While LVRS has produced positive results in patients with emphysema, studies are still under way to establish concrete documentation.

Emphysema is a chronic obstructive pulmonary disease characterized by bullae in the lung tissue. These bullae develop most commonly as a result of cigarette smoking, air pollution, work hazards, or lung infections. Cigarette smoking alters the structure and function of the lungs, causing them to thicken and lose their elasticity.

Due to the volume of carbon dioxide that remains in the bullae, oxygenated air coming into the lung pushes the organ’s walls further outward with each new breath. There is a subsequent decrease in the transfer of air, and the lungs expand and lose their elasticity. This, in turn, causes greater carbon dioxide retention and decreasingly oxygenated air, producing dyspnea as the body’s demand for oxygen increases with exercise. In time, the muscles and ribs surrounding the lungs are stretched to accommodate the expansion of the chest. The diaphragm flattens and loses its effectiveness in the respiratory effort. The muscles in the neck, shoulders, and abdomen must then assist in the work of breathing. The emphysema patient eventually becomes deconditioned because the disease does not permit him or her to remain fit, and a cycle of increasing dyspnea develops.

In the United States, more than 2 million people have emphysema, and the overall death rate has been estimated at 20,000 per year. Emphysema is currently the fifth leading cause of death in this country.1 

Clinical pathologic features

As the pathology of emphysema progresses, various results are seen. Due to the destruction of interalveolar septa, with attendant decreases in elastic recoil and alveolar expiratory driving pressure, there is a reduction in expiratory flow. There is also a reduction in the transmural pressure that is meant to maintain distal airway patency. 

Pulmonary hyperinflation with air trapping develops as a compensatory mechanism aimed at limiting the obstruction to expiratory flow. An increased positive end-expiratory pressure (PEEP) will, in turn, make the inspiratory muscles operate at a length/tension ratio that is disadvantageous. The effort required for each individual breath increases as a result of reduced neuromechanical coupling. As more and more nervous impulses need to be conducted to the muscular structures to obtain the same response and the same ventilatory capacity, dyspnea increases.

Diaphragmatic fibers shorten and reduce the zone of apposition with the thoracoabdominal wall, which results in a decreased pressure gradient between the chest wall and the abdomen.

Dynamic hyperinflation results from a reduction in expiratory time, especially with exercise. This creates compression of the distal airways and further increases the work of respiration. The incomplete expiration produces an additional increase in intra-alveolar PEEP and forces the inspiratory muscles to function at even more of a mechanical disadvantage.

As a result of hyperinflation and auto-PEEP, cardiovascular sequelae develop in relation to the increased pulmonary resistance, reduced venous return to the right heart, and ventilation-perfusion (V/Q) mismatching. The most prominent of these is pulmonary hypertension.

Mechanisms of destruction

Elastic recoil is lost when lung tissue is destroyed by emphysema. This has numerous implications.2 Airways tethered to the lung parenchyma lose their support, so their diameter at any specific lung volume is decreased. This contributes to an increase in specific airway resistance and to decreased maximal expiratory flow. The operational volume of the lungs and chest cavity increases because the outward recoil of the chest wall is opposed by the inward recoil of the lungs (and because reduced expiratory flow causes dynamic hyperinflation). This hyperinflation affects respiratory muscle activity, energetics, and hemodynamics. The inspiratory muscles are placed at a mechanical disadvantage by having to operate at high volumes, and their elastic load is increased due to inadvertent PEEP. Further complicating the problem are the impairment of gas exchange and the tendency promoting the limitation of cardiovascular exercise. Through its effect on physiologic dead space, V/Q mismatching increases the ventilatory requirement of the patient unless, or until, the ventilatory control system begins to tolerate hypercapnia. Pulmonary vasoconstriction, pulmonary hypertension, cor pulmonale, and right heart failure may develop as a result of hypoxemia complicating the V/Q mismatch, hypoventilation, or sleep-related disorders.


Many attempts have been made to correct hyperinflation by reducing lung volume through compression (pneumoperitoneum, abdominal belts, phrenic paralysis, and thoracoplasty) or by enlarging the chest cavity (costochondrectomy).3 Late in the 1950s, Baltimore surgeon Otto Brantigan, MD, pioneered an operation based on the belief that the removal of lung tissue would increase the circumferential pull on small airways and thereby relieve bronchial obstruction and dyspnea.4 The operation was performed through a standard thoracotomy, reducing the volume of only one lung at a time (although Brantigan believed that the procedure should be performed on both lungs). Approximately 75% of patients reported improvement and, in some cases, this lasted for more than 5 years. This operation was, however, associated with a significant mortality of about 16%, and the operation did not gain widespread acceptance. A lack of data from rigorous follow-up care also caused interest to wane. 

