运动疗法与慢性阻塞性肺疾病

运动受限是慢性阻塞性肺疾病(COPD)的特征。运动受限的COPD患者，只要疾病处在稳定期，都可进行运动疗法。但运动时有生命危险的患者、重度肺动脉高压、运动引起晕厥患者、药物治疗无效的顽固性充血性心力衰竭、不稳定心绞痛、近期心肌梗死、终末期肝功能衰竭、严重关节炎、恶性肿瘤骨骼受累、失去学习活动能力患者或精神障碍或破坏性行为患者不宜进行运动疗法。运动疗法通过改善有氧代谢能力、改善呼吸肌肉力量和呼吸肌功能、提高肢体运动效率和协调性及减轻焦虑和恐惧等机制来提高COPD患者的运动耐力，减轻呼吸困难和肢体疲劳，改善生活质量。运动疗法可分为耐力训练和力量训练。确定运动强度的最直接的方法是心肺运动试验。评价运动强度的指标有最大功率的比例、呼吸困难评分及目标心率。运动疗法的实施方法分下肢运动疗法、上肢运动疗法和呼吸肌训练。运动强度和运动类型的选择，应该以病人个人的基础功能状态、病人症状和长期目标为依据。运动耐受程度的改善作用能维持2年。     

慢性阻塞性肺疾病患者居家运动疗法的研究进展

对慢性阻塞性肺疾病患者居家运动疗法进行综述,运动类型包括呼吸肌运动训练,骨骼肌运动训练;运动方法包含运动强度、运动频率及周期和运动程序.以期为慢性阻塞性肺疾病患者居家运动训练提供参考.     

运动疗法与慢性阻塞性肺疾病

运动受限是慢性阻塞性肺疾病(COPD)的特征。运动受限的COPD患者,只要疾病处在稳定期,都可进行运动疗法。但运动时有生命危险的患者、重度肺动脉高压、运动引起晕厥患者、药物治疗无效的顽固性充血性心力衰竭、不稳定心绞痛、近期心肌梗死、终末期肝功能衰竭、严重关节炎、恶性肿瘤骨骼受累、失去学习活动能力患者或精神障碍或破坏性行为患者不宜进行运动疗法。运动疗法通过改善有氧代谢能力、改善呼吸肌肉力量和呼吸肌功能、提高肢体运动效率和协调性及减轻焦虑和恐惧等机制来提高COPD患者的运动耐力,减轻呼吸困难和肢体疲劳,改善生活质量。运动疗法可分为耐力训练和力量训练。确定运动强度的最直接的方法是心肺运动试验。评价运动强度的指标有最大功率的比例、呼吸困难评分及目标心率。运动疗法的实施方法分下肢运动疗法、上肢运动疗法和呼吸肌训练。运动强度和运动类型的选择,应该以病人个人的基础功能状态、病人症状和长期目标为依据。运动耐受程度的改善作用能维持2年。     

慢性阻塞性肺疾病病人肺康复研究进展

本研究对近年来慢性阻塞性肺疾病(COPD)病人肺康复应用情况及相关方面研究进行综述,旨在提高医护人员对COPD病人肺康复效果的认识,为COPD病人肺康复提供临床科学依据,促进我国COPD肺康复的进一步发展。     

血小板与慢性阻塞性肺疾病

慢性阻塞性肺疾病(慢阻肺,COPD)是多种病因引起的慢性气道阻塞,其主要病理生理改变为:阻塞性通气功能障碍,后期发展为肺动脉高压、肺心病.慢阻肺肺动脉血栓形成率达20～50%,合并严重肺动脉高压者血栓形成率更高.血小板具有粘附、促凝和收缩血块的功能,因此在血栓形成和血管损伤中起重要作用.     

自我管理在慢性阻塞性肺疾病患者中的应用研究进展

正慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是危害人类健康的重要疾病。据世界卫生组织预计,到2020年COPD将成为全球世界疾病经济负担第5位~([1])。COPD作为全球公共卫生的重大问题,在我国也正成为国家和个人主要的疾病负担。目前,COPD的治疗手段仅仅是延缓疾病的进展,致使患者在长期患病过程中,心理、生理和社会等方面均受     

肺康复运动疗法在慢性阻塞性肺疾病中的研究进展

慢性阻塞性肺疾病(Chronic obstructive pulmo-nary disease,COPD)简称慢阻肺,是以持续的呼吸道症状和气流受限为特征的疾病,2014～2015年我国40岁以上成年人的患病率约为13.6％[1].慢阻肺患者因进行性呼吸困难出现活动量螺旋式下降,与体力活动降低和死亡率增加相关,故相关学...     

