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Donation after circulatory determination of death (DCDD) has the potential to increase the number of organs available for transplantation. Because consent and management of potential donors must occur before death, DCDD raises unique ethical and policy issues.To develop an ethics and health policy statement on adult and pediatric DCDD relevant to critical care and transplantation stakeholders.A multidisciplinary panel of stakeholders was convened to develop an ethics and health policy statement. The panel consisted of representatives from the American Thoracic Society, Society of Critical Care Medicine, International Society for Heart and Lung Transplantation, Association of Organ Procurement Organizations, and the United Network of Organ Sharing. The panel reviewed the literature, discussed important ethics and health policy considerations, and developed a guiding framework for decision making by stakeholders.A framework to guide ethics and health policy statement was established, which addressed the consent process, pre- and post mortem interventions, the determination of death, provisions of end-of-life care, and pediatric DCDD.The information presented in this Statement is based on the current evidence, experience, and clinical rationale. New clinical research and the development and dissemination of new technologies will eventually necessitate an update of this Statement.

Background CT scan measures of emphysema and airway disease have been correlated with lung function in cohorts of subjects with a range of COPD severity. The contribution of CT scan-assessed airway disease to objective measures of lung function and respiratory symptoms such as dyspnea in severe emphysema is less clear. Methods Using data from 338 subjects in the National Emphysema Treatment Trial (NETT) Genetics Ancillary Study, densitometric measures of emphysema using a threshold of −950 Hounsfield units (%LAA-950) and airway wall phenotypes of the wall thickness (WT) and the square root of wall area (SRWA) of a 10-mm luminal perimeter airway were calculated for each subject. Linear regression analysis was performed for outcome variables FEV 1 and percent predicted value of FEV 1 with CT scan measures of emphysema and airway disease. Results In univariate analysis, there were significant negative correlations between %LAA-950 and both the WT ( r = −0.28, p = 0.0001) and SRWA ( r = −0.19, p = 0.0008). Airway wall thickness was weakly but significantly correlated with postbronchodilator FEV 1 % predicted (R = −0.12, p = 0.02). Multivariate analysis showed significant associations between either WT or SRWA (β = −5.2, p = 0.009; β = −2.6, p = 0.008, respectively) and %LAA-950 (β = −10.6, p = 0.03) with the postbronchodilator FEV 1 % predicted. Male subjects exhibited significantly thicker airway wall phenotypes (p = 0.007 for WT and p = 0.0006 for SRWA). Conclusions Airway disease and emphysema detected by CT scanning are inversely related in patients with severe COPD. Airway wall phenotypes were influenced by gender and associated with lung function in subjects with severe emphysema.

To evaluate correlations between improvement in quality of life (QOL) in patients with severe COPD before and after they undergo lung volume reduction surgery (LVRS) with changes in pulmonary function tests, gas exchange, exercise performance, and alterations in medical management.Case-series analysis.University hospital.Forty-two patients (mean [+/- SD] age, 56+/-8 years; 53% women) with severe airflow obstruction (FEV(1), 0.62+/-0.2 L), and moderate to severe hyperinflation (total lung capacity [TLC], 6.9+/-1.7 L).All patients underwent bilateral LVRS via median sternotomy. Measurements of lung function, symptom-limited cardiopulmonary exercise testing, the total distance the patient was able to walk in 6 min in a corridor, and sickness impact profile (SIP) scores were made before and 3 months after LVRS. SIP scores are inversely proportional to the level of function and QOL.Compared to baseline, FEV(1) increased (0.87+/-0.3 vs. 0.62+/-0.2 L, respectively; p0.01) while residual volume significantly decreased (3.2+/-1.8 vs. 6.3+/-1.2 L, respectively; p0.004) at 3 months post-LVRS. On cardiopulmonary exercise testing, values increased from baseline to post-LVRS for total exercise time (9.0+/-2.2 vs. 6.0+/-1.5 min, respectively; p = 0.045), maximum oxygen uptake (VO(2)) (16+/-3 vs. 11+/-2 mL/kg/min, respectively; p = 0.01), and maximum minute ventilation (VE) (33+/-9 vs. 28+/-5 L/min, respectively; p = 0.03). The percentage change in the oxygen cost of breathing (VO2/VE ratio) from low to high workloads during exercise was significantly lower after LVRS (p = 0.002). There was no significant change in oxygenation after LVRS (PaO(2)/fraction of inspired oxygen, 331+/-27 vs. 337+/-39, respectively; p = 0.76), but PaCO(2) tended to be lower (41+/-9 vs. 48+/-6 mm Hg, respectively; p = 0.07). Overall SIP scores were significantly lower after LVRS than before (8+/-4 vs. 15+/-2, respectively; p = 0.002). Changes in SIP scores correlated with the change in VO2/VE ratio from low to high workloads, with patients having the smallest changes in VO2/VE ratio having the smallest changes in SIP scores after LVRS (r = 0.6; p = 0.01). Improved or lower SIP scores also tended to correlate with a reduction in residual volume/TLC ratio (r = 0.45; p = 0.09), and there was a linear correlation with a statistically significant Pearson r value with decreased steroid requirements (r = 0.7; p = 0.001). Moreover, changes in psychological SIP subscore tended to correlate with diminished oxygen requirements post-LVRS (r = 0.45; p = 0.09). However, there was no significant correlation between changes in SIP scores and routine measurements of lung function, exercise performance, or gas exchange.There is an association between an improvement in QOL and reduced hyperinflation after LVRS. Reduced hyperinflation may lead to more efficient work of breathing during exercise and, therefore, to an increased ability to perform daily activities. Changes in QOL scores correlate best with behaviorally based variables that directly affect the patient's well-being, such as systemic steroid administration.

