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

Haemodynamic studies at rest and during exercise together with radionuclide ventriculography, pulmonary function and clinical well-being assessment were evaluated in ten patients with COPD and secondary pulmonary hypertension (mean PAP 25 mm Hg), before and after 6 months therapy with pirbuterol 20 mg thrice daily. Despite the continued pharmacological action of pirbuterol on the heart and systemic circulation during peak pirbuterol levels at 6 months, no significant effect on the pulmonary circulation was observed. Seven patients reported an improvement in the level of fatigue, the partial pressure of carbon dioxide fell significantly (6.5 +/- 0.9 to 6.1 +/- 0.9 kPa: P less than 0.01) and there was a slight bronchodilator effect [forced expiratory volume in 1s (FEV1) 0.60 +/- 0.18 to 0.71 +/- 0.2 1s-1: P less than 0.02] after 6 months. The drug was generally well tolerated but three patients with pre-existing biliary tract disease developed obstructive jaundice.
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PMID:Long term haemodynamic, pulmonary function and symptomatic effects of pirbuterol in COPD. 251 10

High frequency ventilation (HFV) may be achieved by external oscillation (external HFV) applied around the chest wall (HFCWO) in large animals and humans, or over the entire body (HFBSO) in small animals, instead of being applied via the trachea (internal HFV). We present a synthesis of the results obtained with external HFV in both normal and bronchoconstricted subjects. Whereas external and internal HFV were found to be equivalent in terms of gas exchange in normal rats, external HFV was found to have a beneficial effect in bronchoconstricted rabbits, but internal HFV did not. From the frequency-oscillatory tidal volume relationship determined in normocapnic rabbits, HFBSO at 5 Hz was found to be the optimal frequency at which to ventilate with tidal volumes close to the dead space volume, and which was also shown to be the optimal volume to obtain normocapnia. Moreover, 5 Hz oscillations (HFCWO) at 20 ml and 40 ml superimposed on tidal breathing accelerated nitrogen washout, i.e., gas exchange in normal humans. Unfortunately, only oscillations with much smaller volumes (5-10 ml) were obtainable in COPD patients. Nevertheless, they produced a clear change in breathing pattern associated with a slight improvement in gas exchange and a potentially positive effect on inspiratory muscle fatigue. These results support the concept that non-invasive external HFV technique may be of use in assisting ventilation in bronchoconstricted subjects and may possibly replace conventional controlled ventilation, at least in subjects with high lung compliance, such as babies, neonates and normal adults.
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PMID:The ventilatory effect of external oscillation. 264 42

To estimate the effect of the increase in ventilation induced by exercise on the dynamics of respiratory muscle in normal subjects and cases of respiratory diseases, we measured the changes of transdiaphragmatic pressure (Pdi), gastric pressure (Pga), tension time index of the diaphragm (TTdi) and tension time index of the abdomen (TTab). To confirm the effect of oxygen on exercise endurance, we investigated changes of parameters measured during exercise under air breathing and oxygen inhalation. In normal subjects, we found the increase in diaphragmatic activity as a gradual increase of exercise level, but TTdi always stayed in the non-fatigue zone. On the contrary, patients with COPD showed that TTdi was near fatigue threshold during quiet breathing and crossed easily into fatigue zone during exercise. There was an increase in endurance time with oxygen for COPD patients. Breathing with oxygen was associated with a smooth increase in Pdi during the inspiratory phase which indicates efficient contraction of the diaphragm. During the expiratory phase, the degree of increase in Pga was markedly reduced by oxygen inhalation.
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PMID:[Respiratory muscle fatigue]. 274 68

Diaphragmatic function test was performed at rest and during maximal incremental exercise in six male normal non-smokers (Group A), sixteen male patients with COPD (58 +/- 8 yrs), including 4 with only small airway disorder (B) 6 with mild (C) and 6 with moderate airway obstruction (D) and eight patients with cor pulmonale complicated severe airway obstruction and chronic respiratory failure (E). Maximal transdiaphragmatic pressure (Pdi max) at rest in Group A, B, C, D, E were 13.6 +/- 2.9 kPa, 10.8 +/- 3.1 kPa, 9.9 +/- 3.4 kPa, 6.8 +/- 3.3 kPa and 5.3 +/- 2.5 kPa respectively, the latter two (D and E) being significantly lower than that of the normal control (D, P less than 0.05, E, P less than 0.01). Breathing pattern of the diaphragm at rest was similar to the normal control in all groups except that half of the patients in Group E (4/8) showed diaphragmatic paradoxical motion during inspiration. Ergometer test with incremental workload was performed in all groups except for Group E. During exercise, patients with COPD revealed some extent of diaphragmatic fatigue. All in group D(6/6) and most in group C(4/6) eventually developed inspiratory paradoxical motion of diaphragm before the ventilatory reserve was exhausted.
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PMID:[Diaphragmatic fatigue and its role in the development of respiratory insufficiency and cor pulmonale in COPD]. 280 47