慢性阻塞性肺疾病营养干预的研究进展

慢性阻塞性肺疾病（COPD）患者常发生营养不良,而营养不良可加重病情,延长病期,呈恶性循环。所以在对患者进行临床治疗的同时,合理的营养干预对防止病情恶化和疾病康复起着非常重要的作用。本文对COPD引起营养不良的原因和营养干预等进行综述,以期为临床COPD的营养治疗提供依据。     

慢性阻塞性肺疾病患者的生活质量状态和干预方法

随着人口老龄化，环境污染加重，慢性阻塞性肺病发病率和病死率不断上升，章综述了慢性阻塞性肺疾病患生活质量受损的各个方面，并且提出了改善慢性阻塞性肺疾病患生活质量的有效措施。旨在提高人们对慢性阻塞性肺疾病患生活质量的关注，从而进一步加强对慢性阻塞性肺疾病患的综合治疗。     

Exercise and chronic obstructive pulmonary disease

Patients with chronic obstructive pulmonary disease have abnormal respiratory mechanics, respiratory muscle function, gas exchange, and cardiovascular function during exercise. Their impaired exercise tolerance is at least partly due to altered respiratory mechanics, but factors that increase ventilation during exercise indirectly contribute to exercise limitation. Clinical exercise testing is a very important tool in the assessment of exercise capacity, assessment of factors that contribute to exercise limitation, and differential diagnosis of cardiopulmonary disease.     

Exercise limitation and pulmonary rehabilitation in chronic obstructive pulmonary disease.

Impairment of exercise tolerance is a common problem in patients with severe chronic obstructive pulmonary disease. The cause of exercise intolerance in patients with severe chronic obstructive pulmonary disease is multifactorial and includes impaired lung mechanics, fatigue of inspiratory muscles, impaired gas exchange, right ventricular dysfunction, malnutrition, occult cardiac disease, deconditioning, and psychologic problems; however, impaired lung mechanics and gas exchange abnormalities seem to be the major limiting factors. Recently, the approach to management of pulmonary rehabilitation in patients with chronic obstructive pulmonary disease has changed because improvement in exercise tolerance has been demonstrated after pulmonary rehabilitation. Other adjunctive measures that have been shown to contribute to the observed improvement in exercise tolerance include administration of oxygen, nutritional support, cessation of smoking, and psychosocial support. The roles of ventilatory muscle endurance training, respiratory muscle rest therapy, nasally administered continuous positive airway pressure, and training of the muscles of the upper extremities are less clearly defined.     

Corticosteroid therapy and chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease is characterized in part by a chronic inflammatory state in the airways (largely from chronic noxious stimuli such as tobacco smoke), punctuated with acute inflammatory exacerbations, which are often infectious. Although pathologically and biochemically different from the inflammation of asthma, the chronic inflammation of chronic obstructive pulmonary disease, especially in subgroups with asthma-like features and especially during exacerbations, might be expected to respond to corticosteroid therapy, as does asthma. Complications from long-term corticosteroid use are important, but they appear less when the corticosteroid is given via the inhaled route. Clinical evidence is particularly strong supporting the use of inhaled corticosteroids to prevent exacerbations and oral corticosteroids to reduce the duration and impact of exacerbations.     

慢性阻塞性肺疾病运动能力及运动性肺动脉高压测 …

目的 应用运动心肺负荷试验早期检出慢性阻塞性肺疾病（ＣＯＰＤ）运动性低氧血症及运动性肺动脉高压。方法 实验组分为２组。慢性阻塞性肺疾病组６２例,正常对照组３０例,用ＨＰＳＯＮＳ－１０００型彩色多普勒超声仪,采用三尖瓣返流法于运动前后分别测定２组受试者的肺动脉收缩压,用Ｊａｅｇｅｒ公司产运动心肺功能仪,采用连续递增负荷方案测定最大摄氧量（ＶＯ２ｍａｘ）,最大功率（ＷＡＴＴ）等。结果 ＣＯＰＤ患者运动     

Contemporary therapy of chronic obstructive pulmonary disease and its new directions

Chronic obstructive pulmonary disease (COPD) gives rise to substantial structural changes in the respiratory tract and lungs with the development of chronic inflammation and bronchiolitis, as well as pulmonary parenchymatous destruction and the formation of emphysema. The listed changes substantiate the development of new treatment techniques, which will help correct structural changes in the respiratory tract and will slow down or even reverse progressive worsening of the respiratory function. In the future, the development of blood and/or saliva infection of inflammation biomarkers (e.g. endogenic protease inhibitors, antioxidants, cytokines etc.) will make it possible to find valuable diagnostic signs of forthcoming exacerbation, as well as to evaluate the effectiveness of new therapeutic techniques in clinical studies. COPD, or chronic bronchitis, airway obstruction, and emphysema, should be considered among pathological processes which result in smoking-induced chronic system inflammatory syndrome including cardiovascular diseases, metabolic disorder, and cancer. Possibly, treatment with new preparations, directed towards treating the patient as a whole rather than separate COPD symptoms, will be developed in the future.     

