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

Five children (four boys and one girl) with chronic renal failure (CRF) developed congestive heart failure 0.5 to 11 years after the onset of the disease. Their ages were from 4 to 13 years old. They noticed tachypnea, tachycardia, cough, chest anxiety, general fatigue and their chest X-rays showed cardiomegaly with cardio-thoracic ratio (CTR) of from 55 to 63% and pulmonary congestion. Their echocardiograms showed no cardiomuscular hypertrophy, but the dilatation of left ventricular diastolic diameter (LVDd), and the decreased ejection fraction (EF) were observed. They were treated with water restriction, antihypertensive agents, cardiotonics and dialysis. Their clinical symptoms improved promptly, but their cardiomegary and echocardiographic findings improved gradually. The causes of heart failure in these patients seemed to be due to uremia, fluid overload and hypertension. The echocardiographic examination was useful for the management of the children with CRF in heart failure.
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PMID:[Echocardiographic assessment of cardiac function in the children of chronic renal failure with cardiomegary]. 129 69

Diaphragmatic fatigue (DF) in respiratory distress syndrome (RDS) induced by injection of fat were studied in 7 dogs. After injection of fat, all dogs developed respiratory distress and tachypnea, PaO2 fell to the level lower than 8 kPa. Transdiaphragmatic pressure (Pdi) decreased progressively (P less than 0.05-0.001), Pdi-stimulation frequency (Pdi-F) curve shifted to the right, central frequency (Fc), median frequency (Fm) and high/low frequency ratio (H/L) significantly decreased (P less than 0.05-0.001). It is concluded that the contractile force of the diaphragm progressively decreased after RDS was induced, which suggested the occurrence of DF.
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PMID:[Diaphragmatic fatigue in respiratory distress syndrome in dogs]. 181 79

The purpose of this study was to determine whether induction of inspiratory muscle fatigue might impair subsequent exercise performance. Ten healthy subjects cycled to volitional exhaustion at 90% of their maximal capacity. Oxygen consumption, breathing pattern, and a visual analogue scale for respiratory effort were measured. Exercise was performed on three separate occasions, once immediately after induction of fatigue, whereas the other two episodes served as controls. Fatigue was achieved by having the subjects breathe against an inspiratory threshold load while generating 80% of their predetermined maximal mouth pressure until they could no longer reach the target pressure. After induction of fatigue, exercise time was reduced compared with control, 238 +/- 69 vs. 311 +/- 96 (SD) s (P less than 0.001). During the last minute of exercise, oxygen consumption and heart rate were lower after induction of fatigue than during control, 2,234 +/- 472 vs. 2,533 +/- 548 ml/min (P less than 0.002) and 167 +/- 15 vs. 177 +/- 12 beats/min (P less than 0.002). At exercise isotime, minutes ventilation and the visual analogue scale for respiratory effort were larger after induction of fatigue than during control. In addition, at exercise isotime, relative tachypnea was observed after induction of fatigue. We conclude that induction of inspiratory muscle fatigue can impair subsequent performance of high-intensity exercise and alter the pattern of breathing during such exercise.
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PMID:Effect of respiratory muscle fatigue on subsequent exercise performance. 186 88

We describe the clinical characteristics and actuarial survival of a consecutive cohort of 41 patients with rheumatoid arthritis and clinical pericarditis who were seen at the Mayo Clinic between 1970 and 1987 and followed up until death or through 1987. The survivors were followed up for a median of 5.1 years. Approximately three-fourths of our patients had acute pericarditis, the remainder having recurrent acute pericarditis, chronic pericarditis with effusion, or chronic constrictive pericarditis. Most patients had symmetrical joint swelling, morning stiffness, subcutaneous nodules, rheumatoid factor, and classic radiographic changes of rheumatoid arthritis. Common extra-articular features included fatigue, loss of weight, and fever. Dyspnea or orthopnea, typical pericardial pain, peripheral edema, tachycardia, tachypnea, a diminished mean blood pressure, a pericardial friction rub, jugular venous distension, rales, radiographic evidence of cardiomegaly and pleural effusions, and abnormal echocardiograms were the most common cardiac manifestations. An elevated erythrocyte sedimentation rate and anemia were other common laboratory findings. Our cohort demonstrated decreased survival in comparison with an age- and sex-matched North Central white population (from the upper midwestern United States), especially during the first year after diagnosis. Increasing age, the presence of other heart disease, an increasing total number of other extra-articular manifestations of rheumatoid arthritis, jugular venous distention, and a lower mean blood pressure were associated with decreased survival.
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PMID:Rheumatoid pericarditis: clinical features and survival. 231 40

The most common congenital cardiac defect is VSD. This malady accounts for 20 to 30 per cent of all congenital cardiac defects and is representative of a cardiac lesion that increases pulmonary blood flow. Although lesions, which increase pulmonary blood flow, may vary in incidence, they frequently have common symptomatology. Over time, congestive heart failure becomes a problem. Poor respiratory status leads to weight loss, poor feeding, and failure to thrive. If unrepaired, the child often presents with cyanosis and tachypnea. The history may include frequent respiratory infections, exercise intolerance, generalized malaise, or fatigue. In spite of poor weight gain, the child may be edematous and have a large liver. Definitive diagnosis of each lesion may be made by echocardiogram, cardiac catheterization, or both. With these data and a detailed history, treatment and management decisions are determined. In most cases, as the child gets older, symptoms become more evident. This is the result of high pulmonary pressure. High pressure over time causes a thickening of the alveolar tissue, which decreases the permeability of the alveolar membranes for gas exchange. Lung changes can become irreversible, but it is unusual for irreversible changes to occur before 1 year of age. All the lesions described in this article are amendable to primary repair before 1 year of age, affording the best functional results. Postoperative nursing care includes management of persisting CHF and PVR while maintaining adequate cardiac output. Many factors, including electrolyte balance, nutritional status, conduction disturbances, stress, and parental anxiety, influence the management of these infants. The outcome depends greatly on the assessment skill of a highly competent cardiac intensive care nurse and an environment conducive to collaborative practice.
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PMID:Caring for patients with lesions increasing pulmonary blood flow. 281 77

