肺减容手术治疗慢性阻塞性肺气肿的临床护理研究

目的:探讨慢性阻塞性肺气肿(COPD)予以肺减容手术治疗时的临床护理效果.方法:将收治的64例COPD患者作为研究对象,所有患者均予以肺减容手术治疗,将其随机分为常规组(予以常规护理)和全面组(予以全面护理),每组32例,对比两组患者的护理效果.结果:全面组患者并发症发生率显著低于常规组(P<0.05);全面组的PaO2水平及护理满意度评分显著高于常规组,且PaCO2较常规组更低,差异有统计学意义(P<0.05).结论:在对COPD患者予以肺减容手术治疗时,应从术前、术中及术后加强全面护理,改善血气分析指标、降低术后并发症发生率.     

Pharmacological therapy of chronic obstructive pulmonary disease

None of the available drugs for chronic obstructive pulmonary disease is able to reduce the progressive decline in lung function which is the hallmark of this disease. Smoking cessation is the only intervention that has been shown so far to reduce disease progression. The current pharmacological therapy for chronic obstructive pulmonary disease is largely symptomatic and is based on bronchodilators including selective beta2-adrenoceptor agonists (short- and long-acting), anticholinergics, theophylline, or a combination of these drugs. Due to the lack of efficacy, side effects at high doses, and high costs, glucocorticoids should not be used routinely for management of stable chronic obstructive pulmonary disease, although they are effective for exacerbations. New pharmacological strategies for chronic obstructive pulmonary disease are needed because the current management is inadequate.     

Nutritional status in chronic obstructive pulmonary disease: role of hypoxia

In patients with chronic obstructive pulmonary disease (COPD), malnutrition and limited physical activity are very common and contribute to disease prognosis, whereas a balance between caloric intake and exercise allows body weight stability and muscle mass preservation. The goal of this review is to analyze the implications of chronic hypoxia on three key elements involved in energy homeostasis and its role in COPD cachexia. The first one is energy intake. Body weight loss, often observed in patients with COPD, is related to lack of appetite. Inflammatory cytokines are known to be involved in anorexia and to be correlated to arterial partial pressure of oxygen. Recent studies in animals have investigated the role of hypoxia in peptides involved in food consumption such as leptin, ghrelin, and adenosine monophosphate activated protein kinase. The second element is muscle function, which is strongly related to energy use. In COPD, muscle atrophy and muscle fiber shift to the glycolytic type might be an adaptation to chronic hypoxia to preserve the muscle from oxidative stress. Muscle atrophy could be the result of a marked activation of the ubiquitin-proteasome pathway as found in muscle of patients with COPD. Hypoxia, via hypoxia inducible factor-1, is implicated in mitochondrial biogenesis and autophagy. Third, hormonal control of energy balance seems to be affected in patients with COPD. Insulin resistance has been described in this group of patients as well as a sort of “growth hormone resistance.” Hypoxia, by hypoxia inducible factor-1, accelerates the degradation of tri-iodothyronine and thyroxine, decreasing cellular oxygen consumption, suggesting an adaptive mechanism rather than a primary cause of COPD cachexia. COPD rehabilitation aimed at maintaining function and quality of life needs to address body weight stabilization and, in particular, muscle mass preservation.     

COPD稳定期无创正压通气治疗的评价(综述)

目的:评价COPD稳定期无创呼吸机的应用价值。方法:从无创呼吸机治疗对呼吸肌、肺功能、血气交换、活动耐量、生活质量和生存率的影响,来分析其疗效。结果:COPD稳定期无创呼吸机能明显改善生活质量,提高生存率。结论:无创呼吸机在COPD稳定期的治疗中,可是一种理想的方法。     

观察综合性肺康复疗法在慢性阻塞性肺病稳定期患者治疗中的疗效

目的采用综合性肺康复法为COPD(慢性阻塞肺病)患者进行治疗,对其稳定期的治疗效果进行观察与探讨。方法选取该院2008年1月—2011年1月收治过的符合COPD相关诊断标准的患者,共88例,将其进行随机分组,分为两组,观察组与对照组各分有患者44例,于患者的稳定期开始,进行治疗。结论进行综合性肺康复治疗在COPD患者的稳定期具有非常重要的意义。     

