This review presents an analysis of the literature on the topic of respiratory muscle (RM) dysfunction in various forms of respiratory pathology: chronic obstructive pulmonary disease (COPD), asthma, community-acquired pneumonia, idiopathic pulmonary fibrosis (IPF), sarcoidosis and interstitial lung diseases (ILD), associated with systemic connective tissue diseases (polymyositis, dermatomyositis and systemic lupus erythematosus - SLE). Various clinical and pathophysiological aspects of RM dysfunction and general patterns of its pathogenesis were examined. It was proved that the role of RM in the development of respiratory failure depends on the form and stage of the pulmonary pathology and the severity of systemic manifestations of these diseases: excessive proteolysis, oxidative stress, hypoxia, chronic systemic inflammation. These factors modify the morphofunctional status of RM, worsens their contractile function, which is contributed to the development of respiratory failure. In some cases, the primary weakness of RM precedes the clinical manifestation of pulmonary pathology, which is distinctive for some variants of myositis-associated ILD and SLE. Endogenous intoxication syndrome plays a significant role in the development of RM dysfunction during community-acquired pneumonia. It is noted that sarcoid pulmonary ventilation disorders associate with the RM weakness, but not with the degree of lung damage. In most cases, secondary RM dysfunction predominates that contributes to respiratory failure progression, which is especially noticeable in case of COPD, asthma and IPF.
Literature data of chronic obstructive pulmonary disease (COPD) and cerebrovascular diseases (CVD) comorbidity are represented in this review. Key aspects of this interaction and its importance for clinical medicine have been considered. CVD and COPD are the main mortality factors in adults, which contribute to great economic wastes. The incidence of chronic cerebral ischemia for COPD patients is almost three times as high as for general population. The incidence of ischemic stroke for COPD patients is 1,2 times higher than in general population. For hemorrhagic stroke and subarachnoid haemorrhages, this figures are 1,3 and 1,46 respectively. Chronic systemic inflammation, tissue hypoxia and oxidative stress play the crucial role in respiratory and cerebrovascular comorbidity. Metabolites of these processes (especially proinflammatory cytokines, reactive oxygen species, C-reactive protein and some neurotrophins) increase the permeability of blood-brain barrier, destroy brain cells and activate atherogenesis in pre - and intracerebral arteries. Endothelial dysfunction affects autoregulation of cerebral circulation. Systemic symptoms of COPD are closely associated with different structural-functional disorders of the brain such as reduction in white matter integrity, grey matter volume reduction and cerebral microbleeds. Also, venous encephalopathy is developed as a result of intrathoracic pressure elevation and stasis in superior vena cava system. These processes result in neurological symptomatology. The intensity of symptoms depends on COPD severity. The occurrence of cognitive impairment, psychic tension, depression, panic disorders also increases. However COPD and CVD comorbidity is an important problem of modern medicine, pathophysiologic mechanisms and clinic aspects of this problem remain unresolved. Understanding of their role opens perspectives for rational pharmacotherapy.
ФГАОУ ВО «Дальневосточный федеральный университет» Минобрнауки России, г. Владивосток, РФ 2 ФГБОУ ВО «Владивостокский государственный университет экономики и сервиса» Минобрнауки России, Институт информационных технологий, г. Владивосток, РФ Цель исследования: сравнительная оценка силы дыхательных мышц (ДМ) у больных бронхиальной астмой (БА), хронической обструктивной болезнью легких (ХОБЛ) и с их сочетанием, определение информативности ее индикаторов для верификации этих состояний. Материалы и методы. В стационаре обследовано 130 больных с тяжелым течением БА, ХОБЛ и с сочетанием БА + ХОБЛ. Регистрировали силовые индикаторы экспираторных (MEP) и инспираторных (MIP, SNIP) ДМ на аппарате MicroRPM (CareFusion, Великобритания), рассчитывали их должные величины. Информативность показателей MEP, MIP и SNIP для верификации отдельных форм бронхиальной обструкции определяли с помощью моделей логистической регрессии. Результаты. У больных всех групп зафиксировано снижение силы экспираторных и инспираторных ДМ. Дисфункция экспираторных мышц доминировала при БА, а диафрагмы-при ХОБЛ и сочетании БА + ХОБЛ. Корреляционный анализ показал зависимость силы ДМ от выраженности бронхиальной обструкции и гиперинфляции легких, массы скелетной мускулатуры, индекса массы тела, респираторного дискомфорта и функционального статуса больных. Установлено, что отношение MEP/MIP обладает высоким прогностическим потенциалом и значительно повышает точность моделей стратификации обследованных по нозологическим группам. Заключение. Исследование силы ДМ является информативным инструментом в комплексной оценке респираторных функций у больных с различными клиническими вариантами бронхиальной обструкции.
Respiratory muscles strength is the main indicator of their functional state. The study of respiratory muscles strength is becoming increasingly prevalent in clinical pulmonology, especially in case of chronic obstructive pulmonary disease (COPD) and asthma. However, respiratory muscles strength is used neither for COPD stratification nor for differential diagnosis of COPD and asthma related to the broncho-obstructive syndrome. The aim of the study was to develop models that support medical decision making in broncho-obstructive syndrome diagnostics. Material and methods. 214 patients who were hospitalized with COPD exacerbation (115 people), severe uncontrolled asthma (56 people), and their combination (43 people). Respiratory muscles strength indicators (MEP, MIP and SNIP), 9 anthropometric parameters, spirometry and blood gas parameters, modified medical research council dyspnea scale, COPD assessment test data were recorded. Data processing was carried out by means of Mann-Whitney, Fisher and Tukey tests and correlation analysis. Respiratory muscles strength models were performed by linear and nonlinear regression methods. COPD stratification and differential diagnosis of COPD and asthma models were performed by artificial neural networks. Results. Respiratory muscles strength models of healthy individuals and COPD patients allowed to estimate the effects of various factors on the respiratory muscles functional status. Comparative analysis of COPD severity verification showed that models accuracy increased when we had added a respiratory muscles strength indicator. The most informative indicators were MIP, total body mass, partial pressure of carbon dioxide and fibrinogen. Moreover, MIP increased the accuracy of all the models. Conclusion. Practical application of artificial neural networks models in telemedicine projects allows developing information services to support real-time assessment of the patient's condition.
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