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To evaluate the frequency of the causes of exercise limitation in patients with chronic pulmonary disease and to assess the relationship between the resting pulmonary functional parameters and the degree of exercise dyspnea, we reviewed the data from 88 consecutive stable patients with chronic lung disease (62 COPD, 16 interstitial lung disease [ILD]). In each patient, the intensity of dyspnea was measured by a Borg scale (BS) during an incremental symptom-limited exercise test. COPD patients stopped exercise due to fatigue (46%), dyspnea (36%), cardiac limitation (12%), and peripheral circulatory limitation (6%). ILD patients stopped exercise due to dyspnea (62%), fatigue (25%), and cardiac limitation (12%). In all patients, dyspnea severity increased linearly with exercise intensity as measured as VO2, VE, and VE/MVV. The severity of dyspnea expressed as the slope of the relationship between BS and VE/MVV (DBS/D[VE/MVV]) showed in COPD a significant inverse correlation with VC, FEV1, MIP, and a positive correlation with PaCO2 and VE/MVV at rest. In ILD, DBS/D(VE/MVV) showed a significant inverse correlation with VC, FEV1, TLC, and PaO2 and a positive correlation with VE/MVV at rest. The predicting power of all equations was very low.
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PMID:Dyspnea on exercise. Pathophysiologic mechanisms. 157 44

Restrictive lung disease patients exhibit a wide range of breathing and oxygenation abnormalities during sleep. The combination of degree of restriction, whether it is intrapulmonary or extrapulmonary, and confounding factors, such as obesity, age, and sex, will ultimately determine the degree of disturbed nocturnal physiology. The sleep literature is still sparse in most restrictive diseases. For patients with interstitial lung disease, the role of nocturnal oxygen in chronic established fibrosis, and also in acute alveolitis (e.g., farmer's lung, bird fancier's lung, etc.), has not been addressed. As fibrotic lung disease progresses, the degree of nocturnal desaturation and breathing dysrhythmias will progress. Changes in sleep architecture are likely related to the progression of the disease, but this is not known with certainty. Long-term evaluation of sleep and breathing in interstitial lung disease will give further insight into whether or not sleep changes are primary or secondary events. For kyphoscoliosis patients, again, we need more information on sleep as the thoracic deformity changes. In addition, the use of drugs (acetazolomide, medroxyprogesterone, and almitrine) and/or nasal CPAP to treat nocturnal desaturation needs to be assessed in a controlled fashion. In neuromuscular disease, the dynamics of gas exchange and sleep structure need to be defined in a larger group of patients. Factors such as degree of muscle weakness, degree of underlying lung diseases, and medications must be taken into consideration. Nocturnal hypoxemia may cause muscle weakness and fatigue, which in time, could cause more nocturnal hypoventilation and further hypoxemia. Supplemental nocturnal oxygen should be evaluated in this population.
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PMID:Sleep in restrictive lung disease. 331 24

Inspiratory muscle fatigue and pulmonary edema are both known to cause rapid shallow breathing. It has been suggested that exercise tolerance in patients with pulmonary disease and cardiac disease may be limited by the development of inspiratory muscle fatigue and pulmonary edema, respectively, at maximal exercise. If these hypotheses are correct, breathing pattern during recovery from maximal exercise in these patients should be rapid and shallow compared with that during exercise. This study was performed to test these hypotheses. Seven patients with chronic obstructive pulmonary disease (COPD), 8 patients with interstitial lung disease (ILD), 7 patients with cardiac disease (CD) (mitral valve disease or left ventricular dysfunction) and 8 normal (NR) subjects each performed maximal incremental exercise on a cycle ergometer. Exercise breathing pattern was compared with that during recovery by calculating the mean difference in tidal volume (at the same levels of minute ventilation) between exercise and recovery for each subject. Recovery breathing pattern was similar to that during exercise for the COPD, ILD, and NR subjects. In contrast, breathing pattern during recovery was rapid and shallow compared with that during exercise for the CD patients; recovery tidal volume was less than that during exercise for the same level of minute ventilation. The fact that rapid shallow breathing does not develop during recovery from maximal exercise in patients with COPD or ILD suggests that inspiratory muscle fatigue does not limit their exercise tolerance. The relative rapid shallow breathing during recovery from maximal exercise in patients with CD is probably due to the development of pulmonary edema at maximal exercise, but further studies are needed to confirm this.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Breathing pattern during and after maximal exercise in patients with chronic obstructive lung disease, interstitial lung disease, and cardiac disease, and in normal subjects. 396 26