The ability of theophylline to limit diaphragmatic fatigue and to improve contractility appears to be dependent upon alterations in calcium metabolism. The mechanism responsible for these actions, however, remains unclear. We used perfused, contracting, intact rat diaphragm to measure the influence of therapeutic theophylline levels (10(-4) M) on tension development, in the presence or absence of the three most commonly used calcium channel blocking agents, or in the absence of calcium. Concentrations of diltiazem (10(-4) M), verapamil (10(-5) M), or nifedipine (10(-6) M) sufficient to completely block transmembrane calcium channels, were used. During the experiment, each diaphragm preparation was subjected to one of two fatiguing procedures: one to mimic that encountered during tachypnea and one to mimic that encountered during increased respiratory resistance. Our findings showed that therapeutic levels of theophylline were related to statistically significant (p less than 0.0005) increases in diaphragmatic contractility under control conditions and to statistically significant reductions in the sensitivity of the preparation to fatigue. All three calcium channel blockers negated the positive influence of theophylline. Zero calcium also prevented theophylline from enhancing the contractile properties of the diaphragm. It is our conclusion that theophylline enhances the contractile properties of the diaphragm by altering the transmembrane movement of calcium. Calcium antagonists, in turn, inhibit the beneficial effects of theophylline on diaphragm function.
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PMID:Diltiazem, verapamil, and nifedipine inhibit theophylline-enhanced diaphragmatic contractility. 291 32

This study tests three hypotheses regarding mechanisms that produce rapid shallow breathing during a severe inspiratory resistive load (IRL): 1) an intact vagal afferent pathway is necessary; 2) diaphragm fatigue contributes to tachypnea; and 3) hypoxia may alter the pattern of respiration. We imposed a severe IRL on pentobarbital sodium-anesthetized dogs, followed by bilateral vagotomy, then by supplemental O2. IRL alone produced rapid shallow breathing associated with hypercapnia and hypoxia. After the vagotomy, the breathing pattern became slow and deep, restoring arterial PCO2 but not arterial PO2 toward the control values. Relief of hypoxia had no effect, and at no time was there any evidence of fatigue of the diaphragm as measured by the response to phrenic nerve stimulation. We conclude that an intact afferent vagal pathway is necessary for the tachypnea resulting from a severe IRL, neither hypoxia nor diaphragm fatigue played a role, and, although we cannot rule out stimulation of vagal afferents, the simplest explanation for the increased frequency in our experiments is increased respiratory drive due to hypercapnia.
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PMID:Vagal afferents, diaphragm fatigue, and inspiratory resistance in anesthetized dogs. 313 22

Respiratory muscle strength and endurance should be assessed when dyspnea, respiratory failure, or poor performance on routine pulmonary function tests are unexplained. Respiratory muscle strength can be measured non-invasively from maximal mouth pressures, but measurement of transdiaphragmatic pressure refines the assessment. The maximal voluntary ventilation test is the only simple index of ventilatory or respiratory muscle endurance. Other tests for endurance and fatigue are more difficult, but some newer techniques may be applicable to the clinical laboratory. Some patients who exhibit tachypnea, marked use of neck inspiratory muscles, and chest-abdomen asynchrony may be developing respiratory muscle fatigue.
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PMID:Tests of respiratory muscle function. 329 26

Although the respiratory system is not fully developed at birth, the human newborn infant has flexible strategies to sustain breathing and defend blood gas homeostasis in both health and disease conditions. Initially the thresholds for chemoreceptor response to PO2 and PCO2 closely mimic those of the fetus, but the threshold resets to sustain ventilation adequate for blood gas homeostasis appropriate to the extrauterine milieu. The muscles of respiration have been "trained" in utero and effectively assume the function of the respiratory pump, despite their marginal reserve against fatigue. The pliable chest wall is functionally stabilized by the tonic activity of the intercostal muscles, thereby allowing effective ventilation. Finally, expiration is prolonged by the postinspiratory activity of the diaphragm and laryngeal braking as a means of maintaining an elevated lung volume and augmenting FRC. The ventilatory response of the newborn to respiratory disease is limited. The magnitude of the VE response is smaller than that of the adult, and is characterized by an increase in the respiratory rate and a limited increase in the VT. The poor effort reserve of the muscles, especially the diaphragm, predisposes the newborn to muscle fatigue and ventilatory failure. To avoid fatigue, recruitment of accessory muscles occurs, along with laryngeal braking of expiration, thereby decreasing the work of the diaphragm, recruiting new alveoli by an auto-PEEP effect, increasing the FRC volume, and improving gas exchange by an increase in the pulmonary surface area. These mechanisms help to avoid muscle exhaustion and facilitate adequate gas exchange in the presence of lung disease. We do not know precisely the postconceptual age at which the newborn is sufficiently developed to adopt these various defensive strategies of breathing, but the presence of tachypnea and grunting in 28-week-old premature infants suggests that long before term the human infant is capable of remarkable variation in the defense of breathing.
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PMID:Pulmonary and chest wall mechanics in the control of respiration in the newborn. 331 39

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


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