The effects of acute bronchoconstriction on respiratory activity in patients with chronic obstructive pulmonary disease

Attacks of acute airway obstruction often complicate the course of chronic obstructive pulmonary disease (COPD). In asthmatic subjects, bronchospasm triggers an increase in respiratory drive, which results in hyperventilation and hypocapnia. In the present study, we assessed the effects of acute bronchoconstriction induced by aerosolized methacholine on breathing and lung mechanics in 12 patients with stable COPD. Even low doses of methacholine markedly increased airway resistance and caused hyperinflation and decreased inspiratory muscle performance in the patients. Increasing airway obstruction produced a progressive rise in PCO2 despite an increase in minute ventilation. Breathing frequency and average inspiratory flow were greater, but tidal volume decreased because of shortening of the inspiratory duration. The magnitude of CO2 retention during acute bronchoconstriction was inversely related to the changes in tidal volume and inspiratory time (p less than 0.01 for each). In subjects with COPD, the occlusion pressure response to progressive hypercapnia failed to increase during bronchoconstriction. These results show that patients with COPD retain CO2 during acutely increasing airway obstruction induced by bronchoconstriction partly because of a rapid shallow breathing pattern that reduces alveolar ventilation.     

无创正压通气抑制慢性阻塞性肺疾病急性加重期患者吸气肌肉活动的机制

目的探讨无创正压通气（NIPPV）抑制慢性阻塞性肺疾病（COPD）急性发作期患者吸气肌肉活动的机制。方法12例COPD急性加重期患者接受感觉最舒适通气压力水平时的NIPPV,观察患者吸气肌肉用力和呼吸方式的变化。结果与自主呼吸（SB）相比,NIPPV时的潮气量（VT）显著增高（从408ml升到462ml,P〈0.05）;接受NIPPV后VT的增高很迅速,第一呼吸周期时即明显增高。SB时的跨膜压（Pdi）为14.04cmH2O,而NIPPV时为10.98cmH2O,比SB时约减少22%（P〈0.05）。NIPPV时Pdi的下降从第一个呼吸周期即开始,然后进一步迅速下降,治疗至第5个呼吸周期时与SB时相比开始有显著差异（P〈0.05）。SB时的呼吸肌做功（Wp）分别为0.47J/breath和0.95J/L;而NIPPV时分别为0.34J/breath和0.69J/L,比SB时分别减少28%和27%（P〈0.05）。NIPPV时Wp的下降也是从第一个呼吸周期即开始,然后进一步迅速下降,治疗至第5个呼吸周期时与SB时相比开始有显著差异（P〈0.05）。结论本实验证实了NIPPV治疗COPD急性加重期患者时吸气肌肉活动的非化学性抑制作用的存在;这种非化学性抑制作用的产生与NIPPV治疗的开始基本同步,能有效改善患者的呼吸肌肉疲劳。     

吸入异丙托溴胺对慢性阻塞性肺疾病患者运动肺功能的影响

目的 评价吸入异丙托溴胺(ipratropium bromide,IPB)是否改善慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者的静态肺功能,运动通气功能和运动耐量.方法 随机抽取稳定期COPD患者12例,吸入IPB溶液2 mg,吸人前后分别进行静态肺功能和运动肺功能测定.结果 吸入IPB后,COPD患者最大运动功率(Wmax)、最大耗氧量(VO2max)、最大运动时每分钟通气量(Vemax)和比潮气量(Vtmax/IC),较吸人前均有显著增加;死腔通气(VD/VT)和二氧化碳通气当量(Vemax/VCO2max)无明显改变.Vtmax/IC的变化(⊿Vtmax/IC)与VO2max的变化(⊿VO2max)有显著相关性(r=0.598,P＜0.05);⊿Vtmax/IC与最大运动功率的变化(⊿Wmax)也存在显著相关性(r=0.743,P＜0.05).结论 吸入IPB能够增加COPD患者的运动耐量,COPD患者吸入IPB后,⊿Vtmax/IC可能是运动耐量增加机制中的一个重要环节.     