Study objectives We sought to investigate the effectof lung volume reduction surgery (LVRS) on regional lungventilation. Design Retrospective analysis ofroutinely acquired data before and after LVRS. Setting Large, urban, university medical center. Patients Twenty-nine patients with severe emphysema. Intervention Bilateral LVRS. Measurements and results 133 Xe washout curves during lungscintigraphy exhibit a biphasic pattern (the first component of thewashout curve [m r ] corresponds to an initial rapidphase in washout that reflects larger airways emptying, and the secondcomponent [m s ] reflects a slower phase of washout that isattributed to gas elimination via smaller airways). We analyzed sixstandardized regions of the lung (upper, mid, and lower zones of theright and left lung), and calculated m r and m s for each lung region. The mean (± SE) baseline FEV 1 was0.69 ± 0.04 L, total lung capacity (TLC) was 139 ± 4% predicted, and the residual volume (RV)/TLC ratio was 65 ± 2%. The meanimprovement in FEV 1 3 months post-LVRS was 38%. Post-LVRS,m r and m s increased in 79 and 74 lung regions, respectively, and there was no relationship with respect to lungregions that had or had not been operated on. The increase inm s , however, significantly correlated with the increase in, FEV 1 ( r = 0.66; p r = −0.67; p s also correlated with a decrease in, Pa co 2 ( r = −0.39;p = 0.03), but m r showed no relationship with anyparameter. Conclusions Small airways ventilation inlung regions that had and had not been operated on is associated with agreater improvement in lung mechanics following, LVRS.

