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

The maximal inspiratory pressure (MIP) and the sustainable inspiratory maximal pressure (SIPm) in 79 patients with chronic obstructive pulmonary disease (COPD) which were divided into the mild group (MG) and the mid-severe group (MSG) were measured. The results showed that MIP and SIPm were significantly lower in MSG than the prediction and in MG, the inspiratory fatigue in MSG was taken place in lower load and shorter time. We considered: MIP and SIPm fallen significantly in COPD patients might play a very important role in developing patients' respiratory failure.
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PMID:[Inspiratory muscle strength and endurance in patients with chronic obstructive pulmonary disease]. 187 24

The purpose of this study was to evaluate the usefulness of ratings of perceived exertion (RPE) as an indicator of exercise intensity in patients with chronic obstructive pulmonary disease (COPD). The subjects were ten male patients with COPD, whose mean forced expiratory volume in 1 s was 1.09 1, SD 0.41, and ten healthy middle-aged men. Ramp incremental exercise on a cycle-ergometer was performed and RPE was determined by the Borg 15-point scale. The absolute oxygen uptake at each RPE was significantly greater in the healthy subjects than in the patients with COPD. However, oxygen uptake calculated as a percentage of maximal at any RPE did not differ significantly between the two groups. Arterial blood lactate concentration at points 15 to 19 on the RPE scale was increased in healthy subjects (P less than 0.05-P less than 0.001), while the dyspnoea index at points 11 to 19 on the RPE scale was higher in patients with COPD (P less than 0.05-P less than 0.001). The main complaints on stopping exercise were dyspnoea in the patients with COPD and fatigue in the healthy subjects. Although the nature of RPE may have been different in the two groups, RPE could be a possible indicator of exercise intensity when physicians prescribe exercise to patients with COPD.
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PMID:Ratings of perceived exertion in chronic obstructive pulmonary disease--a possible indicator for exercise training in patients with this disease. 189

A prospective evaluation of the prevalence of CO2 retention and its relationship to lung mechanics and inspiratory muscle strength was carried out in 311 clinically stable patients with chronic obstructive pulmonary disease (COPD). Of these patients 32.8% had hypercapnia (PaCO2 greater than or equal to 43 mm Hg). PaCO2 was directly related to lung resistance (RL; r = 0.53) and inversely related to FEV1 (r = 0.53) and to an expression of the dead space/tidal volume ratio (1 - VD/VT) (r = 0.48). RL was found to be a major determinant of the mean intrathoracic pressure swing developed during inspiration (PI) at rest (r = 0.85). Maximal inspiratory pressure (PImax) was found to improve the predictive value for PaCO2 of several mechanical loads, with RL/PImax the best predictor (r = 0.57). The prevalence of hypercapnia increased from virtually 0 to 100% with increases in the RL/PImax value and was higher in the obese subjects at intermediate RL/PImax values, probably because of the burden placed on the respiratory muscles by chest wall mass loading. Our results show that chronic alveolar hypoventilation is likely to develop in COPD patients who have a combination of high inspiratory loads and inspiratory muscle weakness. hypercapnia may be one strategy available to avoid overloading of the inspiratory muscles leading to fatigue and possible irreversible failure.
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PMID:Inspiratory muscle dysfunction and chronic hypercapnia in chronic obstructive pulmonary disease. 202 40

Patients with chronic respiratory insufficiency due to severe chronic obstructive pulmonary disease (COPD) and presumed respiratory muscle fatigue may benefit from therapeutic maneuvers aimed at reducing the magnitude of inspiratory muscle effort. Recent work has demonstrated that continuous positive airway pressure (CPAP) can significantly reduce inspiratory effort and work of breathing in COPD patients with acute respiratory failure. Accordingly it was reasoned that prolonged CPAP administration may similarly reduce the work of breathing in stable COPD patients with chronic respiratory insufficiency, thereby allowing recovery from respiratory muscle fatigue. The purpose of this study was to determine the feasibility of employing nasal CPAP during sleep as a means of implementing this approach to reducing inspiratory muscle effort in such patients. Standard polysomnographic parameters were recorded during nocturnal administration of nasal CPAP in eight stable patients with severe COPD (FEV1 = 26.7 +/- 3.9% of predicted). Esophageal pressure, diaphragmatic (EMGdi) and parasternal intercostal (EMGic) electromyographic activity, arterial oxyhemoglobin saturation (SaO2), and transcutaneous PCO2 (PtcCO2) were also measured. Breathing pattern was determined by respiratory inductive plethysmography. In each patient an optimum level of nasal CPAP could be determined that produced consistent reductions in indices of inspiratory muscle effort without changing tidal volume or breathing frequency. Highly significant reductions in the tidal excursions of esophageal pressure and the pressure-time integral for the inspiratory muscles occurred at the optimum CPAP level in all patients. EMGdi and EMGic were similarly reduced. SaO2 and PtcCO2 were unaffected by CPAP. These results indicate that nasal CPAP can effectively reduce inspiratory muscle effort during sleep in patients with severe COPD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nasal continuous positive airway pressure facilitates respiratory muscle function during sleep in severe chronic obstructive pulmonary disease. 202 45