Long-term follow-up of symptoms, pulmonary function, respiratory muscle strength, and exercise performance after botulism

Respiratory muscle weakness occurs commonly at presentation in patients with botulism. Although clinical improvement occurs over several months, symptoms such as fatigue and dyspnea persist in many patients in the long term. To determine whether continued respiratory muscle weakness might contribute to these symptoms, we compared lung function tests, respiratory muscle strength, and exercise performance in 13 patients 2 years after type B botulism. We found that residual symptoms including dyspnea and fatigue were common in botulism patients at 2 years postintoxication. Lung function tests had returned to normal in all patients. Maximal inspiratory and expiratory pressures were similar between botulism patients and control subjects. Evaluation of individual results showed evidence of inspiratory muscle weakness in four of 13 patients with botulism (Plmax less than 65% predicted). Maximal oxygen consumption and maximal workload during exercise were reduced in botulism patients in comparison to control subjects. During exercise, botulism patients had a more rapid and shallow breathing pattern and a higher dyspnea score at a given minute ventilation in comparison to control subjects. Reasons for premature exercise termination in botulism patients were multifactorial. Although respiratory muscle weakness may have been contributory in some patients, most appeared to be limited by reduced cardiovascular fitness, leg fatigue, or reduced motivation.     

Neural respiratory drive and neuromuscular coupling in patients with chronic obstructive pulmonary disease (COPD)

In 15 spontaneously breathing patients with chronic obstructive pulmonary disease (COPD) divided into two groups, one with normocapnia (A) and one with chronic hypercapnia (B), we evaluated the maximal voluntary inspiratory muscle strength (MIP), the pattern of breathing, the mouth occlusion pressure (Po.1), the neural respiratory drive (NRD), assessed by surface electromyographic (EMG) activity of the diaphragm (EMGd) and EMG activity of intercostal muscles (EMGint), and the chest wall neuromuscular coupling, assessed in terms of Po.1/EMGd ratio. Compared with an age-matched normal control group, both A and B groups exhibited lower MIP, significantly greater EMGd and EMGint, and lower Po.1/EMGd ratio. However, a similar pattern, along with a rapid and shallow breathing, differentiated group B from group A. In group B we found a significant direct relationship between Po.1/EMGd ratio and MIP, and an inverse relationship between PaCO2 and Po.1/EMGd ratio. These data seem to indicate the following: (1) EMG is a more precise method than Po.1 in assessing the magnitude of the NRD; (2) NRD is increased in these patients; and (3) clinical manifestations probably associated with inspiratory muscle fatigue (marked decrease in muscle strength, rapid and shallow breathing, and alveolar hypoventilation) may be accompanied by a greater NRD and a more marked derangement in chest wall neuromuscular coupling in COPD.     

Dyspnea and diaphragmatic fatigue in patients with chronic obstructive pulmonary disease. Responses to theophylline

This study sought answers to 2 questions: (1) Is severe dyspnea to the point of exhaustion regularly accompanied by diaphragmatic fatigue in patients with moderately severe chronic obstructive pulmonary disease (COPD)? (2) When diaphragmatic fatigue occurs in such patients, does theophylline prevent or delay its onset? Eight eucapnic patients with moderately severe COPD were subjected to 2 different stresses to the point of severe dyspnea requiring cessation of the stress. The stresses were cycle exercise and inspiratory resistive breathing, the latter requiring a tidal Pdi equal to 60% of Pdimax. Despite incapacitating dyspnea, objective evidence of diaphragmatic fatigue was not encountered during cycle exercise. During inspiratory resistive breathing, diaphragmatic fatigue was encountered in all patients as defined by consistent inability to attain a target Pdi during final moments of the resistance run. Patients were uniformly extremely dyspneic at this point. In neither stressful maneuver did oral sustained-release theophylline show a convincing or significant advantage over placebo when administered in a randomized double-blind crossover protocol. These results suggest that the diaphragmatic fatigue encountered in this sort of COPD patient may be of predominantly central rather than peripheral (myogenic) origin and that theophylline may not be effective in this type of fatigue.     

