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

This study examines whether teenage asthmatic wind instrumentalists exhibit fewer bronchoconstrictive symptoms, panic-fear responses, changes of mood, and fatigue symptoms than non-wind instrument players. Eight teenage asthmatic wind instrument players and 10 asthmatic non-wind instrument players kept a diary of asthma symptoms. Panic-fear responses and mood changes were significantly higher in the non-wind players. A general health profile suggested that the wind instrumentalists present a significantly better "asthma health" picture, perceiving themselves better able to cope with the disease. Playing a musical wind instrument has the potential of being a long-term therapeutic agent for asthmatics.
J Asthma 1994
PMID:Effects of playing a musical wind instrument in asthmatic teenagers. 792 33

The cause of respiratory arrest in acute asthma is not known. By its nature, respiratory arrest is difficult to study clinically. The possible causes of respiratory arrest include cardiovascular dysfunction, respiratory muscle fatigue, and central respiratory failure. We used a dog model of respiratory arrest in acute bronchoconstriction that examined the effects of hypoxemia and intrinsic loading in an attempt to establish the mechanism. Our hypothesis was that, in a setting of hypoxemia and intrinsic loading similar to human fatal asthma, respiratory arrest is caused by a central respiratory failure, more specifically, failure of the central rhythm generator. We studied 18 dogs divided into 1) an intrinsically loaded group, 2) a hypoxemic group, and 3) both a loaded and a hypoxemic group. Intrinsic loading was induced with methacholine combined with selective beta 2-blockade, and the hypoxemia was controlled by varying inspired O2 fraction. Respiratory arrest occurred only in animals with both hypoxemia and intrinsic loading. We found no evidence of hemodynamic instability or respiratory muscle fatigue. Instead, there was an abrupt cessation of ventilation while the intensity of the central neural output was maintained. Our results are consistent with a failure of the central rhythm generator as the causal agent in respiratory arrest.
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PMID:Mechanism of respiratory arrest in an animal model of acute fatal bronchoconstriction. 796 Dec 40

We studied the link between chronic fatigue syndrome (CFS) and hyperventilation in 31 consecutive attenders at a chronic fatigue clinic (19 females, 12 males) who fulfilled criteria for CFS based on both Oxford and Joint CDC/NIH criteria. All experienced profound fatigue and fatigability associated with minimal exertion, in 66% developing after an infective episode. Alternative causes of fatigue were excluded. Hyperventilation was studied during a 43-min protocol in which end-tidal PCO2 (PETCO2) was measured non-invasively by capnograph or mass spectrometer via a fine catheter taped in a nostril at rest, during and after exercise (10-50 W) and for 10 min during recovery from voluntary overbreathing to approximately 2.7 kPa (20 mmHg). PETCO2 < 4 kPa (30 mmHg) at rest, during or after exercise, or at 5 min after the end of voluntary overbreathing, suggested either hyperventilation or a tendency to hyperventilate. Most patients were able voluntarily to overbreathe, but not all were able to exercise. Twenty-two patients (71%) had no evidence of hyperventilation during any aspect of the test. Only four patients had unequivocal hyperventilation, in one associated with asthma and in three with panic. Only one patient with severe functional disability and agoraphobia had hyperventilation with no other obvious cause. A further five patients had borderline hyperventilation, in which PETCO2 was < 4 kPa (30 mmHg) for no more than 2 min, when we would have expected it to be normal. There was no association between level of functional impairment and degree of hyperventilation. There is only a weak association between hyperventilation and chronic fatigue syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperventilation and chronic fatigue syndrome. 804 70

Asthma is a chronic disease in which social life is altered. The importance of restrictions on social life may be greater in severe asthma or when symptoms are not adequately controlled. General scales of quality-of-life (QOL) may be used to detect the importance of social life impairment, but it is not yet known whether the scores of such QOL measures are reliable and valid in asthmatic patients. A study was carried out in 252 patients with asthma of variable severity (FEV1 ranging from 25 to 131% of predicted) to assess the validity of a general QOL scale, the first French version of the SF-36 health status questionnaire (SF-36). This is based on 36 items selected to represent nine health concepts (physical, social, and role functioning; mental health; health perceptions; energy or fatigue; pain; and general health). All nine SF-36 category scores were highly significantly correlated with the severity of asthma assessed by the clinical score of Aas (p < 0.0007 to p < 0.0001). Eight SF-36 category scores were highly significantly correlated with FEV1 (p < 0.003 to p < 0.0001). A high internal reliability of SF-36 was found using the alpha coefficient of Cronbach (0.91 for the whole questionnaire). The SF-36 questionnaire is valid and reliable in asthma and can therefore be used to examine QOL in asthmatic and nonasthmatic patients and to determine to what extent asthma impairs social life.
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PMID:Quality of life in asthma. I. Internal consistency and validity of the SF-36 questionnaire. 830 32