早期无创通气治疗煤工尘肺并慢性阻塞性肺病急性期患者的观察

目的观察早期应用无创正压通气(NIPPV)治疗煤工尘肺并慢性阻塞性肺病(COPD)急性加重期患者的临床疗效。方法随机选取17例煤工尘肺并COPD急性加重期患者除常规治疗外经面罩行NIPPV治疗。另取同期住院的12例煤工尘肺并COPD急性加重期患者作为对照组,仅用常规治疗。分别观察两组在治疗前2h、后24h、后48h的生命体征和动脉血气变化情况及最后转归。结果与对照组相比,治疗组患者病情和血气分析指标恢复较快,很少出现呼吸衰竭。结论早期应用NIPPV治疗煤工尘肺并COPD急性加重期患者的临床效果满意,预后较好,应作为本病的常规治疗。     

机械通气在慢性阻塞性肺疾病(COPD)治疗中的应用

慢性阻塞性肺疾病是引起呼吸衰竭的最常见原因之一,在对患者施行机械通气时,应根据其发病机理和病人指征来确定通气模式,设置呼吸机参数,并在通气过程中密切注意观察病人是否有动态过度充气,内原性呼气末正压及人-机是否同步.     

Exacerbations of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease is characterised by a progressive decline in lung function, reduced exercise performance, and worsening of health status. Exacerbations are important clinical events in chronic obstructive pulmonary disease and are defined as sudden worsening of respiratory symptoms and function requiring medical intervention. The most common causes of chronic obstructive pulmonary disease exacerbations are bacterial or viral infections, but comorbidity may be important. A major issue is the decision regarding home management or hospital management of exacerbations. Because of exacerbations, a frequent assessment of severity of chronic obstructive pulmonary disease is required for targeting pharmacological therapy.     

Epidemiology of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is an important cause of morbidity and mortality, all over the world. COPD, which was the sixth leading cause of death worldwide in 1990, will become the third one in 2020. COPD is a complex disease, influenced by genetic, behavioral, and environmental factors. The most important factor for developing COPD is tobacco smoke. Also environmental conditions represents risk for developing COPD. Furthermore, diet and a low socioeconomic status are correlated to the disease. Genetic factors, familial history, and childhood lower respiratory tract infections play an important role in the etiology of COPD. Burden of COPD is very high for community. Furthermore, the disease often is under-diagnosed and treated only at advanced stages, whilst it is a substantial health problem even among young adults. This needs to be taken into account by health personnel and decision-makers.     

Pathology of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder of the lung characterized by poorly reversible airflow limitation. It is not a unique disease entity but rather a complex of conditions which include emphysema, chronic bronchitis and, sometimes, asthma. Moreover, COPD is a progressive disease often associated with exacerbations. Cigarette smoking, which is the most important risk factor for the development of COPD, induces pathological changes involving lung parenchyma, peripheral airways and central airways. Since lung parenchyma and peripheral airways are the sites responsible for airflow limitation and central airways are the main site of mucus hypersecretion, pathological changes in these compartments may be relevant in the development of COPD.     

Pathophysiology of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a disease state characterised by airflow obstruction that is not fully reversible and progressive. Symptoms, as cough, sputum production and dyspnoea, functional impairment and complications of COPD can all be explained on the basis of the underlying lung inflammation and the resulting pathology. The chronic airflow obstruction is caused by a mixture of small airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema). On one hand, chronic inflammation causes remodelling and narrowing of the small airways. On the other hand, destruction of the lung parenchyma, also by an inflammatory process, leads to the loss of alveolar attachments to the small airways and decreases lung elastic recoil. In turn, these changes reduce the ability of the airways to remain open during expiration.     

