was due to an increase in VT by a median value of
0.28 L (range, 0.29 to +0.64 L, p < 0.05), or 43% (range,
16 to +144%) (Figure 2B) as no change in f was observed
(Figure 2C). The median Emax, expressed as a fraction of
maximal voluntary ventilation, was 0.8 (range, 0.7 to 1.2) pre-LVRS and 0.9 (range, 0.6 to 1.1) post-LVRS (p < 0.05) for the
13 patients in whom maximal volume ventilation (MVV) was
measured both pre- and post-LVRS.
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GAS EXCHANGE. Prior to LVRS 16 of the 21 patients in
whom arterial blood gas determinations were obtained both at
rest and at peak exercise developed an acute respiratory acidemia (i.e., an increase in PaCO2 
4 mm Hg with a pH decreasing > 0.05 units to < 7.35). After LVRS, 14 of the 21 patients
developed respiratory acidemia. In the 13 patients breathing
air the PaO2 decreased and the AaPO2 increased going from rest
to exercise both before and after LVRS, but significant changes
in these responses were not observed after the operation (Table 3).
VD/VT at peak exercise after surgery decreased by 0.07 (range, 0.22 to +0.09, p < 0.05), or 13% (range, 41 to +26%)
(Figure 3A). The change in VD/VT resulted from an increase
in VT as VD actually increased slightly after surgery (median
change, 0.05 L; range, 0.18 to +0.35 L, p < 0.05), or 12%
(range, 35 to +54%) (Figure 3B).
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CARDIAC PERFORMANCE. Heart rate at peak exercise increased
a median of 6.5 beats/min (range, 14 to +19 beats/min, p < 0.05), or 5% change (range, 11 to +16%) (Figure 4A). The O2
pulse (O2/HR) increased by 1.2 ml/beat (range, 1.2 to +3.1
ml/beat, p < 0.05), or 20% (range, 11 to +56%) (Figure 4B).
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Isowatt exercise (Table 3). WORK. No difference was observed in the O2 measured at the point of isowatt exercise 3 mo after LVRS.
VENTILATORY PERFORMANCE. No difference was observed in
the E measured at the point of isowatt exercise after LVRS, although VT increased 0.20 L (range, 0.26 to +0.71 L, p < 0.05),
or 22% (range, 14 to +105%), and f decreased 5 breaths/min
(range +7 to 19 breaths/min, p < 0.05) or 18% (range, 49 to
+32%). Arterial blood gas determinations were not obtained
at the point of isowatt exercise after LVRS.
CARDIAC PERFORMANCE. HR decreased at the point of isowatt exercise after LVRS by 3.5 beats/min (range, 28 to +24
beats/min, p < 0.05). No change in the VO2/HR was observed.
Dyspnea
VAS measured at rest decreased from a median of 29 (range, 7 to 76) to 9 (range, 0 to 60, p < 0.05) after LVRS. At peak exercise the VAS decreased a median of 82 (range, 34 to 92) to 47 (range, 28 to 82, p < 0.05).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The major finding of this study is that maximal exercise performance, as measured by work performed or maximal O2
achieved, improved in patients with emphysema 3 mo after
LVRS. At maximal exercise before and after LVRS the ventilation observed approached the MVV, and respiratory acidemia was present in the large majority of the patients, indicating that the primary problem limiting exercise performance
was ventilatory limitation.
Ventilatory Performance
The reduction in elastic recoil seen in emphysema decreases
expiratory air flow such that the maximal ventilatory capacity becomes limited by the boundary of the maximal expiratory
flow volume curve (9). Accordingly, a greater fraction of
the maximal E is used during exercise (i.e., the Emax/MVV
is increased) and respiratory acidemia frequently occurs, as
was seen in our patients. Sciurba and colleagues (6) and Gelb
and colleagues (13) have recently reported that elastic recoil
increases after LVRS. This finding could explain much of the
increase in forced expiratory airflow, MVV, and maximal exercise E that we observed 3 mo after LVRS.
Patients with emphysema have an increased VD/VT that
does not decrease appropriately during exercise (14). The
excess wasted ventilation contributes to the development of
respiratory acidemia and the resulting exercise limitation. After LVRS we found that the VD/VT decreased slightly at rest
and markedly during exercise. The decrease was the result of
an increase in VT rather than a decrease in VD as absolute VD
actually increased, as would be expected with the increase in
VT. Although a reduction in VD/VT should improve ventilatory efficiency, thereby reducing the overall E required for a
given work load, we saw no change in the E measured at the
point of isowatt exercise after LVRS, possibly because the
PaCO2 was lower at this work load after surgery, as a result of
the increased alveolar ventilation.
