慢性阻塞性肺疾病的呼吸肌功能

慢性阻塞性肺疾病患者常存在呼吸肌收缩力和(或)耐力下降,引起呼吸困难,限制患者活动能力,使患者的运动量减少,日常生活质量降低;如果病情得不到控制,可以导致高碳酸性呼吸衰竭,严重者造成患者死亡.呼吸肌功能评价在慢性阻塞性肺疾病患者临床病情评估和预后判断方面很有应用价值.最大吸气压和最大呼气压测定是临床最常用的、可信的、非创伤性的评价呼吸肌功能的指标.研究结果显示最大吸气压较一秒量敏感.呼吸肌本身的病理改变和肺过度充气导致膈肌的收缩初长度缩短等原因可以引起呼吸肌功能障碍.可以应用抗胆碱药物、β2-受体激动剂、运动训练、营养支持及同化激素、心理支持、患者教育等治疗慢性阻塞性肺疾病呼吸肌功能障碍.蛋白酶抑制剂、过氧化物酶体增殖物激活受体、硫酸镁有希望成为治疗慢性阻塞性肺疾病呼吸肌功能障碍的方法.     

Respiratory muscle function and drive in chronic obstructive pulmonary disease

Respiratory, and particularly inspiratory, muscle function is altered in COPD. Many of these alterations are secondary to a mechanical disadvantage related to hyperinflation. Other factors, including corticosteroid therapy and nutritional depletion, are also deleterious to muscle function. In addition, the load imposed on the respiratory muscles is increased in COPD. Combined with the altered respiratory muscle function, this increase induces important changes in respiratory muscle drive and recruitment. Moreover, the imbalance between respiratory muscle function and load is an important determinant of dyspnea and hypercapnia. Because much of the lung and airway derangements are irreversible in COPD, the respiratory muscles appear to be an attractive target for therapeutic interventions.     

慢性阻塞性肺疾病呼吸肌功能不全发病机制

研究发现慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者由于肺气肿、慢性低氧、高碳酸血症、营养不良及医源性因素等多种原因,呼吸肌尤其是膈肌可出现肌纤维发生结构及功能变化,导致呼吸肌功能不全.呼吸肌功能不全是发生呼吸衰竭的重要的病理生理机制之一.本文对COPD发生呼吸肌功能不全机制进行综述.     

Acute bronchodilator trials in chronic obstructive pulmonary disease.

Short-term trials of bronchodilator drugs are widely used to assess patients with stable chronic obstructive pulmonary disease (COPD), but there is an uncertainty about the equivalence of the FEV1 response to beta-agonists and anticholinergic drugs, their relative ability to identify patients likely to improve with corticosteroids, the most appropriate way to express the results of these tests, and whether age or allergic status affects the beta-agonist and anticholinergic response differently. We studied 100 consecutive patients with stable COPD (mean FEV1, 0.96 +/- 0.48 L; mean age, 62 +/- 8 yr). Spirometry was measured before and after either 5 mg of nebulized salbutamol or 500 micrograms of nebulized ipratropium bromide and repeated after 2 wk of 30 mg of oral prednisolone daily. Total IgE, specific RAST, and skin prick testing values were recorded. Using modified American Thoracic Society response criteria, 33 patients failed to bronchodilate after the acute trials, 16 responded only to nebulized salbutamol, 17 to nebulized ipratropium, and 34 to both drugs. Twenty-two patients improved after corticosteroids. This was usually detected by a positive acute trial response (salbutamol 90% specific; ipratropium 84% specific). Baseline FEV1 differed between days, and in those who responded on only 1 day, this variation correlating with the response to ipratropium (r = 0.66). Expressing the response criterion as a percentage change in the available bronchodilatation increased the numbers responding with a high baseline FEV1, and vice versa. Neither age nor allergic status was related to the change in FEV1 after either drug in these patients. In COPD patients, testing with high-dose nebulized bronchodilators identifies a substantial number of partially reversible patients whatever age it is employed.(ABSTRACT TRUNCATED AT 250 WORDS)     

