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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium-channel antagonists may provide an effective approach to the treatment of pulmonary hypertensive disorders. Biochemical evidence suggests that pulmonary vasoconstriction results from the transmembrane flux of calcium into vascular smooth muscle; accordingly, the pulmonary pressor responses in experimental hypoxic pulmonary hypertension can be attenuated by verapamil and nifedipine. In patients with chronic obstructive lung disease, nifedipine decreases pulmonary artery pressures and pulmonary vascular resistance in proportion to the severity of hypoxemia before treatment. However, little pulmonary vasodilator effect is seen when hypoxemia is corrected by inhalation of oxygen, and systemic arterial oxygen desaturation can occur after nifedipine in patients breathing room air; most importantly, long-term studies in patients with chronic lung disease are lacking. In selected patients with primary pulmonary hypertension and other obliterative diseases of the pulmonary vasculature, nifedipine produces short- and long-term hemodynamic improvement at rest and during exercise, and these benefits are frequently paralleled by amelioration of dyspnea and fatigue. However, in patients in whom right ventricular function has been severely compromised by chronic pressure overload, both verapamil and nifedipine may exert notable depressant effects on right ventricular performance, despite the decrease in right ventricular afterload that would be expected to accompany a decrease in pulmonary vascular resistance. These negative inotropic actions may result in serious deleterious clinical reactions. Although calcium-channel antagonists represent a promising approach to the management of patients with pulmonary hypertension, the long-term efficacy and safety of these drugs in this disorder remain to be established.
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PMID:Therapeutic application of calcium-channel antagonists for pulmonary hypertension. 388 14

Sleep and sleep loss have remarkable effects on breathing. Although sleep causes ventilatory disturbances of greater severity and variety than does sleep deprivation, the effects of sleep and sleep loss on respiration are similar. For example, both impair ventilatory drive and arousal responses to a variety of stimuli. Although the mechanism of impaired ventilation after sleep loss is not entirely understood, there is evidence to suggest that both respiratory muscle fatigue and central nervous system depression play a role. Patients who suffer from both disturbed sleep and lung disease are particularly vulnerable to the adverse effects of sleep disruption on breathing. Since sleep restoration returns many respiratory parameters to normal in sleep-deprived individuals, perhaps we should include rest in our treatment of certain patients with respiratory disease.
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PMID:Sleep, sleep loss, and breathing. 390 14

To test the relative merits of administering questionnaires with previous responses available (the informed condition) or unavailable (the blind condition), we administered blind and informed versions of a quality of life questionnaire to two groups of patients. One, a group of 43 stable subjects with chronic cardiorespiratory disease, were seen three times at fortnightly intervals; a separate series of 13 patients with chronic lung disease were evaluated before and after optimization of therapy. In the stable patients the informed strategy resulted in substantial decrease in the variance in the measurement of dyspnea, fatigue, and of emotional function. Large improvements in dyspnea, fatigue, and emotional function seen in patients undergoing treatment optimization were comparable using blind and informed methods. These results suggest that by letting patients see their previous responses we can decrease the sample size needed to detect changes in quality of life in clinical trials.
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PMID:Should study subjects see their previous responses? 406 88

The diseases which are commonly complicated by hypercapnic respiratory failure also compromise the respiratory muscles in several ways. Increased work of breathing, mechanical disadvantage, neuromuscular disease, impaired nutritional status, shock, hypoxemia, acidosis, and deficiency of potassium, magnesium, and inorganic phosphorus are the major non-neurologic factors which contribute to respiratory muscle fatigue and failure. Respiratory muscle fatigue has two components. High frequency fatigue occurs rapidly with intense contractile efforts but is usually not severe. It also recovers rapidly with rest. Low frequency fatigue develops more slowly but is severe and requires hours for recovery. Since the spontaneous rate of neural stimulation is predominantly in the low frequency range, this component of fatigue is of particular clinical importance. Fatigue of the inspiratory muscles leads to acute respiratory acidosis, but before carbon dioxide retention occurs, it can be recognized from characteristic symptoms and signs. These include dyspnea which responds to mechanical ventilation, rapid shallow breathing, and asynchronous movements of the chest and abdomen. Inspiratory muscle fatigue must be treated by putting these muscles to rest, by mechanically supporting ventilation. In addition, underlying metabolic nutritional and circulatory abnormalities must be corrected and infection treated. Aminophylline and isoproterenol can restore inspiratory muscle contractility, but controlled clinical trials remain to be done regarding their application in acute and chronic respiratory failure. Inspiratory muscle training improves strength and endurance in patients with obstructive lung disease, cystic fibrosis, and spinal cord injury, but does not always improve physical exercise performance. Again, more work is needed to develop the indications for inspiratory muscle training and to determine the optimum type and duration of the training regimen.
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PMID:Respiratory muscle failure. 634 27