The procedure was abandoned until the early 1990s, when lung-transplant pioneer Joel Cooper, MD—faced with a chronic lack of lung donors and the fact that many patients died while waiting for a lung—rediscovered Brantigan’s work. Cooper modified the technique and operated on both lungs via median sternotomy. He also used current techniques of anesthesia, pain control, and postoperative intensive care. In addition, objective measurements were used to determine the success of the procedure. 

Cooper’s initial experience was very encouraging. His patients’ pulmonary function testing results showed significant improvement, and most of the patients were able to be weaned from oxygen. The results, however, were not immediate, and took 6 to 12 months to occur.

Current operative techniques

The surgery aims to remove 20% to 30% of each lung. This volume is difficult to estimate because total lung volume cannot be measured without total resection of the organ. The surgical approach may be made through a median sternotomy, through single or sequential anterior thoracotomies, or using monolateral or bilateral video-assisted thoracoscopic surgery (VATS). 

Regardless of the approach, the lung-volume-reduction surgery (LVRS) can be conducted on both lungs in the same operative session, starting with the most compromised. One-lung ventilation allows the sequential exclusion of the lungs and the intraoperative identification of the most diseased areas, which remain hyperinflated. These target areas are resected using staplers. Bovine pericardial strips or polytetrafluoroethylene strips are used to seal the holes produced by the staples. 

Centrilobular emphysema affects predominantly the upper lobes. For surgery in these cases, the line of resection on the peripheral lung follows the curvilinear contour of the lobes in an upside-down U shape.

The middle and lower lobes may also be involved with emphysematous changes (as in panlobular emphysema, which is commonly found in patients with a1-antitrypsin deficiency). Patients with a1-proteinase-inhibitor-deficiency emphysema do less well with LVRS than patients with smoker’s emphysema.5 Most surgeons consider topographic heterogeneity in emphysema a prerequisite for a satisfactory surgical outcome. Patients with uniformly emphysematous (and destroyed) lungs are thought to be much worse candidates for LVRS than are those with predominantly upper-lobe disease.6 

Postoperative care focuses on early extubation, chest-tube removal, and patient mobilization aimed at achieving muscle reconditioning that, in turn, may improve exercise tolerance.7 Pulmonary rehabilitation is started in the recovery room. The most common postoperative complication has been persistent air leakage, which has been minimized by using bovine pericardial strips and by avoiding the use of suction on the chest tubes.8 

Outcomes of LVRS

Operative mortality (deaths occurring within 30 days of surgery) ranges from 4% to 10%.7 This is a vast improvement over the rates seen in the early surgeries performed by Brantigan. The variability of selection criteria, operative indications, and postsurgical results reported in the literature have kept LVRS an experimental procedure to date, however.

LVRS has resulted in substantial improvements in lung function, with higher forced expiratory volume in 1 second (FEV1) and reduced total lung capacity (TLC) and residual volume (RV).9 Postsurgical results generally demonstrate an FEV1 improvement in the range of 50% to 60% 30 months after the procedure. This improvement is more remarkable if one considers only the first 12 months after LVRS, during which results slowly decline to the aforementioned rates. The decreases in TLC and RV demonstrate the beneficial effects of LVRS on lung hyperinflation. In addition, exercise tolerance improves, possibly due to the restoration of the diaphragmatic geometric configuration and function. Accordingly, the thoracoabdominal pressure gradient goes back to normal, thus augmenting venous return to the right heart. 

In addition to improving airflow, goals of the surgery include weaning from oxygen therapy and the reduction of steroid dependency, both to be obtained over a longer period of time. Up to 68% of patients were free of supplemental oxygen within 6 months of LVRS.10 A parallel decrease in steroid use was seen in 85% of the patients who underwent this surgery.10

Further studies are needed to determine the benefits of LVRS in comparison with lung transplantation, with transplantation being limited by a donor shortage and having side effects of prolonged immunosuppression, elevated costs, and 3-year survival rates of only 60%.7

There is no technology for monitoring lung volume in an ambulatory setting. Therefore, only inferences can be made from pulmonary function laboratory assessments of TLC, functional residual capacity, and RV. This places some limitations on those evaluating the effectiveness of LVRS.

Cooper et al11 presented 30-month follow-up data on the first 20 patients who had been subjects in 1995. Despite minor differences in the reported baseline pulmonary function values between the two case series, the FEV1 at 30 months was still 50% greater than it had been preoperatively.