Inspiratory muscle fatigue has been documented during loaded breathing or acute respiratory failure, but its role in exercise limitation is still undetermined. Electromyographic (EMG) signs of diaphragmatic fatigue develop in normal subjects hyperventilating above 70% of maximal voluntary ventilation (MVV), a ventilatory level commonly attained at peak exercise. EMG signs of diaphragmatic fatigue also occur during high power cycling exercise in normal subjects and chronic obstructive pulmonary disease (COPD) patients. However, a loss of respiratory muscle strength has rarely been documented following strenuous physical exercise with techniques independent of the subjects' collaboration. Prior inspiratory muscle fatigue decreases exercise tolerance in normal subjects but its effect is largely unknown in COPD patients. Respiratory muscle rest by negative pressure ventilation was reported to improve exercise tolerance in COPD, but this beneficial effect was not confirmed by controlled studies. The effect of inspiratory muscle training on exercise tolerance is still undefined by existing data, in part because of differences in methods and selection criteria between studies. Although respiratory muscle fatigue may occur during exercise, it is not clearly established whether interventions directed at respiratory muscles may improve exercise tolerance in COPD.
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PMID:Respiratory muscle fatigue limiting physical exercise? 202 29

The percentage of the patients with PaCO2 more than 60 Torr and PaO2 more than 50 Torr were 13% in the patients with tuberculosis sequela (N = 502) and 4% in the patients with chronic obstructive lung disease (COLD, N = 727), who were treated with home oxygen therapy in the western region of Japan. Patients with chronic respiratory failure caused by tuberculosis sequela have higher PaCO2 than patients with COLD. Although the prognosis of patients with hypercapnia and moderate hypoxemia is not necessarily poor, some patients may need treatment for severe hypoventilation to prevent respiratory muscle fatigue and abnormal breathing during sleep. In this study, nine patients with hypercapnic chronic respiratory failure caused by tuberculosis sequela were ventilated by Chest Negative Pressure Ventilation (CNPV). The patients were monitored as in polysomnography by transcutaneous PCO2 (PtcCO2) electrode and Respiratory Inductance Plethysmography (RIP). Tidal volume induced by CNPV was larger during mouth breathing (504 +/- 128 ml, mean +/- s.d.) than during nose breathing (438 +/- 109 ml) calculated from RIP in awake state (N = 7). Oxygen saturation measured by ear oximeter and PtcCO2 were 94.4 +/- 2.9% and 57.8 +/- 12.2 Torr in awake state. Following CNPV SaO2 and PtcCO2 were 95.7 +/- 3.0%, 42.7 +/- 12.1 Torr in awake state (N = 9) and 93.0 +/- 4.4%, 57.0 +/- 15.7 Torr in Non-REM sleep (N = 5), respectively. CNPV is effective in these patients in awake state. During Non-REM sleep, CNPV maintains the PtcCO2 level only in awake state.
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PMID:[Tuberculosis sequelae: pathophysiological aspect (ventilation)]. 207 61

In order to evaluate the hemodynamic effects of INPV, eight patients with COPD (FEV1/FVC, 54 +/- 6 percent; mean +/- SD), respiratory failure (PaO2, 52 +/- 6 mm Hg; PaCO2, 56 +/- 4 mm Hg), and clinical signs of inspiratory muscle fatigue underwent right cardiac catheterization while performing 20 minutes of INPV by a cuirass ventilator at a pressure (-20 to -40 cm H2O) able to reduce the diaphragmatic electromyographic activity. Patients showed a mild basal pulmonary artery hypertension. During INPV, no changes in the mean values of HR (from 79 +/- 20 to 80 +/- 18 beats per minute), systolic BP (141 +/- 19 to 139 +/- 16 mm Hg), CO (5.2 +/- 0.8 to 5.1 +/- 1.3 L/min), mean PAP (23.8 +/- 3.8 to 23.9 +/- 4.4 mm Hg), RAP (4.3 +/- 2.6 to 5.5 +/- 2.5 mm Hg), PWP (10.3 +/- 4.5 to 9.4 +/- 2.9 mm Hg), TPR (369 +/- 76 to 392 +/- 124 dynes.s.cm-5), and PVR (199 +/- 51 to 233 +/- 94 dynes.s.cm-5) were observed. Direct systemic BP monitoring could be performed in six patients. During INPV, three patients showed "pulsus paradoxus," as assessed by an inspiratory fall in systolic BP of 11, 13, and 20 mm Hg, respectively. We conclude that INPV by cuirass ventilator does not induce adverse hemodynamic effects in patients with COPD who have pulmonary artery hypertension.
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PMID:Hemodynamic effects of negative-pressure ventilation in patients with COPD. 218 97