Respiratory muscle fatigue limiting physical exercise?

Inspiratory muscle fatigue has been documented during loaded breathing or acute respiratory failure, but its role in exercise limitation is still undetermined. Electromyographic (EMG) signs of diaphragmatic fatigue develop in normal subjects hyperventilating above 70% of maximal voluntary ventilation (MVV), a ventilatory level commonly attained at peak exercise. EMG signs of diaphragmatic fatigue also occur during high power cycling exercise in normal subjects and chronic obstructive pulmonary disease (COPD) patients. However, a loss of respiratory muscle strength has rarely been documented following strenuous physical exercise with techniques independent of the subjects' collaboration. Prior inspiratory muscle fatigue decreases exercise tolerance in normal subjects but its effect is largely unknown in COPD patients. Respiratory muscle rest by negative pressure ventilation was reported to improve exercise tolerance in COPD, but this beneficial effect was not confirmed by controlled studies. The effect of inspiratory muscle training on exercise tolerance is still undefined by existing data, in part because of differences in methods and selection criteria between studies. Although respiratory muscle fatigue may occur during exercise, it is not clearly established whether interventions directed at respiratory muscles may improve exercise tolerance in COPD.     

Predictors of weaning outcome in chronic obstructive pulmonary disease patients.

Several threshold values for predicting weaning outcome from mechanical ventilation have been proposed. These values, however, have been obtained in nonhomogeneous patient populations. The aim of the present study was to determine the threshold values in chronic obstructive pulmonary disease (COPD) patients and compare them to those reported for nonhomogeneous patient populations. The initial weaning trial included 81 COPD patients. Fifty-three of them underwent a successful weaning trial, whereas 28 failed it. The latter were enrolled into the present investigation, and were restudied during a subsequent successful trial. The weaning indices used were those reported in the literature. The threshold values obtained were within 10% of those reported for a nonhomogeneous patients population only for tidal volume and effective compliance. The classification error was <20% for maximal inspiratory pressure (MIP), occluded inspiratory pressure swing (deltaPI)/MIP, rapid and shallow breathing (respiratory frequency/tidal volume), and compliance, rate, oxygenation, pressure index (CROP), whereas the area under the receiver operating characteristic curves was >0.9 only for deltaPI/MIP and CROP. In conclusion, the threshold values obtained in chronic obstructive pulmonary disease patients who failed the first weaning attempt differed from those previously reported. Although a gold standard weaning index is not available for chronic obstructive pulmonary disease patients, the occluded inspiratory pressure swing/ maximal inspiratory pressure and compliance, rate, oxygenation, pressure index may be candidates for such a role.     

Respiratory and skeletal muscles in hypogonadal men with chronic obstructive pulmonary disease

Hypogonadism, found in about one-third of patients with chronic obstructive pulmonary disease (COPD), has potential for decreasing muscle mass and muscle performance. Compared with eugonadal patients, we hypothesized that hypogonadal patients with COPD have decreased respiratory and skeletal muscle performance. Nineteen hypogonadal and 20 eugonadal men with COPD (FEV(1) 1.14 +/- 0.08 and 1.17 +/- 0.11 L [standard error], respectively) were studied. Diaphragmatic contractility, assessed as transdiaphragmatic twitch pressure generated by phrenic nerve stimulation, was similar in hypogonadal and eugonadal patients: 20.6 +/- 2.2 and 19.8 +/- 2.5 cm H(2)O, respectively. During progressive inspiratory threshold loading, hypogonadal and eugonadal patients had similar respiratory muscle endurance times (302 +/- 29 and 313 +/- 48 seconds, respectively) and airway pressure sustained during the last minute of loading (38.2 +/- 3.0 and 40.5 +/- 4.7 cm H(2)O, respectively) (similar to predicted values in healthy subjects). Hypogonadal and eugonadal patients had equivalent limb muscle strength and endurance. During cycle exercise to exhaustion, exercise performance, gas exchange, and respiratory muscle recruitment (estimated by esophageal and gastric pressure swings during tidal breathing) were similar in both groups. In conclusion, hypogonadism does not decrease respiratory or limb muscle performance and exercise capacity in men with moderate-to-severe COPD who, for the most part, are not underweight.     