Bilateral LVRS has been shown to provide clinical and physiologic improvement for more than 3 years in nine of 26 patients with emphysema, primarily due to increased lung elastic recoil and small airway caliber and decreased hyperinflation. The nine patients had vital capacities and forced vital capacities that were greater at baseline (P<.01), compared with those of 10 short-term responders who died less than 4 years after LVRS.12 In an earlier study, Gelb et al13 reported 1-year follow-up data for 10 patients in whom bilateral stapling LVRS was performed using thoracoscopic techniques. The preoperative mean FEV1 was 0.71 L, the mean 6-month postoperative FEV1 was 1.19 L, and the mean 1-year postoperative FEV1 was 0.95 L. This yields a 68% mean improvement in the FEV1 at 6 months and 34% at 12 months, suggesting that a substantial degradation of the benefit from LVRS may be noted as early as 1 year postoperatively. The 30-month value declined from 69% above baseline at 6 months and 60% above baseline at 12 months.11 In a recent interview, Gelb states that the results of the ongoing study of the same cohort demonstrate “not only the mortality rate from year to year, but also the improvement in lung function, rather objectively—that is, the FEV1 greater than 0.2 L or the forced vital capacity greater than 0.4 L. Of course, we also looked at improvements in dyspnea in decrease in oxygen utilization.” He adds, “The results of the study demonstrate that the majority of the patients gained benefit for 2 to 3 years following LVRS, and approximately a quarter still showed benefits 4 years after surgery. Of course, the high mortality of 46% by the fourth year is probably still better than that among patients who have not undergone surgery. It is important to remember that the patients who undergo LVRS suffer from very severe, far-advanced emphysema and without surgery, not only is their lifestyle progressively deteriorating, but there is also a very high mortality. Probably the mortality without surgery would be close to 50%.” 


LVRS was initially reimbursable under the Medicare program because there was no Current Procedural Terminology code for the new procedure; it was usually billed as multiple wedge resections or excision-plication of bullae. Funding decisions were ultimately the responsibility of regional carriers because there was no national Medicare reimbursement policy in place. Naturally, this led to variability in coverage for the procedure.

In December 1995, the Health Care Financing Administration (HCFA) decided not to reimburse for LVRS, based on two independent assessments. A National Heart, Lung, and Blood Institute workshop held in September 199510 found that a more systematic study of selection criteria and the long-term efficacy of the procedure needed to be done. A second study10 by the Agency for Health Care Policy and Research determined that the available data on the risks and benefits of LVRS were not conclusive enough for the agency to recommend unrestricted Medicare funding. Based on these studies, HCFA and the National Institutes of Health decided to cosponsor a large, multicenter trial to assess the safety and efficacy of LVRS when combined with maximal medical therapy. 

This is the National Emphysema Treatment Trial (NETT), begun in early 1998. It is a multicenter randomized trial comparing maximal medical therapy with maximal medical therapy plus LVRS in patients with moderate to severe emphysema. The primary objective of NETT is to determine whether the addition of LVRS to medical therapy improves survival and increases exercise capacity. The secondary objective is to determine whether LVRS reduces symptoms and improves quality of life as related to health. Additional objectives include determination of the relative value of VATS in comparison with medial sternotomy, determination of the durability of potential improvements, and identification of patients who may be at high risk for death and complications associated with LVRS.10


The median charge for LVRS was $26,669 (range, $20,032 to $75,561).14 Studies14 estimated that even if only 10% of US patients with emphysema were candidates for LVRS, the expense of surgery would exceed $4.6 billion. Further studies are needed to determine whether the operation would result in less money being spent on outpatient visits, hospitalizations, medications, oxygen, and other expenses associated with emphysema.15 Lengths of stay for patients undergoing LVRS range from 13 to 22 days.10


Although LVRS has produced positive results in patients with emphysema, the safety and efficacy of the operation have yet to be determined. Studies are under way to establish documentation of these outcomes, and these will facilitate decisions to modify or abandon the procedure. Many patients have been excluded from studies on the basis of criteria that might not hold up under the rigor of a well-designed clinical trial. The long-term risk of LVRS compared to medical therapy is still to be determined, as are the optimal selection criteria, the best measures of efficacy, the mechanisms of improvement (or lack thereof), the duration of benefit, the cost-effectiveness of the procedure, and the optimal surgical technique. It is hoped that the NETT will answer many of these questions. N 

Linda Kerby, RNC, MA, is a contributing writer for RT Magazine.


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