Hyperinflation and inspiratory muscle dysfunction can also
limit the Emax attained during exercise (17). Recent data
presented by O'Donnell and colleagues (18) in patients undergoing bullectomy indicates that end-expiratory lung volume is
reduced after surgery. Similar changes might explain the improvement in muscle function that we demonstrated after
LVRS (5), and they could also contribute to the increased VT
observed during exercise.
Cardiac Performance
A number of cardiac abnormalities occur in patients with emphysema during exercise, including a reduced cardiac output
at peak exercise (15, 19) and a reduced stroke volume and
more rapid heart rate than is seen in normal subjects when
these variables are measured at the same level of work (15, 19,
20). These abnormalities are attributable to an increased pulmonary vascular resistance, which increases right ventricular
afterload, and/or to gas trapping, which reduces right ventricular filling (8, 22, 23). We found that the O2 pulse and HR measured at maximal exercise increased after LVRS. These
changes may simply have resulted from the improvement in
Emax, which allowed a greater amount of work to be accomplished (with or without a greater degree of O2 extraction as a
manifestation of this increased work). Alternatively, the increase in O2 pulse after LVRS may have resulted from improved right ventricular filling because of a reduction in the
degree of compression of the cardiac fossa or the inferior vena
cava associated with a reduction in dynamic hyperinflation.
This latter possibility is supported by the increase in right ventricular dimensions that has been observed after LVRS (6).
Heart rate decreased at the point of isowatt exercise after LVRS. This finding may be explained by improved right or left ventricular performance caused by increases in cardiac filling or improvement in overall conditioning.
Dyspnea
Breathlessness in patients with emphysema has been attributed to abnormal control of ventilation, the abnormal position of the respiratory muscles on their length-tension curves, to respiratory muscle fatigue, and to the increased work of breathing (24). We believe that the explanation for reduction in dyspnea after LVRS relates to a change in ventilatory muscle recruitment pattern with greater use of the diaphragm and less use of accessory and abdominal muscles after LVRS (5). Other factors that might contribute post-LVRS have not yet been studied.
Maximal Exercise Capacity
The increase in maximal exercise capacity after LVRS appears to be related to the increase in maximal ventilation resulting from the operation as the Emax/MVV approached 1 both before and after LVRS, and most of the patients developed a respiratory acidosis at maximal exercise. The improvement in Emax was, however, poorly correlated with the increase in exercise capacity (r = 0.23, with exercise capacity
measured either as O2max or watts). Accordingly, we suggest
that changes in dyspnea, improvements in the oxygen cost of
breathing, and/or improved conditioning may also be involved.
Although we cannot exclude the possibility of a non-specific or placebo effect as an explanation for our findings, we
feel such a possibility is unlikely for two reasons. First, a recent well-done study found that a highly motivated and carefully monitored group of subjects with emphysema increased
their O2max by only 8.8% after completing a pulmonary rehabilitation program that included a rigorous exercise training
component (28). Because the large majority of these patients
have a ventilatory limitation to exercise performance, the results of this and other similar studies in the literature imply
that this degree of improvement may be the maximum attainable in patients with emphysema who have not undergone
LVRS. The O2max in our patients improved 29% after LVRS, even though none of them underwent any form of exercise training. Second, there is substantial evidence providing
a sound physiologic rationale for the improvement in exercise
capacity after LVRS, including improvements in static lung
volumes, airflow, changes in breathing and ventilatory patterns, augmented tidal volumes, reduction in the work of
breathing and an increased use of the diaphragm that we and
others have previously reported (1, 13, 18).
The duration of the beneficial effect on exercise capacity associated with LVRS is unknown. Accordingly, it will be important to determine whether these improvements persist, are augmented, or diminish over time.
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Footnotes |
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Correspondence and requests for reprints should be addressed to Joshua O. Benditt, M.D., University of Washington Medical Center, Pulmonary and Critical Care Medicine, Box 356522, Seattle, WA 98195-6522.
(Received in original form November 11, 1996 and in revised form January 21, 1997).
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References |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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1.