In COLD, the inspiratory muscles are severely disadvantaged by virtue of the hyperinflation that accompanies this disorder. Such mechanical disadvantage will lead clinically, in the stable patient, to the active recruitment of the accessory muscles of inspiration and to a pattern of rapid, shallow breathing that may be due to either peripheral (muscle) or central (neurogenic) influences thought to be linked to a critical tension-time index of the inspiratory muscles. This pattern appears to be all the more pronounced in the patient with acute respiratory failure and is frequently accompanied by disordered rib cage-abdominal movements. While these movements may reflect the muscles' attempts to stave off fatigue, they may also imply that if the imposed mechanical stress is unrelieved, muscle failure will ensue. In the laboratory, mechanical disadvantage is marked by diminished inspiratory mouth pressures. Because of wide scatter, a low mouth pressure beyond that which can be explained by hyperinflation alone should be confirmed by an assessment of Pesosniff or by the measurement of transdiaphragmatic pressure. Muscle endurance, also compromised in this condition, can be assessed indirectly by the measurement of MVV or MSVC, or more directly by an invasive assessment of the tension-time index and endurance time of the diaphragm or noninvasively by the Endurance Index of McKenzie and Gandevia. And finally, once muscle failure is pending or has been established, a program of muscle rest, either complete or partial, pharmacotherapy, and goal-specific training should be instituted.
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PMID:Assessment of respiratory muscle dysfunction in chronic obstructive lung disease. 218 36

In 15 spontaneously breathing patients with chronic obstructive pulmonary disease (COPD) divided into two groups, one with normocapnia (A) and one with chronic hypercapnia (B), we evaluated the maximal voluntary inspiratory muscle strength (MIP), the pattern of breathing, the mouth occlusion pressure (Po.1), the neural respiratory drive (NRD), assessed by surface electromyographic (EMG) activity of the diaphragm (EMGd) and EMG activity of intercostal muscles (EMGint), and the chest wall neuromuscular coupling, assessed in terms of Po.1/EMGd ratio. Compared with an age-matched normal control group, both A and B groups exhibited lower MIP, significantly greater EMGd and EMGint, and lower Po.1/EMGd ratio. However, a similar pattern, along with a rapid and shallow breathing, differentiated group B from group A. In group B we found a significant direct relationship between Po.1/EMGd ratio and MIP, and an inverse relationship between PaCO2 and Po.1/EMGd ratio. These data seem to indicate the following: (1) EMG is a more precise method than Po.1 in assessing the magnitude of the NRD; (2) NRD is increased in these patients; and (3) clinical manifestations probably associated with inspiratory muscle fatigue (marked decrease in muscle strength, rapid and shallow breathing, and alveolar hypoventilation) may be accompanied by a greater NRD and a more marked derangement in chest wall neuromuscular coupling in COPD.
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PMID:Neural respiratory drive and neuromuscular coupling in patients with chronic obstructive pulmonary disease (COPD). 222 64

Patient with severe chronic obstructive pulmonary disease (COPD) can develop respiratory muscle weakness and fatigue. Arterial hypoxemia can predispose to this condition. To assess whether O2 administration improved respiratory muscle function and respiratory pattern in COPD 11 patients with chronic hypoxemia were examined. Each patient was first submitted to respiratory function studies, including lung volumes, in normal and recumbent position, respiratory frequency, Ti/Te, Ti/Tot, maximal inspiratory and expiratory pressures (Pimax, Pemax) and arterial gas analysis breathing room air. All these tests were repeated during oxygen Administration through a nasal cannula. The arterial PO2 improved from 50 +/- 7 mmHg to 81 +/- 28 mmHg but the breathing pattern, Pimax and Pemax as well as lung volumes remained unchanged. It is concluded that oxygen, in short term administration, doesn't influence respiratory pattern and muscle function.
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PMID:Respiratory function during oxygen administration in chronic obstructive pulmonary disease. 226 98


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