Pulmonary rehabilitation and non-invasive ventilation in COPD

A multidisciplinary pulmonary rehabilitation program has become an important part of the treatment of chronic obstructive pulmonary disease. It can improve both exercise tolerance and health related quality of life in these patients. Exercise training has to be included for the program to be successful. The intensity of the training is of great importance: there is more physiological benefit in high-intensity training, compared to moderate-intensity training. High-intensity training results in reduced levels of blood lactate and pulmonary ventilation at a given heavy work rate. High-intensity training is limited in COPD patients because of exercise-induced dyspnoea. Flow limitation, as a consequence of increased ventilatory demands of exercise, causes a breathing pattern with greater demands on their inspiratory muscles: this results in a pattern of low tidal volume and high-frequency breathing. Increased inspiratory muscle work causes dyspnoea and limitation in exercise intensity. Artificial ventilatory assistance could improve exercise tolerance and hence help severe COPD patients to achieve a higher level of training. It could help to unload and assist the overburdened ventilatory muscles and give a possibility for higher levels of exercise intensity. In this review article we will discuss the effectiveness and feasibility of training with ventilatory aids.     

Evaluation of dynamic hyperinflation parameters and exercise capacity at maximal exercise in patients with COPD

Hyperinflation is an important limiting factor for exercise performance in patients with chronic obstructive pulmonary disease (COPD). Hyperinflation can be determined by measuring residual volume (RV), functional residual capacity (FRC), and total lung capacity (TLC) at rest, and by measuring inspiratory capacity (IC) and end-expiratory lung volume (EELV) at maximal exercise. This study aimed to evaluate changes in hyperinflation parameters on maximal exercise in subjects with COPD. Patients with clinically stable COPD (n= 43) and healthy controls (n= 14) were included. Subjects performed pulmonary function tests and an incremental exercise test on cycle ergometry. Statistically significant differences (p< 0.05) were found regarding exercise test parameters including exercise duration, maximum oxygen uptake, breathing reserve, maximum minute ventilation, and breathing pattern between groups. There was significant increase in EELV (p< 0.05) and decrease in IC (p< 0.05) at maximum exercise when hyperinflation parameters were compared at baseline and maximum exercise. Our results showed that hyperinflation was evident at maximal exercise, although there were no hyperinflation findings at rest in subjects with COPD. We believe that in patients with COPD, it is better to evaluate hyperinflation at maximal exercise than at rest.     