It has been difficult to confirm that a given building is responsible for allergic symptomatology, exacerbation of asthma, or immunological dysfunction. In fact, in most studies, few objective immunological parameters have been studied and only rarely has there been any quantitation of IgE or secondary mediators. Furthermore, although many studies deal with rhinitis or respiratory tract irritation, there is a misconception that all such symptoms are allergic in nature, and studies attempting to prove that allergies are caused by buildings frequently neglect to prove that these are indeed true allergic responses. In addition, many of the symptoms that people attribute to sick building syndrome (SBS) or building-related illness, such as headaches, dizziness, fatigue, nausea, cough, and eye irritation, are subjective, and studies often fail to take into account other possible causes that may be inherent in the subjects, such as sinusitis, hyperventilation syndrome, or psychosomatic illness. Unfortunately, most clinical studies on SBS pay little attention to the preexisting conditions that a subject may have and discount the possibility that the inciting agent does not cause symptoms, but merely exacerbates a preexisting condition. Moreover, they offer no information about the nature of the mechanisms of action or pathophysiological relationships. Clearly, further studies are necessary to further explain the complexity of complaints that currently exist. Indeed, SBS might properly be paraphrased as "what is it?--if it is!"
J Asthma 1993
PMID:The sick building syndrome. I. Definition and epidemiological considerations. 833 Oct 40

Maximal voluntary drive to the diaphragm and a non-respiratory muscle group (elbow flexors) was compared in 10 control subjects and 11 asthmatics who were studied when well. The degree of voluntary activation during repeated attempted maximal quasi-static efforts was determined using the twitch interpolation technique in the absence of contractile fatigue under both control conditions and following bronchial challenge with histamine. Diaphragm activation was assessed using bilateral phrenic stimulation at the normal resting end-expiratory lung volume after exhalation from TLC. Asthmatic subjects showed lower and more variable voluntary activation than control subjects for both diaphragm (82.0% +/- 18.4 [SD], vs 87.8% +/- 12.0, P < 0.01) and elbow flexors (91.3% +/- 7.6 vs 95.8% +/- 4.1, P < 0.01). Histamine challenge decreased FEV1 in asthmatic subjects to 50% of the initial value, but had no significant effect on voluntary activation in either subject group. The decreased voluntary drive to the diaphragm observed in some asthmatic subjects may predispose to rapid development of ventilatory failure during severe airway narrowing.
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PMID:Reduced voluntary drive to breathe in asthmatic subjects. 836 14

A random sample of subjects over 65 years of age who had replied to a postal questionnaire on respiratory symptoms was asked to attend for lung function studies and, if fit, an inhaled methacholine bronchial challenge. Of 283 subjects, 180 (63.6%) agreed to attend. Most (98%) subjects performed reproducible spirometry, with no evidence of fatigue on repeated testing. However, 20 subjects were found to be unsuitable for challenge (forced expiratory volume in 1 s, (FEV1) < 1 litre or unable to perform spirometry reproducibly). The dose of methacholine producing a 20% fall in FEV1 was termed the PD20. A positive challenge with PD20 < 6.13 mumol methacholine was found in 69 of 160 (43%) subjects studied, with highly reactive airways (PD20 < 1.0 mumol methacholine) in 19 of 160 (12%). Bronchial hyperreactivity, which is closely associated with clinical asthma, was found to be far more common amongst the elderly than previously recognised. Low initial FEV1 (1-1.5 litres) predisposed to both a positive challenge (p < 0.01) and also to highly reactive airways (p < 0.01), generally associated with respiratory symptoms. Subjects with low (1-1.5 litres) baseline FEV1 were five times more likely to have highly reactive airways than those with FEV1 > 1.5 litres, confirming a relationship between baseline airway calibre and bronchial reactivity. Early detection of subjects with low FEV1, who are therefore more likely to have increased airway reactivity, may help to reduce respiratory morbidity in the elderly with considerable benefit both to patients and to the Health Service.
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PMID:How common is increased airway reactivity amongst the elderly? 844 Apr 89