细菌-病毒负荷在慢性阻塞性肺疾病中作用的研究进展

细菌和病毒在慢性阻塞性肺疾病(COPD)急性加重和疾病进展中起着举足轻重的作用,稳定期COPD患者气道内细菌和病毒负荷与气道炎症直接相关,能起到维持炎症状态的作用。该综述对不同临床条件下相关宿主肺微生物动力学及其与免疫反应的相互作用进行了回顾分析,对细菌-病毒负荷在慢性阻塞性肺疾病中的研究进展作一综述。     

肺康复有氧运动对缓解期慢性阻塞性肺疾病患者疲劳的影响

目的 探讨肺康复有氧运动对缓解期慢性阻塞性肺疾病患者疲劳的干预效果.方法 将门诊60例缓解期慢性阻塞性肺疾病患者随机分为试验组30例和对照组30例,对照组30例仅接受常规护理,试验组在接受常规护理的基础上给予8周的肺康复有氧运动干预.使用修订的Piper疲乏量表（RPFS）评价干预效果.结果 8周干预结束后,试验组RPFS及各维度得分明显低于对照组,差异有统计学意义（P〈0.05）,而对照组RPFS及各维度得分较8周前降低,但变化不明显,差异无统计学意义（P〉0.05）.结论 肺康复有氧运动可减轻慢性阻塞性肺疾病患者的疲劳.     

Circulating visfatin in chronic obstructive pulmonary disease

ObjectiveMalnutrition and continuous systemic inflammation occur frequently in patients with chronic obstructive pulmonary disease (COPD). Visfatin is a new adipokine, which increases in some inflammatory diseases. Its plasma level and relation with nutritional status and inflammation in COPD remain unknown. This study compared visfatin levels, nutritional status, and inflammation markers in patients with COPD and healthy controls.MethodsPlasma visfatin, tumor necrosis factor-α (TNF-α) and C-reactive protein (CRP) were measured in 35 patients with COPD and 28 healthy controls. Body composition was assessed with bioelectrical impedance analysis.ResultsSignificantly lower body mass index and percentage of body fat were observed in patients with COPD compared with control subjects. The levels of plasma visfatin were higher in the COPD group compared with healthy controls (2.07 ± 0.18 versus 1.88 ± 0.15 ng/mL, P < 0.001). Levels of TNF-α and CRP were also significantly higher in patients with COPD compared with controls. Plasma CRP and TNF-α were positively correlated with visfatin in the COPD group. No significant correlations were found between visfatin and body mass index or percentage of body fat in both groups.ConclusionPlasma visfatin levels increased in patients with COPD. This increased adipocytokine was significantly correlated with TNF-α and CRP. Visfatin may be a new proinflammatory adipocytokine in this disease.     

Efficacy of nutritional supplementation therapy in depleted patients with chronic obstructive pulmonary disease

OBJECTIVE: Weight loss and muscle wasting adversely affect morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD). Maintenance systemic glucocorticosteroids, prescribed in a substantial number of patients, further contribute to muscle weakness. We investigated the efficacy of oral nutritional supplementation therapy in depleted patients with COPD. METHODS: The therapy consisted of daily two to three oral liquid nutritional supplements (mean +/- standard deviation: 2812 +/- 523 kJ/24 h) incorporated into an 8-wk inpatient pulmonary rehabilitation program in 64 (49 men) depleted patients with COPD. Endpoints were body weight, fat-free mass by bioelectrical impedance analysis, respiratory and peripheral muscle function (maximal inspiratory mouth pressure and handgrip strength, respectively), exercise performance (incremental bicycle ergometry), and disease-specific health status by St. George's Respiratory Questionnaire. Forty-eight percent of the patients were treated with low-dose oral glucocorticosteroids as maintenance medication (dose equivalent to 7.6 +/- 2.5 mg of methylprednisolone per day). RESULTS: Increases in body weight (2.1 +/- 2.1 kg, P < 0.001) and fat-free mass (1.1 +/- 2.0 kg, P < 0.001) were seen. Further, maximal inspiratory mouth pressure (4 +/- 10 cm of H(2)O, P = 0.001), handgrip strength (1.2 +/- 3.1 kg, P = 0.004), and peak workload (7 +/- 11 W, P = 0.001) significantly improved. Clinically significant improvements in the items symptoms (9 +/- 16 points, P < 0.001) and impact (4 +/- 15 points, P = 0.043) of St. George's Respiratory Questionnaire were achieved. Oral glucocorticosteroid treatment significantly impaired the response to nutritional supplementation therapy with respect to maximal inspiratory mouth pressure, peak workload, and St. George's Respiratory Questionnaire symptom score. CONCLUSIONS: Nutritional supplementation therapy implemented in a pulmonary rehabilitation program was effective in depleted patients with COPD. However, oral glucocorticosteroid treatment attenuated the anabolic response to nutritional supplementation.