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

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

Patients with chronic obstructive pulmonary disease (COPD) may incur exercise limitation by any one or combination of disturbances in breathing mechanics, oxygen transport, respiratory muscle metabolism or respiratory regulation and sensation. In spite of the increased ventilation demand/capacity ratio in these patients, the relationship between breathing mechanics, respiratory muscle fatigue, the adequacy of alveolar ventilation and the development of exertional dyspnoea is neither clearly defined nor predictable from data obtained with the patient at rest. The issue of oxygen transport during exercise has been complicated by confusion between arterial hypoxia and inadequate volume of oxygen transported to the tissues, which frequently may differ qualitatively and quantitatively. The cardiac output response to exercise in patients with COPD is therefore critical in determining oxygen transport. This response is also impossible to predict from resting lung mechanics, pulmonary arterial blood pressure, arterial oxygen tension or clinical disease profile. Without exercise testing, which includes measurement of all the variables mentioned, it is impossible to define clearly the cause of exercise-induced symptoms in patients with COPD. Exercise training with and without supplemental oxygen has been shown to improve exercise tolerance in these patients, but the precise mechanism of this improvement remains obscure.
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PMID:Exercise in patients with chronic obstructive pulmonary disease. 388 Sep 31

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

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

Bellemare and Grassino (J. Appl. Physiol. 53: 1196-1206, 1982) have reported that the diphragmatic time-tension index (TTdi) (i.e., the product of mean transdiaphragmatic pressure/maximum transdiaphragmatic pressure and the inspiratory duty cycle) can be used as a predictor of diaphragmatic fatigue in humans. However, the publications of these authors do not directly address the question of whether inspiratory flow or transdiaphragmatic pressure should be used to calculate the inspiratory duty cycle. To gather data on this point, we computed TTdi by both methods in spontaneously breathing normal adult males (AMN) and age-matched males with chronic obstructive pulmonary disease (COPD) at rest and during treadmill exercise. During rest and exercise in both AMN and COPD, the fraction of the breathing cycle over which diaphragmatic tension was maintained (Tdi/TT) exceeded the fraction of the breathing cycle over which inspiratory airflow was maintained (TI/TT). Therefore, TTdi calculations using Tdi/TT were greater (P less than 0.05) than TTdi computations using TI/TT. However, this difference in TTdi values was relatively small (approximately 15%).
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PMID:Critique on application of diaphragmatic time-tension index to spontaneously breathing humans. 395 22

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 purpose of this study was to evaluate whether the previously demonstrated improvement in contractile tension of diaphragmatic muscle with aminophylline results in improved ventilatory endurance. We measured the maximal sustained ventilatory levels during prolonged isocapnic hyperpnea as an index of ventilatory muscle function. This measurement was made in 7 normal subjects and 7 patients with chronic obstructive pulmonary disease during the intravenous administration of saline and aminophylline on 2 separate days. The order of administration of the infusions was randomized. Although both groups showed slightly higher sustained ventilatory levels during aminophylline infusion, the magnitude of change was small and unlikely to have a significant clinical benefit in the setting of respiratory muscle fatigue.
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PMID:Aminophylline and its influence on ventilatory endurance in humans. 397 Apr 54

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

The purpose of this study was to evaluate inspiratory muscle force reserve in children with chronic obstructive pulmonary disease (COPD). In 15 hyperinflated (FRC/TLC, 65 +/- 0.7%) children, maximal mouth inspiratory static pressure (PImax) at FRC, mouth occlusion pressure (P0.1), tidal volume (VT), inspiratory time (TI), and total duration of the respiratory cycle (Ttot) were all measured. It was found that PImax at FRC was reduced compared with predicted values. However, after lung volume correction, PImax was in the normal range, and P0.1 was higher, TI was shorter, and Ti/Ttot was lower than predicted. The estimated mean inspiratory pressure for breathing at rest (PI) was significantly higher than predicted and was related to total pulmonary resistance (r = 0.74, p less than 0.001). The fraction of PImax developed by the respiratory muscles for breathing at rest (PI/PImax) significantly increased. The higher the PI/PImax ratio, the more the TI/Ttot ratio decreased (r = -0.64, p = 0.01). At rest, our subjects had to develop a mean inspiratory power (W) of as much as 48% (range, 30 to 76%) of the critical W above which fatigue occurs. Thus, even minimal increases in breathing load might expose children with COPD to respiratory muscle fatigue and to respiratory failure.
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PMID:Inspiratory force reserve of the respiratory muscles in children with chronic obstructive pulmonary disease. 400 28

The fatigue threshold of the human diaphragm in normal subjects corresponds to a transdiaphragmatic pressure (Pdi)-inspiratory time integral (TTdi) of about 15% of Pdimax. The TTdi of resting ventilation was measured in 20 patients with chronic obstructive pulmonary disease (COPD) and ranged between 1 and 12% of Pdimax (mean 5%). TTdi was significantly related to total airway resistance (Raw) (r = 0.57; P less than 0.05). Five of these patients were asked to voluntarily modify their TI/TT (ratio of inspiratory time to total cycle duration; from 0.33 to 0.49) so as to increase their TTdi from a control value of 8% to an imposed value of 17% of Pdimax. The imposed pattern induced a progressive decline in the high-frequency (150-350 Hz)/low-frequency (20-40 Hz) power ratio (H/L) of the diaphragm electromyogram (fatigue pattern), quantitatively similar to that seen in normal subjects breathing with similar TTdi levels. The decay in H/L was followed by a progressive fall in mean Pdi meanly due to decrease in gastric pressure swings. It is concluded that 1) the force reserve of the diaphragm in COPD patients is decreased because of a decrease in Pdimax; 2) the remaining force reserve of the diaphragm can be exhausted by even minor modifications in the breathing pattern; and 3) at a TI/TT of 0.40 our COPD patients can increase their mean Pdi 3-fold before reaching a fatiguing pattern of breathing compared with 8-fold in normal subjects.
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PMID:Force reserve of the diaphragm in patients with chronic obstructive pulmonary disease. 641 67


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