Study objectives Hyperinflation in patients with severe COPD is associated with an increased anteroposterior (AP) rib cage diameter. We sought to determine whether bilateral lung volume reduction surgery (LVRS) affects bony thorax configuration. Design Prospective of clinical data collection before and after LVRS. Setting Tertiary-care university medical center. Patients We measured multiple AP and transverse thoracic diameters, by using plain chest roentgenograms (CXRs) in 25 patients (11 men, 14 women), and thoracic CT scans in 14 patients (7 men, 7 women), preoperatively and 3 months postoperatively. A subgroup of 7 patients (reference data) also had CXR thoracic diameter measurements made, using films obtained previously within a year of their presurgical evaluation. Another subgroup of 10 patients had CT scan measurements also made 12 months postoperatively. Measurements and results CXR dimensions were taken at the level of the manubrium sterni (M) and thoracic T7 and T11 levels. CT dimensions were taken at T4, T6, T8, and T10 levels. At each level, left (L), midsagittal (C), and right (R) AP and maximal transverse diameters were measured. The sum of the three AP diameters (Total) was used for calculations. Patients also underwent tests such as spirometry, lung volumes, diffusing capacity of the lung for carbon monoxide, 6-min walk distance (6MWD), and transdiaphragmatic pressures during maximum static inspiratory efforts (Pdimax sniff) measured before and 3 months after LVRS. Patients were (mean ± SD) 58 ± 8 years old, with severe COPD and hyperinflation (FEV 1 , 0.68 ± 0.23 L; FVC, 2.56 ± 7.3 L; and total lung capacity[TLC], 143 ± 22% predicted). After LVRS, AP diameters were reduced at thoracic level T7 (from 24.2 ± 2.0 cm to 23.3 ± 2.2 cm, p = 0.0002), and transverse diameters were reduced at T7 (from 26.8 ± 1.9 cm to 26.4 ± 1.7 cm, p = 0.001) and T11 (from 29.9 ± 2.2 cm to 29.5 ± 2.2 cm, p = 0.03), as measured using the CXR. In contrast, thoracic diameters were similar in subjects with CXRs before LVRS and within 1 year before evaluation. CT-measured AP diameters were significantly reduced 3 months after LVRS at T6, (from 48.8 ± 6.0 cm to 46.7 ± 5.4 cm, p = 0.02), T8 (from 54.2 ± 7.0 cm to 52.3 ± 6.5 cm, p = 0.004), and T10 (from 53.8 ± 7.5 cm to 51.2 ± 8.0 cm, p = 0.001), but not at T4. These AP diameter reductions directly correlated with the postoperative reductions in TLC and residual volume, and also with the increases in Pdimax sniff and 6MWD after LVRS. The reduction in AP diameters at thoracic levels T8 and T10 seen 3 months after LVRS remained stable at 12-month follow-up, whereas those measured at T6 lost statistical significance. CT-measured transverse diameters were unchanged at all levels after LVRS. Conclusions We conclude that LVRS decreases mid-to-lower AP rib cage diameter as assessed by CXR and thoracic CT. Although transverse diameters were reduced on CXR, the magnitude was small and was not confirmed with CT. After LVRS, AP diameter reductions are most likely the result of reduction in lung volume, and they are associated with improvements in diaphragm strength and exercise endurance.

Patients with severe chronic obstructive pulmonary disease (COPD) have varying degrees of hypercapnia. Recent studies have demonstrated inconsistent effects of lung volume reduction surgery (LVRS) on PaCO2 ; however, most series have excluded patients with moderate to severe hypercapnia. In addition, no study has examined the mechanisms responsible for the reduction in PaCO2 post-LVRS. We obtained spirometry, body plethysmography, diffusion capacity, respiratory muscle strength, 6-min walk test, and incremental symptom-limited maximal exercise data in 33 consecutive patients pre- and 3 to 6 mo post-LVRS, and explored the relationship between changes in PaCO2 and changes in the measured physiologic variables. All patients underwent bilateral LVRS via median sternotomy and stapling resection by the same cardiothoracic surgeon. Patients were 57 ± 8 yr of age with severe COPD, hyperinflation, and air trapping (FEV1, 0.73 ± 0.2 L; TLC, 7.3 ± 1.6 L; residual volume [RV], 4.8 ± 1.4 L), and moderate resting hyper...