Described is a 67-year-old man whose initial symptoms evoked an obesity-hypoventilation syndrome. Polysomnography showed hypopneas associated with O2 desaturation episodes, and no apnea; maximal changes were noted during REM sleep. A few months later, in spite of marked weight loss, acute alveolar hypoventilation occurred and necessitated mechanical ventilatory support. Tracheostomy was performed. The patient appeared to be dependent on nocturnal ventilatory assistance. Diaphragmatic paralysis was noted in addition to clinical and electrodiagnostic evidence of amyotrophic lateral sclerosis. While the patient was not ventilated, a nocturnal recording of SaO2 again revealed desaturation episodes partly corrected by O2 2 L/min administered through the tracheostomy tube. With volume-controlled ventilation, desaturations completely disappeared, although no oxygen enrichment of the air was provided. We speculate that sleep disorders with hypopneas and O2 desaturation episodes were the initial symptoms of amyotrophic lateral sclerosis. This leads us to suggest that nonspecific respiratory muscle fatigue frequently seen in COPD might be included in the hypothetic causes of nocturnal hypoxemia.
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PMID:Amyotrophic lateral sclerosis presenting with sleep hypopnea syndrome. 337 Nov 13

The medium-term outcome of weaning from mechanical ventilation in COPD patients is not easy to anticipate because a respiratory fatigue may eventually develop. We evaluated the diaphragmatic function and the breathing pattern during 40 weaning trials on 15 patients ventilated after acute respiratory failure. We formed two groups according to the success (group B, n = 18) or failure (group A, n = 19) of the medium-term attempt (group A/less than 10 hours; group B/more than 12 hours). Provided the patients showed the classic weaning criteria (tidal volume greater than 5 ml/kg, respiratory frequency less than 30 breaths per minute, PaO2 greater than 50 mm Hg), the study of the breathing pattern did not allow differentiation between the groups. However, the transdiaphragmatic pressure (Pdi) and the Pdimax, which gave an indication of the power of diaphragm contraction, dropped early in the group that could not stand weaning, with an increase in the Pdi/Pdimax ratio. In addition, this same group showed a diaphragmatic dysfunction attested for by a frequent negative gastric pressure associated with or shortly preceded by an abdominal paradoxic motion.
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PMID:Diaphragmatic fatigue and breathing pattern during weaning from mechanical ventilation in COPD patients. 376 72

Inspiratory muscle function is impaired in many patients with severe COPD. This functional impairment often leads to hypercapnic respiratory failure via inspiratory muscle fatigue. Factors responsible for this functional impairment are: (1) an excessive mechanical load (high resistance and low compliance) for the inspiratory muscles to overcome; (2) the low, flat configuration of the diaphragm owing to lung hyperinflation; (3) reduced inspiratory muscle blood flow relative to the increased respiratory work requirement; and (4) tachypnea which increases the duty cycle (TI/Ttot) for inspiratory muscles, increases hyperinflation, wastes ventilation, and otherwise causes deterioration of gas exchange. Therapy is directed toward improving inspiratory muscle function and has three strategic goals: (1) to reduce the load imposed on the inspiratory muscles and reduce their mechanical disadvantage; (2) to improve the contractile characteristics of the inspiratory muscles; and (3) if goals 1 and 2 cannot be attained otherwise, to rest the inspiratory muscles using mechanical ventilation. Inspiratory muscle training offers promise as a means of preventing hypercapnic respiratory failure. Available data suggest that some COPD patients benefit from it. To be determined are which patients will benefit from it and which will not, as well as which training regimens are most effective.
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PMID:Therapeutic considerations in respiratory muscle function. 389 24

Acute respiratory failure in chronic obstructive lung disease (COPD) is characterized by abnormal gas exchange and respiratory muscle fatigue; mechanical ventilation would appear to be particularly well suited to the management of COPD patients, because the respirator is a reliable oxygenator and a mechanical power supplier. However, many clinicians are reluctant to prescribe this therapy. The author discusses the indications and practical use of mechanical ventilation in COPD patients. Data are presented which show no correlation between the duration of mechanical ventilation, the age of the patients and pulmonary function tests. During acute respiratory failure, COPD patients require active management in an intensive care unit.
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PMID:[Mechanical ventilation in acute decompensation in chronic obstructive bronchopneumopathy]. 397 86

This article reviews factors that may limit exercise performance in patients with COPD. These factors include alteration in pulmonary mechanics, respiratory muscle fatigue, impairment in pulmonary gas exchange, abnormal perception of breathlessness and ventilatory control, cor pulmonale, and poor nutritional status. The clinical application of exercise testing in patients with COPD and the role of various therapeutic modalities in altering exercise performance in COPD are discussed.
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PMID:Exercise impairment in chronic obstructive pulmonary disease. 672 35

1. Normal respiratory muscles have a large functional reserve. 2. Muscles have a tremendous capacity for adaptation. Adaptation is task-specific (eg, muscles use similar motor units for the same tasks). 3. Muscular fatigue results when motor units are required to perform an unaccustomed task. Continued effort in the face of fatigue, especially high-tension low-repetition effort, may produce a reversible "use atrophy" (eg, fiber damage, splitting, and regeneration). 4. Exercising damaged or regenerating muscle may produce irreversible damage. 5. Exercising the respiratory muscles of some patients may make them more susceptible to fatigue or, at least, produce no further improvement in function. Alternating rest and exercise improves pulmonary function tests in some patients. 6. Retraining a weak or damaged muscle requires that it first be "shut down" and rested before attempting retraining. 7. Training a rested muscle to different tasks--before these tasks are needed--may be the critical step in successful rehabilitation. 8. Resistance breathing probably improves both respiratory muscle strength and respiratory muscle endurance. 9. There are at least three immediate tasks for clinicians to define: Where in the present natural history of COPD should respiratory muscles be rested? How long should they be rested? How best can they be retrained?
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PMID:When should respiratory muscles be exercised? 686 48


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