慢性阻塞性肺疾病急性发作期患者对比例辅助通气的生理反应

目的　探讨比例辅助通气 (PAV)不同辅助水平对慢性阻塞性肺疾病 (COPD)急性发作期患者生理反应的影响。方法　 9例COPD急性发作期患者接受三个不同比例辅助水平的PAV通气 ,观察患者吸气肌肉用力情况和呼吸方式的变化。结果　 (1)与自主呼吸 (SB)相比 ,PAV各辅助水平时的潮气量 (VT)、分钟通气量 (V·E)和呼吸频率 (RR)均稍增高 (P >0 0 5 )。各比例辅助水平之间的VT、V·E 和RR比较差异无显著性 (P >0 0 5 )。 (2 )与SB相比 ,各比例辅助水平时的跨膈压 (Pdi)、压力时间乘积 (PTP)和患者呼吸做功均明显减少 (P >0 0 1) ,Pdi、PTP和患者呼吸做功分别平均减少 8 36cmH2 O、11 4 9cmH2 O·s-1·L-1和 0 5 3J/L。随比例辅助水平的升高 ,Pdi、PTP和患者呼吸功无明显变化(P >0 0 5 )。 (3)PAV可减轻患者呼吸困难 (P <0 0 5 )。结论　本试验证实了无创PAV在COPD急性发作期患者中应用的可行性。患者感觉最舒适的PAV辅助比例水平是 (5 7± 11) %。根据患者感觉舒适情况而设定比例辅助水平的无创PAV可减轻患者的呼吸肌肉负担 ,最舒适水平时呼吸功减少5 7% ,Pdi减少 72 % ,PTP减少 6 5 % ;并改善患者的呼吸方式和呼吸困难     

Mechanism of CO(2) retention in patients with neuromuscular disease

BACKGROUND: In many studies of patients with muscle weakness, chronic hypercapnia has appeared to be out of proportion to the severity of muscle disease, indicating that factors other than muscle weakness are involved in CO(2) retention. In patients with COPD, the unbalanced inspiratory muscle loading-to-strength ratio is thought to trigger the signal for the integrated response that leads to rapid and shallow breathing and eventually to chronic hypercapnia. This mechanism, although postulated, has not yet been assessed in patients with muscular dystrophy. SUBJECTS: Twenty consecutive patients (mean age, 47.6 years; range, 23 to 67 years) were studied: 11 patients with limb-girdle dystrophy, 3 with Duchenne muscular dystrophy, 1 with Charcot-Marie-Tooth syndrome, 1 with Becker muscular dystrophy, 1 with myotonic dystrophy, 1 with facioscapulohumeral dystrophy, and 2 with amyotrophic lateral sclerosis, without any respiratory complaints. Seventeen normal subjects matched for age and sex were studied as a control group. METHODS: Routine spirometry and arterial blood gases, maximal inspiratory and expiratory muscle pressures (MIP and MEP, respectively), and pleural pressure during maximal sniff test (Pplsn), were measured. Mechanical characteristics of the lung were assessed by evaluating lung resistance (RL) and dynamic elastance (Eldyn). Eldyn was assessed as absolute value and as percent of Pplsn; Eldyn (%Pplsn) indicates the elastic load per unit of inspiratory muscle force. Breathing pattern was assessed in terms of time (inspiratory time [TI]; respiratory frequency [Rf]) and volume (tidal volume [VT]) components of the respiratory cycle. RESULTS: A rapid shallow breathing pattern, as indicated by a greater Rf/VT ratio and a lower TI, was found in study patients compared to control subjects. Eldyn was greater in study patients, while MIP, MEP, and Pplsn were lower. PaCO(2) inversely related to VT, TI, and Pplsn (p = 0.012, p = 0.019, and p = 0.002, respectively), whereas it was directly related to Rf, Rf/VT, Eldyn, and Eldyn (%Pplsn) (p < 0.004 to p < 0.0001). Also Eldyn (%Pplsn) inversely related to TI, and the latter positively related to VT. In other words, increase in Eldyn (%Pplsn) was associated with decrease in TI, and the latter was associated with lower VT and greater PaCO(2). Mechanical and breathing pattern variables were introduced in a stepwise multiple regression that selected Eldyn (%Pplsn) (p < 0.0001; r(2) = 0.62) as a unique independent predictor of PaCO(2). CONCLUSIONS: The present study shows that in patients with neuromuscular disease, elastic load and respiratory muscle weakness are responsible for a rapid and shallow breathing pattern leading to chronic CO(2) retention.     

Threshold pressure training, breathing pattern, and exercise performance in chronic airflow obstruction

The effects of six weeks of threshold pressure inspiratory muscle training (IMT) on inspiratory muscle performance, breathing pattern and exercise performance were studied in eight patients with severe airflow obstruction. The results indicated that IMT improved inspiratory muscle performance but did not affect exercise performance or breathing pattern during maximal exercise.     