推拿治疗慢性阻塞性肺疾病的疗效

目的：观察推拿治疗慢性阻塞性肺疾病、改善肺功能的效应。方法：选择2003—07／2005—08来自上海交通大学附属第一人民医院呼吸科和推聿科收治的缓解期的慢性阻塞性肺疾病患者30例，男28例，女2例，随机分为两组，推拿组和对照组各15例，所有患者均给予常规按需治疗。推拿组患者给于每周5次推拿，每次20min，共8周。头面部及项部操作：①从头顶部到枕部用五指拿法，从枕部到项部用三指拿法。②推桥弓穴。③面部分法。④扫散法。躯干部操作：①横擦前胸部。②横擦肩背、腰部。③斜擦两肋。上肢操作：①直擦上肢。②拿上肢。③运肩关节，理手指，最后搓抖上肢。④重复头面部操作，加震百会、大椎、命门穴。按揉心俞、肺俞、脾俞、肾俞、命门，擦肾俞、命门。治疗前后给予测定肺功能（第1秒用力呼出量、用力肺活量、一秒率）；呼吸困难分级评分；6min步行距离实验。结果：30例均进入结果分析，无脱落者。①两组患者康复治疗前后呼吸功能变化：推拿组呼吸凼难减轻的有效率明显高于对照组（67％，40％）。②两组患者康复治疗前后肺功能变化：推拿组治疗屙第1秒用力呼气最，用力肺活量比治疗的升高[（1．419&;#177;0.953），（1．248&;#177;0．743）L；（2．628&;#177;0．921），（2.311&;#177;0．875）L，P＜0．01]，对照组的升高差异没有显著性。推拿组治疗后肺功能改善情况明屁高于对照组（P〈0．05）。③两组患者康复治疗前后6min步行距离实验的变化：两组患者6min步行距离实验均有增加，对照组的增加差异不显著（由328111增加到346111），推拿治疗前后差异显著（由330m增加到389m，P＜0．01），而且治疗后推拿组较对照组差异有显著性（P＜0．05）。结论：推拿治疗缓解期的慢性阻塞性肺疾病，可改善肺功能、减轻呼吸困难，增强运动耐力，值得推广。     

推拿治疗慢性阻塞性肺疾病的疗效

目的:观察推拿治疗慢性阻塞性肺疾病、改善肺功能的效应。方法:选择2003-07/2005-08来自上海交通大学附属第一人民医院呼吸科和推拿科收治的缓解期的慢性阻塞性肺疾病患者30例,男28例,女2例,随机分为两组,推拿组和对照组各15例,所有患者均给予常规按需治疗。推拿组患者给予每周5次推拿,每次20min,共8周。头面部及项部操作:①从头顶部到枕部用五指拿法,从枕部到项部用三指拿法。②推桥弓穴。③面部分法。④扫散法。躯干部操作:①横擦前胸部。②横擦肩背、腰部。③斜擦两肋。上肢操作:①直擦上肢。②拿上肢。③运肩关节,理手指,最后搓抖上肢。④重复头面部操作,加震百会、大椎、命门穴。按揉心俞、肺俞、脾俞、肾俞、命门,擦肾俞、命门。治疗前后给予测定肺功能(第1秒用力呼出量、用力肺活量、一秒率);呼吸困难分级评分;6min步行距离实验。结果:30例均进入结果分析,无脱落者。①两组患者康复治疗前后呼吸功能变化:推拿组呼吸困难减轻的有效率明显高于对照组(67%,40%)。②两组患者康复治疗前后肺功能变化:推拿组治疗后第1秒用力呼气量,用力肺活量比治疗前升高犤(1.419±0.953),(1.248±0.743)L;(2.628±0.921),(2.311±0.875)L,P<0.01犦,对照组的升高差异没有显著性。推拿组治疗后肺功能改善情况明显高于对照组(P<0.05)。③两组患者康复治疗前后6min步行距离实验的变化:两组患者6min步行距离实验均有增加,对照组的增加差异不显著(由328m增加到346m),推拿治疗前后差异显著(由330m增加到389m,P<0.01),而且治疗后推拿组较对照组差异有显著性(P<0.05)。结论:推拿治疗缓解期的慢性阻塞性肺疾病,可改善肺功能、减轻呼吸困难,增强运动耐力,值得推广。     

New drug therapy of chronic obstructive pulmonary disease

The progression of chronic obstructive pulmonary disease(COPD) can be inhibited by smoking cessation. As adjunct drugs, nicotine replacement therapy and an antidepressant bupropion are found to improve the abstinence rate from smoking. The mainstay of drug therapy of COPD consists of bronchodilators. Inhaled long-acting anticholinergic agents are in development. Inhaled long-acting beta 2-agonists are newly available. Theophylline has weak antiinflammatory effects. The significance of corticosteroids and mucolytic drugs in stable COPD is yet to be elucidated. In severely hypoxemic patients with COPD long-term domicillary oxygen therapy improves the survival rate. There is no drug therapy which can prevent the long-term deterioration of pulmonary function in patients with COPD. New class of drugs are now in development.