Since lung volume reduction surgery (LVRS) reduces end-expiratory lung volume, we hypothesized that it may improve diaphragm strength. We evaluated 37 patients for pulmonary rehabilitation and LVRS. Before and 8 wk after pulmonary rehabilitation, 24 patients had spirometry, lung volumes, diffusion capacity, incremental symptom limited maximum exercise test, 6-min walk test, maximal static inspiratory and expiratory mouth pressures, and transdiaphragmatic pressures during maximum static inspiratory efforts and bilateral supramaximal electrophrenic twitch stimulation measured. Twenty patients (including 7 patients who crossed over after completing pulmonary rehabilitation) had baseline measurements postrehabilitation, and 3 mo post-LVRS. Patients were 58 +/- 8 yr of age, with severe COPD and hyperinflation (FEV1, 0.69 +/- 0.21 L; RV, 4.7 +/- 1.4 L). Nineteen patients had bilateral LVRS performed via median sternotomy and stapling, and 1 patient had unilateral LVRS via thorascopy with stapling. After rehabilitation, spirometry and DL(CO)/VA were not different, and lung volumes showed a slight worsening in hyperinflation. Gas exchange, 6-min walk distance, maximum oxygen uptake (VO2max), and breathing pattern during maximum exercise did not change after rehabilitation, but total exercise time was significantly longer. Inspiratory muscle strength (PImax, Pdi(max combined), Pdi(max sniff), Pdi(max), Pdi(twitch)), was unchanged after rehabilitation. In contrast, after LVRS, FVC increased 21%, FEV1 increased 34%, TLC decreased 13%, FRC decreased 23%, and FRC(trapped gas) and RV decreased by 57 and 28%, respectively. PCO2 was lower (44 +/- 6 versus 48 +/- 6 mm Hg, p < 0.003) and 6-min walk distance increased (343 +/- 79 versus 250 +/- 89 m, p < 0.001), as did total exercise time during maximum exercise (9.2 +/- 1.9 versus 6.9 +/- 2.7 min, p < 0.01). Minute ventilation (29 +/- 8 versus 21 +/- 6 L/min, p < 0.001) and tidal volume (1.0 +/- 0.33 versus 0.84 +/- 0.25 L, p < 0.001) during maximum exercise increased whereas respiratory rate was lower (28 +/- 6 versus 32 +/- 7 breaths/min, p < 0.02). Measurements of respiratory muscle strength (PImax, 74 +/- 28 versus 50 +/- 18 cm H2O, p < 0.002; Pdi(max combined), 80 +/- 25 versus 56 +/- 29 cm H2O, p < 0.01; Pdi(max sniff), 71 +/- 7 versus 46 +/- 27 cm H2O, p < 0.01; Pdi(twitch), 15 +/- 5 versus 7 +/- 5 cm H2O, p < 0.01) were all greater post-LVRS. Inspiratory muscle workload as measured by Pdi TTI was lower following LVRS (0.07 +/- 0.02 versus 0.09 +/- 0.03, p < 0.03). On multiple regression analysis, increases in PImax correlated significantly with decreases in RV and FRC(trapped gas) after LVRS (r = 0.67, p < 0.03). We conclude that LVRS significantly improves diaphragm strength that is associated with a reduction in lung volumes and an improvement in exercise performance. Future studies are needed to determine the relationship and stability of these changes over time.

Postpneumonectomy syndrome has only been described after a right pneumonectomy except in cases of congenital mediastinal anomalies or right-sided aortic arch. Placement of Silastic prostheses into the empty hemithorax is the preferred surgical treatment; however, other nonsurgical options exist. Herein, we report a case of left postpneumonectomy syndrome in an adult who was successfully treated with the placement of an endobronchial stent.

Several uncontrolled studies report improvement in lung function, gas exchange, and exercise capacity after bilateral lung volume reduction surgery (LVRS). We recruited 200 patients with severe chronic obstructive pulmonary disease (COPD) for a prospective randomized trial of pulmonary rehabilitation versus bilateral LVRS with stapling resection of 20 to 40% of each lung. Pulmonary function tests, gas exchange, 6-min walk distance, and symptom-limited maximal exercise testing were done in all patients at baseline and after 8 wk of rehabilitation. Patients were then randomized to either 3 additional months of rehabilitation or LVRS. Thirty-seven patients met study criteria and were enrolled into the trial. Eighteen patients were in the medical arm; 15 of 18 patients completed 3 mo of additional pulmonary rehabilitation. Thirty-two patients underwent LVRS (19 in the surgical arm, 13 crossover from the medical arm). After 8 wk of pulmonary rehabilitation, pulmonary function tests remained unchanged compared with baseline data. However, there was a trend toward a higher 6-min walk distance (285 +/- 96 versus 269 +/- 91 m, p = 0.14) and total exercise time on maximal exercise test was significantly longer compared with baseline values (7.4 +/- 2.1 versus 5.8 +/- 1.7 min, p < 0.001). In 15 patients who completed 3 mo of additional rehabilitation, there was a trend to a higher maximal oxygen consumption (V O(2)max) (13.3 +/- 3.0 versus 12.6 +/- 3.3, p < 0.08). In contrast, at 3 mo post-LVRS, FVC (2.79 +/- 0.59 versus 2.36 +/- 0.55 L, p < 0.001) and FEV(1) (0.85 +/- 0.3 versus 0.65 +/- 0.16 L, p < 0.005) increased whereas TLC (6.53 +/- 1.3 versus 7.65 +/- 2.1 L, p < 0.001) and residual volume (RV) (3.7 +/- 1.2 versus 4.9 +/- 1.1 L, p < 0.001) decreased when compared with 8 wk postrehabilitation data. In addition, Pa(CO(2)) decreased significantly 3 mo post-LVRS compared with 8 wk postrehabilitation. Six-minute walk distance (6MWD), total exercise time, and V O(2)max were higher after LVRS but did not reach statistical significance. However, when 13 patients who crossed over from the medical to the surgical arm were included in the analysis, the increases in 6MWD (337 +/- 99 versus 282 +/- 100 m, p < 0.001) and V O(2)max (13.8 +/- 4 versus 12.0 +/- 3 ml/kg/min, p < 0.01) 3 mo post-LVRS were highly significant when compared with postrehabilitation data. The Sickness Impact Profile (SIP), a generalized measure of quality of life (QOL), was significantly improved after 8 wk of rehabilitation and was maintained after 3 mo of additional rehabilitation. A further improvement in QOL was observed 3 mo after LVRS compared with the initial improvement gained after 8 wk of rehabilitation. There were 3 (9.4%) postoperative deaths, and one patient died before surgery (2.7%). We conclude that bilateral LVRS, in addition to pulmonary rehabilitation, improves static lung function, gas exchange, and QOL compared with pulmonary rehabilitation alone. Further studies need to evaluate the risks, benefits, and durability of LVRS over time.