Some conditions that predispose to ventilatory failure increase the work of breathing (chronic obstructive pulmonary disease [COPD], obesity, kyphoscoliosis), whereas others cause severe respiratory muscle weakness. Specific reasons for muscle weakness include critical illness (electrolyte imbalance, acidemia, shock, sepsis), chronic illness (poor nutrition, cachexia), and neuromuscular diseases. Inspiratory muscle weakness from mechanical disadvantage to the diaphragm is characteristic of asthma and COPD. The increased work of breathing combined with muscle weakness increases the pressure needed to inspire a breath and decreases maximal inspiratory pressure. When this pressure exceeds 0.4, dyspnea and inspiratory muscle fatigue ensue. One way to lower this pressure and avert fatigue is to lower the tidal volume. Ventilatory drive is high, not low, in ventilatory failure. Concomitant shortening of inspiration and breath duration cause the small tidal volume and increased respiratory rate. Gas exchange is compromised by ventilation/perfusion imbalance, and the ratio of dead space to tidal volume is also increased by rapid, shallow breathing. Reduction in tidal volume minimizes dyspnea, but the small tidal volume is inadequate for gas exchange. Acute treatment of respiratory muscle failure involves respiratory muscle rest through mechanical ventilation and removal of noxious influences (infection, metabolic disarray), whereas chronic treatment involves rebuilding the contractile apparatus by nutritional repletion and training.
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PMID:Respiratory muscles and ventilatory failure: 1993 perspective. 850 1

The estuarine dinoflagellate Pfiesteria piscicida gen. et sp. nov. produces exotoxin(s) that can be absorbed from water or fine aerosols. Culture filtrate (0.22 microns porosity filters, > 250 toxic flagellated cells/ml) induces formation of open ulcerative sores, hemorrhaging, and death of finfish and shellfish. Human exposure to aerosols from ichthyotoxic cultures (> or = 2000 cells/ml) has been associated with narcosis, respiratory distress with asthma-like symptoms, severe stomach cramping, nausea, vomiting, and eye irritation with reddening and blurred vision (hours to days); autonomic nervous system dysfunction [localized sweating, erratic heart beat (weeks)]; central nervous system dysfunction [sudden rages and personality change (hours to days), and reversible cognitive impairment and short-term memory loss (weeks)]; and chronic effects including asthma-like symptoms, exercise fatigue, and sensory symptoms (tingling or numbness in lips, hands, and feet; months to years). Elevated hepatic enzyme levels and high phosphorus excretion in one human exposure suggested hepatic and renal dysfunction (weeks); easy infection and low counts of several T-cell types may indicate immune system suppression (months to years). Pfiesteria piscicida is euryhaline and eurythermal, and in bioassays a nontoxic flagellated stage has increased under P enrichment (> or = 100 micrograms SRP/L), suggesting a stimulatory role of nutrients. Pfiesteria-like dinoflagellates have been tracked to fish kill sites in eutrophic estuaries from Delaware Bay through the Gulf Coast. Our data point to a critical need to characterize their chronic effects on human health as well as fish recruitment, disease resistance, and survival.
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PMID:Insidious effects of a toxic estuarine dinoflagellate on fish survival and human health. 852 74

Asthma is a condition in which there is airway hyperresponsiveness, with the propensity for widespread, reversible airways narrowing on exposure to diverse inciting factors (triggers). Inhalation of nonspecific agents such as methacholine or histamine leads to bronchoconstriction in most cases, and in some, the bronchoconstriction follows exposure to specific agents such as antigen or occupational irritants. Chest tightness and cough, which are the most common symptoms of asthma, are probably the result of inflammation mucus plugs, edema, or smooth muscle constriction in the small peripheral airways. Because major obstruction of the peripheral airways can occur without recognizable increases of airway resistance or FEV1, the physiologic alterations in acute exacerbations are generally subtle in the early stages. Poorly ventilated alveoli subtending obstructed bronchioles continue to be perfused, and as a consequence, the P(A-a)O2 increases and the PaO2 decreases. At this stage, ventilation is generally increased, with excessive elimination of carbon dioxide and respiratory alkalemia. In the more severe exacerbation, lung volume is increased and the static volume-pressure curve is shifted up (lung volume is greater) and to the left (pressure is lower) while the shape of the curve is unaltered. The airway obstruction is reversible and there is generally improvement in air flow rates following administration of beta-agonists and anti-inflammatory agents. The changes in mechanical properties are also reversible, and therapeutic intervention usually results in a shift of the PV curve downward toward the normal position, for example, a decrease in TLC and an increase in the elastic recoil pressure at any particular lung volume. Failure to take these changes into account may underestimate the impact of therapy. The PaO2 decreases (and the P(A-a)O2 increases) as the work of breathing increases, and when it becomes excessive (and/or the FEV1 falls below 20% to 25%), the PaCO2 begins to increase. Therefore, in any patient with asthma, a decreasing PaO2 and an increasing PaCO2, even into the normal range, indicates severe airway obstruction that is leading to respiratory muscle fatigue and patient exhaustion.
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PMID:Physiologic diagnosis and function in asthma. 856 1


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