踏车锻炼对慢性阻塞性肺疾病患者吸气肺功能的影响及与运动能力改善的关系

目的 探讨踏车锻炼对慢性阻塞性肺疾病(COPD)患者吸气肺功能的影响及与运动能力改善的关系.方法 对12例中、重度COPD患者进行12周的下肢踏车运动训练.在运动训练前后分别进行常规肺通气功能、弥散功能、肺容积、最大用力吸气峰流速(PIF)、最大吸气压(MIP)、症状限制递增功率心肺运动试验和高强度恒定功率心肺运动试验.在高强度恒定功率运动中,每隔1 min记录受试者潮式呼吸流速-容积(TBFV)曲线.结果 踏车锻炼后COPD患者运动持续时间(T)(t=7.357,P＜0.001)和峰运动功率(WRpeak)(t=3.614,P＜0.05)显著增加;MIP(t=4.754,P＜0.001)和PIF(t=2.440,P＜0.05)显著增加;踏车锻炼后COPD患者在等时间点潮式呼吸吸气峰流速(t=-2.747,P＜0.05)和呼气峰流速(t=-4.487,P＜0.05)均较前显著下降,最大吸气流速储备较前显著增加(t=2.755,P＜0.05),最大呼气流速储备较前无显著变化(t=1.326,P＞0.05).受试者下肢踏车锻炼后MIP的增加(r=0.613,P＜0.05)、PIF的增加(r=0.497,P＜0.05)和等时间点最大吸气流速储备的增加(r=0.592,P＜0.05)分别与运动持续时间的增加呈显著正相关.结论 下肢运动训练可改善COPD患者吸气肺功能指标;运动训练后吸气肌肉力量、PIF和运动中吸气流速储备的增加可能是COPD患者运动能力改善的主要原因.

Abstract：

Objective To explore the effect of treadmill training on inspiratory function and its association with improvement of exercise capacity in patients with chronic obstructive pulmonary disease (COPD). Methods The 12 moderate to severe COPD patients were allocated to lower-limb exercise training for 12weeks. The routine tests of pulmonary ventilation function, diffusion function,lung volume, peak inspiratory flow (PIF), maximal inspiratory pressure (MIP), symptom-limited progressive cycle ergometer exercise tests and constant work rate exercise tests were administered before and after the training program. During the constant work rate exercise tests, tidal breathing flow volume (TBFV) curves were recorded every 1 mir. Results After treadmill training, the exercise duration (T) (t=7. 357, P＜0. 001), peak work rate (WRpeak) (t=3. 614, P＜0.05), MIP (t=4.754, P＜0. 001) and PIF (t=2. 440, P＜0. 05) increased significantly. The tidal PIF (t=- 2.747, P＜0.05) and peak expiratory flow (PEF) (t = - 4.487, P＜ 0.05 ) decreased significantly at isotime. Maxium inspiratory flow reserve (△FLOWinsp) (t = 2. 755, P ＜ 0. 05 ) increased significantly at isotime, and maxium expiratory flow reserve (△FLOWexp) (t = 1. 326, P ＞ 0.05)showed no significant changes; The△T were positively correlated with △MIP (r=0. 613, P＜0. 05),△PIF (r=0.497, P＜0.05) and △FLOWinsp (r=0.592, P＜0.05). Conclusions Lower limb exercise training improves inspiratory function of COPD patients. The improvement of exercise endurance in moderate to severe COPD patients after lower limb exercise training is due to increases of inspiratory muscle strength, maxium PIF and inspiratory flow reserve.     