Previous studies have shown the acute effects of noninvasive positive pressure ventilation (NPPV) in chronic respiratory failure; however, information on the chronic effects of NPPV is limited. We examined the acute and chronic effects of NPPV on gas exchange, functional status, and respiratory mechanics in patients with chronic respiratory failure related to restrictive ventilatory disorders or COPD.Descriptive analysis of prospectively collected clinical data.Inpatient noninvasive respiratory care unit and outpatient clinic of university hospital.Forty patients with chronic respiratory failure (20 with severe COPD and 20 with restrictive ventilatory disorders).All patients were admitted to a noninvasive respiratory care unit for 20 +/- 3 days for inpatient evaluation consisting of medical treatment, rehabilitation, and NPPV evaluation and instruction. NPPV was titrated via a ventilatory support system (BiPAP; Respironics Inc; Monroeville, PA) or a portable volume ventilator (PLV 102; Lifecare, Inc; Boulder, CO) to achieve aor = 20% increase in baseline minute ventilation while monitoring gas exchange, expired volume, and clinical evidence of a decrease in the patient's work of breathing.The patients' mean age (+/- SD) was 65 +/- 9.7 years, and there was a 3:1 female:male predominance. In the noninvasive respiratory care unit, 36 patients used NPPV for 7.31 +/- 0.26 h/night. Four patients (three with COPD, one with restrictive disorder) withdrew from the study during the 3-week inpatient stay because they could not tolerate NPPV. Six patients (5 with COPD, 1 with restrictive disorder) used a portable volume ventilator and 34 patients used BiPAP (15 with COPD, 19 with restrictive disorders). At discharge, compared with at admission, daytime PaO2/fraction of inspired oxygen (FIO2) increased (327 +/- 10 vs 283 +/- 13 mm Hg; p = 0.01), PaCO2 was reduced (52 +/- 2 vs 67 +/- 3 mm Hg; p = 0.0001), and functional score increased (4.76 +/- 1.16 vs 2.7 +/- 1.64 arbitrary units (AUs); p0.01). Six months after discharge, improvements in PaO2/FIO2 (317 +/- 10 vs 283 +/- 13; p = 0.05), PaCO2 (52 +/- 2 vs 67 +/- 3 mm Hg; p = 0.0001), and functional score (5.66 +/- 0.41 vs 2.7 +/- 0.3 AUs; p0.001) were maintained compared with admission values. FVC, FEV1, and maximum inspired and expired mouth pressures were unchanged before and after long-term NPPV. Ten patients (7 with COPD, 3 with restrictive disorders) discontinued NPPV at 6 months, and 3 progressed to tracheostomy. The remaining 26 patients continued to use NPPV at the 6-month follow-up. They claimed to use NPPV for 7.23 +/- 0.24 h/night, but logged metered use was 4.5 +/- 0.58 h/night. Problems that required adjustment in either the mask (36%) or ventilator source (36%) included mask leaks (43%), skin irritation (22%), rhinitis (13%), aerophagia (13%), and discomfort from mask headgear (7%).NPPV acutely and chronically improves gas exchange and functional status in patients with chronic respiratory failure, but a significant number of patients do not tolerate NPPV on a chronic basis. Comprehensive follow-up is required to correct problems with NPPV and ensure optimal patient compliance.

