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Background Patients with severe pulmonary emphysema have a greatly increased oxygen cost of breathing (O 2 cost), and this is the cause of serious malnutrition, or respiratory cachexia, in such patients. Study objectives To clarify the effect of lung volume reduction surgery (LVRS) on respiratory function and the nutritional state of these patients through a reduction in the O 2 cost of the respiratory muscles. Design Prospective cohort study. Setting, patients, and interventions Twenty-three patients who underwent LVRS in Tohoku University Hospital. Measurements Pulmonary function and O 2 cost were measured perioperatively by utilizing a method of continuous dead space. In addition, we calculated the proportion of oxygen consumption ( V ˙ o 2 ) of respiratory muscles to total V ˙ o 2 (% V ˙ o 2 resp) from the measured energy expenditure and the predicted values. Results FEV 1 and arterial oxygen pressure increased after surgery while lung volume and dyspnea decreased (p 2 cost was also reduced from 0.044 to 0.026 log(mL/min)/(L/min) [p 2 cost had a strong negative correlation with that of FEV 1 ( r = − 0.70, p r = 0.54, p < 0.01). % V ˙ o 2 resp was 23.1% at rest and 55.5% at maximal ventilation. LVRS reduced % V ˙ o 2 resp at maximal ventilation to 49.0% (p < 0.05), but % V ˙ o 2 resp at rest did not decrease after surgery. Conclusions LVRS reduces energy expenditure of respiratory muscles especially during exercise by decreasing small airway obstruction and hyperinflated lung volume. This may reverse the malnourished state in end-stage emphysema.

Study objectives Repeated episodes of upper-airwayocclusion are the main characteristics of patients with obstructivesleep apnea (OSA) during sleep. It has been reported that an impairmentin the sensation of detection and a depression of ventilatorycompensation to added load could be observed in such patients. In thisstudy, we examined patients with OSA to evaluate the inspiratory effortsensation (IES), ventilation, and mouth occlusion pressures duringadded resistive loading while awake and to determine whether they canbe reversed by nasal continuous positive airway pressure (CPAP)treatment. Design A hospital-based case-controlstudy. Setting A sleep laboratory of a medical unitin Japan. Subjects Seventeen patients with moderateto severe OSA and 10 control subjects were included in this study. Measurements All patients with OSA had undergone standardnocturnal polysomnography. Patients with OSA and control subjects wereevaluated for IES measured by a modified Borg score, ventilation, andmouth occlusion pressure during control and inspiratory resistiveloaded breathing. These tests were repeated in all patients with OSAafter 2 weeks of nasal CPAP treatment. Results IES toinspiratory resistive loading was lower in patients with OSA than incontrol subjects. There were no differences in ventilation and mouthocclusion pressure between patients and control subjects during loadedbreathing. After 2 weeks of nasal CPAP, the decreased IES was increasedin patients with OSA. Conclusion In patients withOSA, the decreased IES to inspiratory resistive loaded breathing isreversible with nasal CPAP. This could be one additional benefit ofnasal CPAP in the treatment of OSA.

We measured electromyograms (EMGs) of genioglossus muscle (GG) and inspiratory intercostal muscle (IIM) in both rapid eye movement (REM) sleep and non-REM sleep of 12 patients with obstructive sleep apnea (OSA) to examine the influence of different sleep stages on upper airway muscle activity during sleep apnea. Quantifications of both muscle activities were assessed by their individual peak amplitude of integrated inspiratory EMG. Genioglossus and IIM activities showed a qualitatively similar cyclic change with an alteration of apneic and ventilatory phases during both non-REM and REM sleep. Both muscle activities increased gradually in the late apneic phase and reached each peak at the opening of the upper airway and, subsequently, decreased gradually. There were no significant differences in both muscles activities in either the ventilatory or early apneic phase between non-REM sleep and REM sleep. On the other hand, GG and IIM activities in the late apneic phase during REM sleep were significantly lower than those during non-REM sleep. The relative activity of GG to IIM in the late apneic phase was significantly lower during REM sleep than that during non-REM sleep. These results indicate that upper airway and intercostal muscle activation in the later apneic phase during REM sleep were inhibited compared with those during non-REM sleep and that this inhibition was observed predominantly in upper airway muscles.

We examined changes in P wave height in lead 2 of an ECG obtained during progressive exercise in 23 patients with COPD, and measured both P wave changes and pulmonary hemodynamics during exercise at a constant workload corresponding to approximately 50 to 60 percent of VO2 max in nine patients. The P wave response to exercise (delta P/delta VO2, %/ml/min), estimated by the relationship between percentage of change in P wave height and VO2, was significantly greater (p less than 0.01) in 15 patients who had a decrease in PaO2 with exercise (group A) than eight patients who did not have a fall in PaO2 with exercise (group B). There was a significant negative correlation between change in PaO2 and change in P wave height from rest to maximal exercise (r = -0.68, p less than 0.001). Oxygen therapy in nine patients in group A reduced the increase in P wave height during exercise. Furthermore, change in P wave height from rest to exercise correlated significantly with that of mean pulmonary artery pressure (r = 0.75, p less than 0.01). These results suggest that increase in P wave height during exercise in COPD patients is related partly to oxygen desaturation during exercise, and continuous measurement of P wave change may be useful for noninvasively predicting the pulmonary vascular pressure response to exercise.

We examined airway responsiveness to allergen inhalation using a novel technique by which dynamic compliance (Cdyn) and pulmonary resistance (Rl) are simultaneously calculated by Fourier-series analysis of flow and transpulmonary pressure during tidal breathing. C0 and C0.5 (Cdyn at the frequency of zero and 0.5 Hz, respectively) were computed using the regression line of Cdyn versus frequency measured at the fundamental and first three harmonics in each breathing cycle. First, the validity of this system was tested by comparing Rl, C0 and C0.5 during five consecutive breaths with those obtained by the conventional method. A good correlation was seen in Rl, C0 and C0.5 between the two methods. Second, we studied airway response to allergen inhalation before and after oral administration of a long-acting β 2 -stimulant (procaterol, 50 μg or 100 μg) or placebo in a double-blind crossover trial in six atopic asthmatic subjects. In control allergen inhalation tests by administration of placebo, Rl increased progressively, and C0.5, expressed as percentage of control compliance at zero frequency (C0.5/C0cont), decreased progressively. After 100 μg procaterol, Rl response to allergen was almost completely inhibited. However, a decrease in C0.5/C0cont was still observed. These findings suggest that pretreatment of asthmatic patients with procaterol can release allergen-induced bronchoconstriction of the central airways, but cannot release that of the peripheral airways.

We report a new device for examining the bronchial hyperresponsiveness by directly writing the dose-response curve of respiratory resistance (Rrs) during the continuous inhalation of the methacholine in stepwise incremental concentrations. Respiratory resistance was measured by the forced oscillation method. We found that the Rrs began to increase at a certain threshold concentration of methacholine (bronchial sensitivity) and that it has a curvilinear slope (bronchial reactivity). Subsequent inhalation of the bronchodilator drug returned the Rrs to the control level. Thus, we were able to examine bronchohyperresponsiveness in the patterns of the cumulative dose-response curves of methacholine. All normal subjects were nonresponders; while all of the asthmatic subjects, 63 percent (10) of the 16 patients with chronic bronchitis and 50 percent (7) of the 14 patients with acute bronchitis were responders. The dose-response curves were reproducible. Our device may be clinically applicable for examinations of bronchial hyperresponsiveness and for screening tests.