The question of respiratory factors limiting exercise has been examined in terms of possible limitations arising from the function of gas exchange, the respiratory mechanics, the energetics of the respiratory muscles, or the development of respiratory muscle fatigue. Exercise capacity is curtailed in the presence of marked hypoxia, and this is readily observed in patients with chronic airflow limitation and interstitial lung disease and in some athletes at high intensities of exercise. In patients with interstitial lung disease, gas exchange abnormality--partly the result of diffusion disequilibrium for oxygen transfer--occurs during exercise despite abnormally high ventilations. In contrast, in certain athletes arterial hypoxemia has been documented during heavy exercise, apparently as a result of relative hypoventilation. During strenuous exercise the maximum expiratory flow volume curves are attained both by patients with chronic airflow limitation and by normal subjects, in particular when they breathe dense gas, so that a mechanical constraint is imposed on further increases in ventilation. Similarly, the force velocity characteristics of the inspiratory muscles may also impose a constraint to further increases in inspiratory flows that affects the ability to increase ventilation. In addition, the oxygen cost of maintaining high ventilations is large. Analysis of results from blood flow experiments reveal a substantial increase in blood flow to the respiratory muscles during exercise, with the result that oxygen supply to the rest of the body may be lessened. Alternatively, high exercise ventilations may not be sustained indefinitely owing to the development of respiratory muscle fatigue that results in hypoventilation and reduced arterial oxygen tension.
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PMID:Respiratory factors limiting exercise. 634 20

Lung volumes were measured at rest and during exercise by an open-circuit N2-washout technique in patients with interstitial lung disease (ILD). Exercise tidal flow-volume (F-V) curves were also compared with maximal F-V curves to investigate whether these patients demonstrated flow limitation. Seven patients underwent 4 min of constant work rate bicycle ergometer exercise at 40, 70, and 90% of their previously determined maximal work rates. End-expiratory lung volume and total lung capacity were measured at rest and near the end of each period of exercise. There was no significant change in end-expiratory lung volume or total lung capacity when resting measurements were compared with measurements at 40, 70, and 90% work rates. During exercise, expiratory flow limitation was evident in four patients who reported stopping exercise because of dyspnea. In the remaining patients who discontinued exercise because of leg fatigue, no flow limitation was evident. In all patients, the mean ratio of maximal minute ventilation to maximal ventilatory capacity (calculated from maximal F-V curves) was 67%. We conclude that lung volumes during exercise do not significantly differ from those at rest in this population and that patients with ILD may demonstrate expiratory flow limitation during exercise. Furthermore, because most patients with ILD are not breathing near their maximal ventilatory capacity at the end of exercise, we suggest that respiratory mechanics are not the primary cause of their exercise limitation.
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PMID:Lung volumes and expiratory flow limitation during exercise in interstitial lung disease. 800 54

Except for benign pleural effusion, asbestos-related pulmonary complications, including asbestosis, malignant mesothelioma and bronchogenic carcinoma, usually occur more than 20 years after exposure. Pleural plaques and pleural thickening serve as markers for asbestos exposure, but they are not associated with an increased risk of malignancy. Clinical criteria for the diagnosis of asbestosis include a reliable history of asbestos exposure, an appropriate interval between exposure and disease detection, radiographic evidence of pulmonary fibrosis, decreased vital capacity and diffusing capacity, and bilateral posterior inspiratory crackles. A lung biopsy is indicated only to rule out other causes of interstitial lung disease. A history of dyspnea, pleuritic chest pain, fatigue, weight loss and pleural effusion in a former asbestos worker is suggestive of mesothelioma. Cigarette smoking greatly increases the risk of lung cancer in asbestos workers.
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PMID:Pulmonary complications of asbestos exposure. 804 65