Study Objectives To determine whether biapical stapling resection alone or resection of diseased, nonapical areas of emphysematous lung provides comparable physiologic outcomes or alters morbidity and mortality after lung volume reduction surgery (LVRS). Design Consecutive case-series analysis. Setting Urban university hospital. Patients Forty-seven patients ([mean ± SD] aged 58 ± 8 years; 18 men) with severe emphysema (FEV 1 , 0.7 ± 0.2 L; total lung capacity [TLC], 139 ± 23% predicted). Interventions Thirty-two patients underwent biapical LVRS, 27 by median sternotomy (MS) and 5 by video-assisted thoracoscopic surgery (VATS), and 15 underwent nonapical resection, 9 by MS and 6 by VATS. Patients were assessed for postoperative complications (respiratory tract infections, air leak duration, and death), length of stay, and physiologic parameters, which included a 6-min walk distance, spirometry, lung volume, gas exchange, diaphragm strength, and quality-of-life measures. Measurements and Results Patients were studied at baseline and at 3 months postoperatively. At the preoperative baseline, both groups had similar ages (57 vs 60 years; p = 0.2), 6-min walk distance (294 vs 263 m; p = 0.3), FEV 1 (28% vs 29% predicted; p = 0.6), degree of hyperinflation (TLC, 138% vs 141% predicted; p = 0.8), gas exchange (PaO 2 /fraction of inspired oxygen, 344 vs 313, p = 0.1; PaCO 2 46 vs 48 mm Hg, p = 0.4), and diaphragm strength (maximal transdiaphragmatic pressure sniff, 54 vs 46 cm H 2 O, p = 0.4). Resected tissue weight was similar in both groups (94 vs 93 g, p = 0.9). There were no differences in the mean percentage of change from baseline for these physiologic parameters or for quality-of-life measures between the two groups. The 6-min walk distances increased by 20% and 33%, FEV 1 increased by 37% and 38%, the degrees of hyperinflation (residual volume/TLC) decreased by 16% and 15%, and the quality-of-life scores improved by 51% and 41%, respectively, in the groups that underwent biapical and nonapical resections at 3 months post-LVRS. The length of stay in the hospital for LVRS (18 vs 23 days; p = 0.4) and the duration of air leak (10 vs 15 days; p = 0.4) were also similar. Complications between the two groups (biapical vs nonapical) were similar (respiratory tract infection, 47% vs 60%, p = 0.2; reintubation, 34% vs 33%, p = 0.2; reoperation, 9% vs 20%, p = 0.4; and death, 9% vs 7%, p = 0.2). Conclusions LVRS, by biapical or nonapical resection, produces similar improvements in lung function, exercise, diaphragm strength, and quality of life, with comparable morbidity and mortality.

Low frequency diaphragm fatigue (LFF) may play a major role in the pathogenesis of ventilatory failure; however, recovery from LFF is not well studied. We measured transdiaphragmatic twitch pressure (PdiT) at FRC (using a reduction of PdiT as an index of LFF) and maximum transdiaphragmatic pressure (Pdimax) before and after the induction of diaphragm fatigue in seven normal subjects, age 31 +/- 3 yr (mean +/- SD). Fatigue was induced by breathing through an inspiratory resistive load. PdiT produced by bilateral transcutaneous supramaximal electrophrenic stimulation was measured at baseline, 15, 30 min, 1, 2, 3, 4 h, and then 1 to 3 times between hour 20-25 post-fatigue. Pdimax estimated by twitch occlusion was measured at baseline, 30 min, 2-3, and 20-25 h post-fatigue. Pre-fatigue values (mean +/- SE) were: PdiT 23.6 +/- 2.5 cm H2O. The mean +/- SD time to fatigue was 25.3 +/- 12.3 min. Post-fatigue PdiT was reduced to 50%, and by 3 h was 72% of the initial value; 100% by 25 h. Pdimax was reduced to 75% post-fatigue, but recovered to 87% by 3 h, and 100% by 25 h. We concluded that recovery of PdiT and Pdimax in normal subjects starts to occur within the first few hours following diaphragm fatigue, and is complete by 25 h.