Sternomastoid muscle function and fatigue in normal subjects and in patients with chronic obstructive pulmonary disease

Four normal subjects and 5 patients with chronic obstructive pulmonary disease (COPD) (mean FEV1, 1.03 L) had frequency:force curves of their sternomastoid muscle measured before and 5 min after a 12-min walk on a flat treadmill, a progressive exercise test (normal subjects only), and a 10-min period of sustained maximal voluntary ventilation (SMVV). Before each test, all subjects had a normal frequency:force curve, and the ratio of the force response at 20 Hz to that at 50 Hz was normal. After SMVV, all the normal subjects and 4 of the 5 patients developed a greater than 15% fall in 20:50 ratio, and this was taken to indicate the presence of low frequency fatigue (LFF). During SMVV, all the subjects achieved minute ventilation greater than 70% of predicted maximal breathing capacity (MBC). During the 12-min walk, all the patients exceeded 70% MBC, and 4 developed LFF. The normal subjects performing progressive exercise also exceeded 70% MBC, and all showed LFF. The 12-min walk did not cause LFF in the normal subjects, but no subject reached 70% of MBC. Despite the presence of LFF in the sternomastoid muscle, the patients were all able to walk the same distance during a second 12-min walk. In both the normal and patient groups, the ventilatory response to CO2 was not changed by the presence of LFF. There were no changes in maximal inspiratory and expiratory mouth pressures or spirometry with LFF. High, sustained levels of minute ventilation cause sternomastoid LFF, but the clinical significance of this phenomenon is not yet certain.     

慢性阻塞性肺疾病撤机困难呼吸力学特征10例分析

目的为提高慢性阻塞性肺疾病(COPD)患者撤机成功率提供生理学依据。方法检测2006年1月至2009年12月广州医学院第一附属医院收治的10例撤机困难COPD患者的呼吸力学指标,观察患者自主呼吸(SB)及机械通气时的呼吸力学指标变化。结果 SB时的呼吸频率(RR)、潮气量(VT)和分钟通气量(Ve)分别为(27.94±8.23)次/min、(0.266±0.107)L和(6.843±1.333)L/min,机械通气时的RR降低,而VT和Ve时升高(均P<0.05)。SB和机械通气时的动态内源性呼吸末正压分别为(0.82±0.19)kPa和(0.41±1.12)kPa,SB时明显增高(P<0.01),吸气中期气道阻力(RL)(2.43±0.94)kPa/(L.S)。SB时的P0.1为(0.61±0.16)kPa。SB时的最大跨膈压、最大食管负压和最大吸气口腔压分别为(5.08±0.93)kPa、(-5.00±0.95)kPa和(-3.78±0.86)kPa。SB时跨膈压(Pdi)和吸气压力时间乘积(PTPins)分别为(0.82±0.20)kPa和(48.93±11.94)kPa.s;机械通气时较SB显著降低,分别为(0.67±0.17)kPa和(30.33±11.72)kPa.s(P均<0.05)。结论撤机困难COPD患者存在显著的呼吸力学异常,SB时呼吸浅快,动态内源性呼吸末正压、RL与呼吸中枢驱动等均增高,吸气肌肉无力;应用PSV(1.57 kPa)联合PEEP(48%动态内源性呼吸末正压)可降低约50%的动态内源性呼吸末正压、17.8%的Pdi和38%的PTPins。     

Effect of salmeterol on the ventilatory response to exercise in chronic obstructive pulmonary disease.