PH is an uncommon manifestation of SLE. The symptoms of PH develop within a few years after the onset of the multisystem disease. The most common presenting complaints of SLE patients with PH are dyspnea on exertion, chest pain, nonproductive cough, edema, and fatigue or weakness. The important physical findings are a loud second pulmonic heart sound and a right ventricular lift. The chest roentgenogram shows a cardiomegaly, a prominent pulmonary segment, and usually clear lung fields. Pulmonary function tests may show evidence of restrictive lung disease; however, the physiologic abnormalities are mild and out of proportion to the severity of the PH. The diagnosis of PH is established by cardiac catheterization showing elevated pulmonary artery pressure, normal capillary wedge pressure, and no evidence of intracardiac or extracardiac shunts. Pathologic examination of the lung demonstrates angiomatoid lesions involving muscular pulmonary arteries. There is a thickening of the media and subintima of the arterioles. Immunoglobulin and complement deposits are found in the walls of pulmonary arteries. Immunoglobulin eluted from the lung contains rheumatoid factor and antinuclear antibody including antibody to DNA activity. DNA antigen is also present in walls of blood vessels. These results suggest an immune complex deposition process as a mechanism in the pathogenesis of PH in SLE. The clinical course of PH in SLE is variable. Symptoms may be mild and the disease follows a stable and protracted course for several years. It can, however, develop a progressive course ending in death in a few years. The clinical response of SLE patients with PH to treatment with high doses of systemic corticosteroids is not consistent or predictable.
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PMID:Immunopathologic and clinical studies in pulmonary hypertension associated with systemic lupus erythematosus. 637

To evaluate the effect of breathing 50 ppm carbon monoxide (CO) on exercise capacity in persons with anemia, 10 nonsmoking subjects with chronic anemia (mean hemoglobin 8.9 g%) were studied. No subject had heart or lung disease. By double-blind, randomized, crossover design, duration of fatigue-limited exercise after breathing CO and purified air for 1 hr was compared. Mean carboxyhemoglobin levels increased from 2.14 to 3.38% after breathing CO and decreased from 2.15 to 1.86% after breathing purified air, P less than 0.004. Mean exercise duration decreased from 270.8 to 221.0 sec after breathing CO in contrast to an increase from 267.9 to 271.6 sec after breathing purified air, P less than 0.0001. Hence, in the absence of clinical heart or lung disease, increasing carboxyhemoglobin concentrations aggravate exercise performance in nonsmokers with chronic anemia.
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PMID:Aggravation of exercise performance in patients with anemia by 3% carboxyhemoglobin. 651 Mar 89

Total lymphoid irradiation (TLI) was administered to 11 patients who had intractable rheumatoid arthritis that was unresponsive to conventional medical therapy, including aspirin, multiple nonsteroidal antiinflammatory drugs, gold salts, and D-penicillamine. Total lymphoid irradiation was given as an alternative to cytotoxic drugs such as azathioprine and cyclophosphamide. After radiotherapy, 9 of the 11 patients showed a marked improvement in clinical disease activity as measured by morning stiffness, joint tenderness, joint swelling, and overall functional abilities. The mean improvement of disease activity in all patients ranged from 40-70 percent and has persisted throughout a 13-28 month followup period. This improvement permitted the mean daily steroid dose to be reduced by 54%. Complications included severe fatigue and other constitutional symptoms during radiotherapy, development of Felty's syndrome in 1 patient, and an exacerbation of rheumatoid lung disease in another. After therapy, all patients exhibited a profound T lymphocytopenia, and a reversal in their T suppressor/cytotoxic cell to helper cell ratio. The proliferative responses of peripheral blood mononuclear cells to phytohemagglutinin, concanavalin A, and allogeneic leukocytes (mixed leukocyte reaction) were markedly reduced, as was in vitro immunoglobulin synthesis after stimulation with pokeweed mitogen. Alterations in T cell numbers and function persisted during the entire followup period, except that the mixed leukocyte reaction showed a tendency to return to normal values.
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PMID:Sustained improvement of intractable rheumatoid arthritis after total lymphoid irradiation. 688 88

Ventilation depends on the proper functioning of the respiratory muscles. These muscles, like other skeletal muscles, can endure high work loads for only short time periods. The work of breathing in patients with lung disease in increased and it has therefore been argued that respiratory muscle fatigue may develop and contribute to respiratory failure. We have studied the contractile function and fatigue of the sternomastoid muscle and the diaphragm in normal subjects and found that these respiratory muscles have the same contractile properties as limb muscles. If subjected to a high load they develop similar patterns of fatigue. Studies on the sternomastoid muscle in patients with lung disease also confirmed that respiratory stress produces fatigue.
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PMID:Contractile function and fatigue of the respiratory muscles in man. 691 71

We studied the pressure developed by the diaphragm in response to stimulation of the phrenic nerve in the neck, in three normal men. When the phrenic was electrically stimulated at increasing frequencies the diaphragm responded by increasing transdiaphragmatic pressure to give a frequency-pressure curve similar to the frequency-force curve for other skeletal muscles. The subjects than breathed through an inspiratory resistance for as long as possible and the frequency-pressure curve was repeated. It was found that the diaphragm developed low frequency fatigue, in the same way as previously described for other muscles. We conclude that the diaphragm has contractile properties similar to these of other skeletal muscles. Low frequency fatigue of the diaphragm could contribute to respiratory failure in patients with lung disease.
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PMID:Contractile properties and fatigue of the diaphragm in man. 728 Oct 80

This article presents a brief overview of respiratory muscle mechanics and the effects of lung disease and neuromuscular disease on pulmonary function. A variety of current specific and general muscle training techniques are described and discussed. Also presented is a current review of training studies and the effects of muscle training on cardiopulmonary function, muscle strength, endurance and fatigue, and exercise tolerance.
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PMID:Respiratory muscle function, assessment, and training. 731 44


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