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C. W. Butler, M. Snyder, D. E. Wood, J. R. Curtis, R. K. Albert, and J. O. Benditt Underestimation of Mortality Following Lung Volume Reduction Surgery Resulting From Incomplete Follow-up Chest, April 1, 2001; 119(4): 1056 - 1060. [Abstract] [Full Text] [PDF]
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M. Yoshikawa, T. Yoneda, H. Takenaka, A. Fukuoka, Y. Okamoto, N. Narita, and K. Nezu Distribution of Muscle Mass and Maximal Exercise Performance in Patients With COPD Chest, January 1, 2001; 119(1): 93 - 98. [Abstract] [Full Text] [PDF]
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D. L. Serna, M. Brenner, K. E. Osann, R. J. McKenna Jr, J. C. Chen, R. J. Fischel, B. U. Jones, A. F. Gelb, and A. F. Wilson SURVIVAL AFTER UNILATERAL VERSUS BILATERAL LUNG VOLUME REDUCTION SURGERY FOR EMPHYSEMA J. Thorac. Cardiovasc. Surg., December 1, 1999; 118(6): 1101 - 1109. [Abstract] [Full Text] [PDF]
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G. J. CRINER, F. C. CORDOVA, S. FURUKAWA, A. M. KUZMA, J. M. TRAVALINE, V. LEYENSON, and G. M. O'BRIEN Prospective Randomized Trial Comparing Bilateral Lung Volume Reduction Surgery to Pulmonary Rehabilitation in Severe Chronic Obstructive Pulmonary Disease Am. J. Respir. Crit. Care Med., December 1, 1999; 160(6): 2018 - 2027. [Abstract] [Full Text]
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J. Young, A. Fry-Smith, and C. Hyde Lung volume reduction surgery (LVRS) for chronic obstructive pulmonary disease (COPD) with underlying severe emphysema Thorax, September 1, 1999; 54(9): 779 - 789. [Abstract] [Full Text]
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Y. Lando, P. Boiselle, D. Shade, J. M. Travaline, S. Furukawa, and G. J. Criner Effect of Lung Volume Reduction Surgery on Bony Thorax Configuration in Severe COPD Chest, July 1, 1999; 116(1): 30 - 39. [Abstract] [Full Text] [PDF]
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Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease . A Statement of the American Thoracic Society and European Respiratory Society Am. J. Respir. Crit. Care Med., April 1, 1999; 159(4): S2 - 40. [Full Text] [PDF]
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Y. LANDO, P. M. BOISELLE, D. SHADE, S. FURUKAWA, A. M. KUZMA, J. M. TRAVALINE, and G. J. CRINER Effect of Lung Volume Reduction Surgery on Diaphragm Length in Severe Chronic Obstructive Pulmonary Disease Am. J. Respir. Crit. Care Med., March 1, 1999; 159(3): 796 - 805. [Abstract] [Full Text]
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P. D. Wagner Functional Consequences of Lung Volume Reduction Surgery for COPD Am. J. Respir. Crit. Care Med., October 1, 1998; 158(4): 1017 - 1019. [Full Text] [PDF]
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M. OSWALD-MAMMOSSER, R. KESSLER, G. MASSARD, J.-M. WIHLM, E. WEITZENBLUM, and J. LONSDORFER Effect of Lung Volume Reduction Surgery on Gas Exchange and Pulmonary Hemodynamics at Rest and during Exercise Am. J. Respir. Crit. Care Med., October 1, 1998; 158(4): 1020 - 1025. [Abstract] [Full Text] [PDF]
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R. K. ALBERT, J. O. BENDITT, J. HILDEBRANDT, D. E. WOOD, and M. P. HLASTALA Lung Volume Reduction Surgery Has Variable Effects on Blood Gases in Patients with Emphysema Am. J. Respir. Crit. Care Med., July 1, 1998; 158(1): 71 - 76. [Abstract] [Full Text] [PDF]
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G. T. FERGUSON, E. FERNANDEZ, M. R. ZAMORA, M. POMERANTZ, J. BUCHHOLZ, and B. J. MAKE Improved Exercise Performance Following Lung Volume Reduction Surgery for Emphysema Am. J. Respir. Crit. Care Med., April 1, 1998; 157(4): 1195 - 1203. [Abstract] [Full Text] [PDF]
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H. E. FESSLER and S. PERMUTT Lung Volume Reduction Surgery and Airflow Limitation Am. J. Respir. Crit. Care Med., March 1, 1998; 157(3): 715 - 722. [Abstract] [Full Text] [PDF]
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