This study examined the effects of bronchodilator-induced reductions in lung hyperinflation on breathing pattern, ventilation and dyspnoea during exercise in chronic obstructive pulmonary disease (COPD). Quantitative tidal flow/volume loop analysis was used to evaluate abnormalities in dynamic ventilatory mechanics and their manipulation by a bronchodilator. In a randomised double-blind crossover study, 23 patients with COPD (mean +/- SEM forced expiratory volume in one second 42 +/- 3% of the predicted value) inhaled salmeterol 50 microg or placebo twice daily for 2 weeks each. After each treatment period, 2 h after dose, patients performed pulmonary function tests and symptom-limited cycle exercise at 75% of their maximal work-rate. After salmeterol versus placebo at rest, volume-corrected maximal expiratory flow rates increased by 175 +/- 52%, inspiratory capacity (IC) increased by 11 +/- 2% pred and functional residual capacity decreased by 11 +/- 3% pred. At a standardised time during exercise, salmeterol increased IC, tidal volume (VT), mean inspiratory and expiratory flows, ventilation, oxygen uptake (VO2) and carbon dioxide output. Salmeterol increased peak exercise endurance, VO2 and ventilation by 58 +/- 19, 8 +/- 3 and 12 +/- 3%, respectively. Improvements in peak VO2 correlated best with increases in peak VT; increases in peak VT and resting IC were interrelated. The reduction in dyspnoea ratings at a standardised time correlated with the increased VT. Mechanical factors play an important role in shaping the ventilatory response to exercise in chronic obstructive pulmonary disease. Bronchodilator-induced lung deflation reduced mechanical restriction, increased ventilatory capacity and decreased respiratory discomfort, thereby increasing exercise endurance.     

Inspiratory force reserve of the respiratory muscles in children with chronic obstructive pulmonary disease

The purpose of this study was to evaluate inspiratory muscle force reserve in children with chronic obstructive pulmonary disease (COPD). In 15 hyperinflated (FRC/TLC, 65 +/- 0.7%) children, maximal mouth inspiratory static pressure (PImax) at FRC, mouth occlusion pressure (P0.1), tidal volume (VT), inspiratory time (TI), and total duration of the respiratory cycle (Ttot) were all measured. It was found that PImax at FRC was reduced compared with predicted values. However, after lung volume correction, PImax was in the normal range, and P0.1 was higher, TI was shorter, and Ti/Ttot was lower than predicted. The estimated mean inspiratory pressure for breathing at rest (PI) was significantly higher than predicted and was related to total pulmonary resistance (r = 0.74, p less than 0.001). The fraction of PImax developed by the respiratory muscles for breathing at rest (PI/PImax) significantly increased. The higher the PI/PImax ratio, the more the TI/Ttot ratio decreased (r = -0.64, p = 0.01). At rest, our subjects had to develop a mean inspiratory power (W) of as much as 48% (range, 30 to 76%) of the critical W above which fatigue occurs. Thus, even minimal increases in breathing load might expose children with COPD to respiratory muscle fatigue and to respiratory failure.     

Effect of respiratory muscle fatigue on breathing pattern during incremental exercise

We examined the breathing pattern during incremental exercise before and after induction of inspiratory muscle fatigue. Our aim was to determine whether induction of fatigue alters the ventilatory response to exercise and in particular whether such changes are most apparent at high levels of exercise when minute ventilation and thus inspiratory load are greatest. A group of 10 healthy subjects was studied on a cycle ergometer. Fatigue was achieved by having the subject breathe against an inspiratory threshold load that required the subject to generate 80% of the predetermined maximal mouth pressure to initiate airflow. Breathing pattern, oxygen consumption (VO2), mouth occlusion pressure (P0.1), and a visual analog scale (VAS) for respiratory effort were obtained for 3 min at rest and at 25, 50, 75, and 100% of the subject's maximal work load (Wmax) as determined by preliminary testing. Exercise was performed on two separate occasions, once immediately after induction of fatigue and the other as a control. Induction of fatigue had no effect on resting breathing and only minimal effects at the lower work loads (25 and 50% Wmax). At the higher work loads (75 and 100% Wmax) induction of fatigue significantly altered the pattern of breathing during exercise. At 75% of Wmax the respiratory frequency (f) increased from 22.5 +/- 4.4 (SD) during control to 27.0 +/- 6.7 breaths/min (p less than 0.02) following induction of fatigue; tidal volume was not significantly altered, 2.15 +/- 0.65 versus 2.24 +/- 0.74 L during control. The increase in f was due to reductions in both inspiratory and expiratory time because fractional inspiratory time remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)