Muscle may suffer from a number of diseases or disorders, some being fatal to humans and animals. Their management or treatment depends on correct diagnosis. Although no single method may be used to identify all diseases, recognition depends on the following diagnostic procedures: (1) history and clinical examination, (2) blood biochemistry, (3) electromyography, (4) muscle biopsy, (5) nuclear magnetic resonance, (6) measurement of muscle cross-sectional area, (7) tests of muscle function, (8) provocation tests, and (9) studies on protein turnover. One or all of these procedures may prove helpful in diagnosis, but even then identification of the disorder may not be possible. Nevertheless, each of these procedures can provide useful information. Among the most common diseases in muscle are the muscular dystrophies, in which the newly identified muscle protein dystrophin is either absent or present at less than normal amounts in both Duchenne and Becker's muscular dystrophy. Although the identification of dystrophin represents a major breakthrough, treatment has not progressed to the experimental stage. Other major diseases of muscle include the inflammatory myopathies and neuropathies. Atrophy and hypertrophy of muscle and the relationship of aging, exercise, and fatigue all add to our understanding of the behavior of normal and abnormal muscle. Some other interesting related diseases and disorders of muscle include myasthenia gravis, muscular dysgenesis, and myclonus. Disorders of energy metabolism include those caused by abnormal glycolysis (Von Gierke's, Pompe's, Cori-Forbes, Andersen's, McArdle's, Hers', and Tauri's diseases) and by the acquired diseases of glycolysis (disorders of mitochondrial oxidation). Still other diseases associated with abnormal energy metabolism include lipid-related disorders (carnitine and carnitine palmitoyl-transferase deficiencies) and myotonic syndromes (myotonia congenita, paramyotonia congenita, hypokalemic and hyperkalemic periodic paralysis, and malignant hyperexia). Diseases of the connective tissues discussed include those of nutritional origin (scurvy, lathyrism, starvation, and protein deficiency), the genetic diseases (dermatosparaxis, Ehlers-Danlos syndrome, osteogenesis imperfecta, Marfan syndrome, homocystinuria, alcaptonuria, epidermolysis bullosa, rheumatoid arthritis in humans, polyarthritis in swine, Aleutian disease of mink, and the several types of systemic lupus erythematosus) and the acquired diseases of connective tissues (abnormal calcification, systemic sclerosis, interstitial lung disease, hepatic fibrosis, and carcinomas of the connective tissues). Several of the diseases of connective tissues may prove to be useful models for determining the relationship of collagen to meat tenderness and its other physical properties. Several other promising models for studying the nutrition-related disorders and the quality-related characteristics of meat are also reviewed.
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PMID:Diseases and disorders of muscle. 839 47

Pulmonary Langerhans' cell histiocytosis and eosinophilic granuloma are the terms used to describe a Langerhans' cell granulomatous interstitial lung disease of unknown aetiology, occurring predominantly in smokers and involving primarily lungs, bones, skin and lymph nodes. In this report a patient with fever, fatigue, dyspnoea, nocturnal perspiration and thoracic pain is described. The high-resolution computed tomography of the chest and histological examination of lung biopsies suggested the diagnosis of pulmonary Langerhans' cell histiocytosis. The disease was limited to the lung, since further investigations did not show any other localization. The patient had a good clinical outcome with avoidance of smoking and steroid therapy. The computed tomography scan follow-up showed a partial resolution of pulmonary lesions.
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PMID:Favourable outcome of a case of pulmonary Langerhans' cell histiocytosis. 1078 15

Lymphangioleiomyomatosis (LAM) is a progressive and usually fatal interstitial lung disease characterized by an abnormal smooth-muscle proliferation in the lung and axial lymphatics. It affects almost exclusively young women of childbearing age. The presenting features most commonly include dyspnea, symptoms of pneumothorax and cough. Less commonly patients can present with chest pain, pleural or pericardial effusion and lymphedema. Our patient, a 41-year-old woman, complained mainly of fatigue that had lasted for 2 months and finally became febrile and dispneic, especially when lying down. Pulmonary diagnostic procedures revealed several multicystic destruction of lung parenchyma. There was also respiratory insufficiency with O2 saturation of 87% and lung diffusion capacity reduced to 48%. The retroperitoneum was filled with neoplastic mass as shown on an abdominal CT scan. Pathohistologic analysis of retroperitoneal mass together with the radiologic finding of the lungs correlated with the diagnosis of LAM. The patient was prescribed corticosteroid therapy, which led to rapid clinical improvement. After making a definite diagnosis, the patient was recommended further treatment with medroxyprogesterone. This case shows that LAM, although rare, can present a diagnostic problem to clinicians and should always be considered as one of the diagnostic possibilities in young women with nonspecific pulmonary symptoms.
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PMID:[Lymphangioleiomyomatosis]. 1550 89

Pulmonary hypertension (PH) is a serious form of pulmonary complication that occurs less frequently in lupus than in other connective tissue diseases like scleroderma; however, it is likely that it is under-recognized in lupus. The symptoms of PH in lupus are non-specific (dyspnea, fatigue, impaired exercise tolerance) and can also be caused by other factors such as pleural or pericardial effusions, interstitial lung disease and many more, making it possible to miss the diagnosis. There are several potential causes of PH in lupus including thromboembolic disease, pulmonary vasculitis, and hypoxia and fibrosis from interstitial lung disease. Endothelin-1 is elevated in lupus and may be associated with PAH. In some studies, pulmonary arterial hypertension (PAH) has been found to be a major cause of mortality in lupus patients. Echocardiograms are a screening tool, but may yield false positives, and a right heart catheterization must be performed to confirm PAH. Early identification is important and can alter the natural history of this dangerous complication of lupus. Treatment of PAH associated with lupus includes standard PAH treatment as well as immunosuppression.
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PMID:An update in pulmonary hypertension in systemic lupus erythematosus - do we need to know about it? 1907 76


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