The response to inhaled and oral steroids in patients with stable chronic obstructive pulmonary disease

BACKGROUND: A significant minority of patients with COPD have favourable response to corticosteroid treatment. In addition, the benefit of corticosteroid treatment may be outweighed by the side-effects. Long-term administration of inhaled steroids is a safe means of treatment. However, only a few studies have addressed the role of inhaled steroids in patients with COPD, with conflicting results. METHODS: Forty-four patients with stable COPD were defined as 'responders to bronchodilators' (increase in FEV1 > or = 20% following administration of beta 2-agonist) (group A), and 124 as 'non-responders to bronchodilators' (group B). All patients were randomized to receive a 6-week course of either a daily dose of 800 micrograms of inhaled budesonide or placebo, separated by 4 weeks when no medication was taken; were randomized again to receive a 6-week course of either 1600 micrograms day-1 of inhaled budesonide, or 800 micrograms day-1 of inhaled budesonide plus placebo; and were randomized once again to receive a 6-week course of either 40 mg day-1 of prednisone or placebo. All stages were performed in a double-blind cross-over design. RESULTS: Following administration of 800 micrograms day-1 of inhaled budesonide, there was an increase in the mean FEV1 from 1.40 +/- 0.20 to 1.92 +/- 0.22 L (P < 0.001) and a significant decrease in inhaled beta 2 agonist consumption in group A. These changes remained almost stable during the increased dose of inhaled budesonide or during prednisone treatment. The mean FEV1 did not change during the placebo period, or in group B in either treatments. CONCLUSIONS: Treatment with inhaled steroids improved spirometry data and inhaled beta 2-agonist consumption in about one-quarter of patients with stable COPD, and this rate increased to about three-quarters in patients who responded to beta 2-agonist inhalation. There was no additional benefit in using a higher dose of inhaled budesonide or prednisone.     

Peripheral muscle dysfunction in chronic obstructive pulmonary disease

Patients with chronic obstructive pulmonary disease (COPD) often develop systemic complications of their disease. Peripheral muscle dysfunction is one such complication and is characterised by atrophy, weakness, and low oxidative capacity. These muscle changes influence exercise tolerance and quality of life independent of the impairment in lung function. In the following article, the evidence for peripheral muscle dysfunction in patients with COPD and the possible clinical implications of this problem will be discussed. Lastly, the available therapeutic options to improve peripheral muscle function in COPD will be reviewed.     

Peripheral muscle dysfunction in chronic obstructive pulmonary disease

Peripheral muscle dysfunction is a common systemic complication of moderate to severe COPD and may contribute to disability, handicap, and premature mortality. In contrast to the lung impairment, which is largely irreversible, peripheral muscle dysfunction is potentially remediable with exercise training, nutritional intervention, oxygen, and anabolic drugs. Therapeutic success is often incomplete, however, and a better understanding of the mechanisms involved in the development of peripheral muscle dysfunction in COPD is needed to help develop innovative and more effective therapeutic strategies.     

慢性阻塞性肺疾病与骨骼肌功能异常

COPD是一种以气流受限不完全可逆为特征,同时伴有全身多系统损害的慢性炎症反应性疾病.骨骼肌功能异常(skeletal muscle dysfunction,SMD)或无力是COPD全身效应(即肺外作用)的突出表现之一,与患者的生命质量和病情加重密切相关[1].SMD常始于早期COPD,且有较高的发病率.因此,对COPD患者SMD防治的研究,有可能为防治COPD提供新的途径.     

慢性阻塞性肺疾病与骨骼肌功能异常

COPD是一种以气流受限不完全可逆为特征,同时伴有全身多系统损害的慢性炎症反应性疾病.骨骼肌功能异常(skeletal muscle dysfunction,SMD)或无力是COPD全身效应(即肺外作用)的突出表现之一,与患者的生命质量和病情加重密切相关[1].SMD常始于早期COPD,且有较高的发病率.因此,对COPD患者SMD防治的研究,有可能为防治COPD提供新的途径.     

Response to oral corticosteroid in patients with chronic obstructive pulmonary disease.