Free radical injury is believed to be important in diaphragm dysfunction. N-Acetylcysteine (NAC) is a potent free radical scavenger shown in animal models to attenuate diaphragm fatigue; however, its effects on human diaphragm function are unknown. We assessed diaphragm function by electrophrenic twitch stimulation (PdiT) and twitch occlusion (to yield Pdimax) in four healthy subjects 35 +/- 3 yr of age (mean +/- SD). We intravenously administered NAC (150 mg/kg in 250 ml D5W) or placebo (CON) (250 ml D5W) in a randomized manner after subjects were premedicated with antihistamines. There were no significant side effects with the infusion. After infusion, we measured baseline Pdimax and PdiT at FRC. Diaphragm fatigue was then induced by subjects breathing through an inspiratory resistive load. Pdimax and PdiT were then measured at 15 to 30 min and 1, 2, 3, 4, and 20-25 h after fatigue. Times to fatigue were 13 +/- 4 min (CON) and 21 +/- 6 min (NAC) (p = 0.04). At 15 min after fatigue, PdiT was reduced to 40% (CON) compared with 30% (NAC) initial PdiT value (p = 0.05). Other twitch characteristics (maximal rate of relaxation and maximal contraction rate) were reduced to a greater degree after placebo compared with NAC. There were no significant differences in the rate of recovery between CON and NAC. Pdimax at 30 min after fatigue was significantly greater with NAC; however, at 1 h after fatigue, Pdimax for CON and NAC were not different, suggesting similar rates of recovery in high-frequency fatigue. These data suggest that NAC may attenuate low-frequency human diaphragm fatigue.

Study objective To evaluate the long-term stability of improvements in exercise capacity and quality of life (QOL) after lung volume reduction surgery (LVRS). Design Case-series analysis. Setting University hospital. Patients Twenty-six patients with severe airflow obstruction (mean FEV 1 of 0.67±0.18 L) and moderate to severe hyperinflation (mean total lung capacity of 7.30±1.90 L). Intervention and measurements All patients underwent bilateral LVRS via median sternotomy. Serial measurement of lung function, symptom-limited cardiopulmonary exercise tests, 6-min walk distances (6MWD), and sickness impact profile (SIP) scores were done before, and at 3, 6, 12, and 18 months after surgery. Results FEV 1 (0.93±0.29 vs 0.68±0.19 L, p

Previous studies have shown that noninvasive positive pressure ventilation (NPPV) improves gas exchange in acute and chronic respiratory failure. However, some patients are unable to tolerate NPPV due to air leaks around the mask, facial discomfort, and claustrophobia. A new mask that covers the entire face (Total, Respironics, Monroeville, Pa), attempts to overcome these obstacles. We studied the efficacy of NPPV via the Total face mask (TFM) in nine patients with chronic respiratory failure. In three patients, respiratory failure was due to chronic obstructive lung disease, and in six patients, it was secondary to restrictive disorders. None of the patients were previously able to tolerate NPPV via nasal (N) or nasal-oral (NO) masks. At baseline, all patients had impaired gas exchange with low PaO2/FIO2 (241 +/- 14), elevated PaCO2 (79 +/- 5 mm Hg), and poor functional status (1.89 +/- 1.45, on a scale of 1 to 7). After NPPV in the hospital for 7.1 +/- 1.5 h per night for 22 +/- 26 days, the PaCO2 fell to 59 +/- 3 mm Hg, and the PaO2/FIO2 rose to 304 +/- 27. Following nocturnal NPPV via the TFM for 6.7 +/- 1.5 h a night 6 +/- 5 weeks after hospital discharge, sustained improvements in PaCO2 (58 +/- 3 mm Hg, p0.05), PaO2/FIO2 (304 +/- 18), and functional status (5.38 +/- 1.06, p0.05) were observed. In four patients, measurements of respiratory rate, tidal volume, minute ventilation, dyspnea, discomfort with the face mask, and mask and mouth leaks were made during 30-min sessions of NPPV applied at constant levels via all three masks (N, NO, TFM). Discomfort with the face mask (0.38 +/- 0.18 vs 1.44 +/- 0.34 vs 2.38 +/- 0.32, p0.05) and mask leaks (0.44 +/- 0.18 vs 1.89 +/- 0.39 vs 1.89 +/- 0.35, p0.05) were least during NPPV via TFM compared with the N or NO masks, respectively. Moreover, expired tidal volume was highest (804 +/- 10 vs 498 +/- 9 vs 537 +/- 13 ml, p0.05) and PaCO2 lowest (51 +/- 2 vs 57 +/- 2 vs 58 +/- 3, p0.05) during NPPV via the TFM compared with N or NO masks. We conclude that NPPV delivered via a Total mask ensures a comfortable, stable patient-mask interface and improves gas exchange in selected patients intolerant of more conventional N or NO masks.