Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with severe COPD may be in a state of ventilatory muscle (VM) fatigue. In these patients, rapid and shallow breathing has been hypothesized to be a compensatory mechanism that prevents more severe fatigue from taking place. To test these hypotheses, we studied the effects of VM resting in a group of patients with severe COPD. Eleven clinically stable patients with COPD and chronic hypercapnia were studied. Six of them (group A) had a seven-day period of negative pressure-assisted ventilation (NPV), and five (group B) with similar functional characteristics served as a control group. Compared with a normal age-matched control group, both A and B groups exhibited significantly lower tidal volume (VT), inspiratory time (TI), total time of the respiratory cycle (Ttot) and Ti/Ttot ratio, decrease in muscle strength, and greater electromyographic activity of diaphragm (EMGd) and parasternal muscles, but similar ventilation and VT/TI. After the study period, group A exhibited significant increase in VT, Ti, and TI/Ttot (p less than 0.05), and decrease in PaCO2 (p less than 0.05), EMGd, and EMGint (p less than 0.05 for both), and a slight but significant increase in maximal inspiratory pressure (MIP) (p less than 0.05). These data suggest that NPV rests VM, increases their strength, and reduces hypercapnia in patients with severe COPD.
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PMID:Changes in ventilatory muscle function with negative pressure ventilation in patients with severe COPD. 229 58

Nine subjects with severe chronic obstructive pulmonary disease (COPD) in acute respiratory failure (ARF) and with marked weakness of the respiratory muscles (Group A) underwent intermittent negative pressure ventilation by means of an iron lung (8 h daily for 7 days). Seven subjects with COPD in stabilized chronic respiratory failure (Group B) were studied as controls and submitted to the same medical therapy without ventilator treatment. Functional respiratory tests were performed before and after 7 days of treatment. After ventilatory treatment, Group A showed an increase of maximum inspiratory pressure (PImax), maximum expiratory pressure (PEmax), vital capacity (VC), arterial oxygen tension (PaO2), pH and a decrease of residual volume (RV), total lung capacity of (TLC) and arterial carbon dioxide tension (PaCO2) (all statistically significant). No improvement was ascertained in the functional parameters of Group B. The expiratory muscles seem to play a determining role in ARF. We conclude that the iron lung is a useful therapeutic defence in removing muscular fatigue and in restoring a good level of respiratory compensation of ARF in severe COPD.
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PMID:Respiratory muscle insufficiency in acute respiratory failure of subjects with severe COPD: treatment with intermittent negative pressure ventilation. 237 75

Theophylline improves diaphragmatic contractility of the respiratory muscles both in isolated muscle preparations, as well as in animals and normal human beings. Furthermore, theophylline restores diaphragmatic fatigue and prevents fatigue of the diaphragm when given prophylactically. Finally, it was recently shown that theophylline improves diaphragmatic function in COPD patients, all of whom were CO2 retainers (PaCO2 53 +/- 3 mm Hg) and hypoxemic (PaO2 57 +/- 8 mm Hg). Patients improved transdiaphragmatic pressure and were less susceptible to fatigue. Presently the mechanisms of action of theophylline regarding its effects on diaphragmatic function are not fully elucidated. Experimental evidence, however, suggests that theophylline may have an effect on transmembrane calcium movements by blocking adenosine receptors.
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PMID:Effect of theophylline on respiratory muscle function. 241 Feb 4

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

Hypophosphatemia has been recently highlighted as a reversible cause of respiratory muscle hypocontractility and reduced tissue oxygen extraction in patients with chronic obstructive lung disease and asthma. To define the prevalence and mechanism of hypophosphatemia under these circumstances, we studied phosphate homeostasis in 22 patients with chronic asthma, who had been hospitalized for emergency bronchodilator therapy. Serum phosphate concentration was normal in all patients on presentation, and fell after the initiation of bronchodilator therapy. Twelve patients (54%) developed hypophosphatemia (serum phosphate, less than 0.8 mmol/L). Urinary phosphate level fell in parallel. A negative correlation was observed between serum phosphate and serum theophylline concentrations, and a positive correlation between serum and urinary phosphate concentrations. No correlation was found between serum phosphate and serum albumin or urea concentration. These data indicate that hypophosphatemia is a common metabolic abnormality during the emergency treatment of asthma. The underlying mechanism appears to be drug-induced phosphate flux from the extra-cellular to the intracellular space. We suggest that the serum phosphate level be monitored in patients undergoing emergency treatment of bronchospasm, particularly if a prolonged period of bronchodilator therapy is required or if respiratory muscle fatigue supervenes.
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PMID:Hypophosphatemia complicating bronchodilator therapy for acute severe asthma. 280 3

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

The effect of a sustained-release aminophylline preparation on diaphragmatic contractility was investigated in patients with stable chronic obstructive lung disease (FEV1 = 22.6% of predicted value). Ten such patients were tested before (control) and after a week's course of oral aminophylline. Diaphragmatic contractility was evaluated by measuring the transdiaphragmatic pressure generated at residual functional capacity by bilateral electrical stimulation of the phrenic nerves. The nerves were stimulated supramaximally at 1 Hz, using needle electrodes. Plasma aminophylline levels (12.5 +/- 0.9 mg/l) were within therapeutic range in all patients. After treatment with aminophylline, for each stimulation the transdiaphragmatic pressure increased significantly from 14 +/- 1.3 to 17 +/- 1.3 cm H2O (+21%; P less than 0.005). These results confirm that aminophylline increases the force of contraction of the diaphragmatic fibres electively tested by the technique used. Long-term treatment with theophylline in therapeutic doses may be of interest in such patients, as it might improve their diaphragmatic contractility and result in better control of both respiratory muscle fatigue and episodes of acute respiratory failure.
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PMID:[Action of aminophylline on the strength of contraction of the diaphragm in patients with chronic obstructive respiratory insufficiency]. 295 24

The reduced respiratory muscle strength and increased work of breathing in patients with severe chronic obstructive pulmonary disease (COPD) may predispose these patients to the development of respiratory muscle fatigue and consequent respiratory failure. To test the hypothesis that these patients may be experiencing chronic respiratory muscle fatigue, we studied the effects of resting the respiratory muscles in a group of patients with severe COPD. Fifteen stable patients with severe COPD were randomized into study and control groups. In 8 study group patients (Group B), breathing was assisted with a negative pressure ventilator 3 to 6 h daily for 3 consecutive days. The remaining 7 patients served as controls (Group A) and did not receive any intervention. Baseline lung function was evaluated by spirometry and arterial blood gas determinations. Respiratory muscle strength and endurance were evaluated by maximal inspiratory and expiratory pressures (MIP and MEP, respectively) and the maximal duration that isocapnic hyperventilation equal to 50 and 70% of the 12-s maximal voluntary ventilation could be sustained (DSV). Baseline DSV was determined as the best effort of several practice trials. All measurements were repeated on the final day of assisted ventilation approximately 2 to 3 h after its discontinuation. After assisted ventilation, the DSV at 50 and 70% of the maximal voluntary ventilation improved significantly (p less than 0.05). Maximal inspiratory pressure and MEP increased to 114% (p less than 0.05) and 112% (p = 0.05) of baseline values, respectively. Mean arterial PCO2 in the hypercapnic subgroup of Group B patients decreased from 60 mm Hg before to 52 mm Hg after assisted ventilation (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of intermittent negative pressure ventilation on respiratory muscle function in patients with severe chronic obstructive pulmonary disease. 310 44


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