We studied the effect of 30 mg of prednisolone on 29 Japanese patients with chronic obstructive pulmonary disease (COPD). The mean value of the baseline forced expiratory volume in one second (FEV1; mean +/- SEM) was 1.14 +/- 0.12 l (46.9 +/- 3.9% pred) and the FEV1 following the steroid trial was 1.30 +/- 0.12 l (53.7 +/- 4.3% pred). Post-trial FEV1--baseline FEV1/predicted FEV1 was 6.8 +/- 1.9%. Five patients (17%) had more than a 15% increase in FEV1 as a percentage of predicted FEV1. Post-trial FEV1/baseline FEV1 was 117.3 +/- 4.3%, and 12 patients (41%) had more than a 20% increase in FEV1 after the trial. Acute bronchodilator response to beta-agonist correlated positively with the response to corticosteroid. Baseline spirometries, blood eosinophil counts, serum IgE levels, sputum eosinophil counts, family history of asthma, and history of paroxysmal dyspnea did not vary across responders and non-responders. Patients with severe COPD should be treated to achieve the best possible pulmonary functions indicated by a steroid trial within the limit of acceptable levels of adverse effects.     

Acute effects of exercise on cognition in patients with chronic obstructive pulmonary disease.

Prior data indicate positive effects of long-term exercise interventions for cognitive functioning among patients with chronic obstructive pulmonary disease (COPD), but no prior studies have examined acute effects of individual bouts of exercise among patients with COPD. This study evaluated acute effects of exercise on cognitive performance in a community-based sample of patients with COPD and a healthy control group, matched by age, sex, and education. Twenty-nine older adults with COPD (mean age = 67.8 yr [+/- 7.4]; range: 56-85; 17 women) and 29 matched healthy control subjects (mean age = 68.7 yr [+/- 6.0] ) were recruited from the community. All participants completed a 20-min exercise session in which they exercised to a peak level and a video control condition in which they were provided information about exercise and cholesterol. Conditions were separated by a 1-wk interval, and order of participation in conditions was randomly assigned. Assessments of cognitive performance (Trail Making Test, Digit Symbol, Verbal Fluency, Digit Span, Finger Tapping) were administered before and after each condition (exercise and video). Among patients with COPD, acute exercise was associated with improved performance on the Verbal Fluency test, a measure of verbal processing, suggesting that acute exercise may benefit aspects of cognitive performance among patients with COPD.     

Expiratory muscle pressure and breathing mechanics in chronic obstructive pulmonary disease.

Expiratory muscle recruitment is common in stable chronic obstructive pulmonary disease (COPD) patients. Due to airway obstruction, there is little reason to believe that active expiration in COPD would be mechanically effective in lowering operating lung volume. The physiological significance of expiratory muscle recruitment in COPD, therefore, remains unknown. The purpose of this study was to assess, in COPD patients breathing at rest, the effect of expiratory muscle contraction on force generating ability of the diaphragm. The force generating ability of the diaphragm was evaluated from its pressure swing (Pdi) for a given diaphragm electrical activity (Edi), where Edi was normalized as % of its maximal value (Pdi/Edi/Edi,max). Phasic expiratory muscle contraction was measured as the total expiratory rise in gastric pressure (Pga,exp.rise). Nineteen seated patients with moderate to severe COPD, participated in the study and 10 exhibited phasic rise in Pga during expiration with a mean Pga,exp.rise of 1.91+/-0.89 cmH2O. The patients were thus divided into passive expiration (PE) and active expiration (AE) groups. There was no significant difference in various lung function and breathing pattern parameters between the two groups. Pdi/Edi/Edi,max was 0.63+/-0.07 and 0.54+/-0.07 cmH2O/% in PE and AE groups, respectively, and was not significantly different between each other. Compared with PE group, AE group not only recruited expiratory muscles, but also preferentially recruited inspiratory rib cage muscles and derecruited the diaphragm. The results do not support a significant improvement of the force-generating ability of the diaphragm by phasic contraction of expiratory muscles at rest in chronic obstructive pulmonary disease patients.