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

Illness associated adenovirus infection is described in 15 immunocompromised patients. Patients were immunocompromised by severe underlying disease, immunosuppressive or corticosteroid therapy or by age (prematurity). Evidence of adenovirus infection was obtained by either viral isolation or, in two cases, characteristic adenovirus inclusion bodies at postmortem study. All clinical illness was associated with high fever (temperature greater than 39 degrees C). Eighty per cent of the patients had severe systemic complaints including malaise, lethargy, fatigue and night sweats; a similar number of gastrointestinal symptoms. Pulmonary complaints were described in 11 of 15 cases and included cough (67 per cent) and tachypnea (53 per cent). Roentgenologic evidence of pneumonia was demonstrated in 12 of 15 patients (80 per cent). Elevation of serum hepatic enzyme levels (serum glutamic pyruvic transaminase (SGPT)) occurred in eight of 11 patients (73 per cent) and was moderate to severe (serum glutamic pyruvic transaminase greater than 450 IU/liter) in five of 11 (45 per cent). Nine patients died; seven after a rapid downhill course and two after a prolonged illness. Evidence of adenovirus infection microscopically by autopsy in the lung, liver or both is demonstrated in four patients with fulminant systemic illness. Adenovirus infection should be considered in the etiology of severe overwhelming illness in the immunocompromised host.
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PMID:Adenovirus infection in the immunocompromised patient. 624 99

When the ventilatory muscles are unable to develop the required force as it occurs during fatigue, hypercapnic respiratory failure ensues. We present evidence that when the respiratory muscles work in a fatiguing load domain the central controllers respond at an early stage with tachypnea, while when the muscles fail bradypnea ensues which is followed by apnea. Although bradypnea and apnea in addition to muscle inability to develop force may reduce alveolar ventilation by virtue of reducing the total minute ventilation, tachypnea may also be followed by hypercapnia at constant total minute ventilation by virtue of a reduction in tidal volume (VT). Such a strategy will increase the ratio of dead space (VD) to tidal volume (VD/VT) and PCO2 will rise. It is argued that this mechanism could satisfactorily explain the high levels of CO2 in patients with chronic obstructive lung disease, as well as the CO2 retention at an early stage in acute cases of fatigue during, for example, the weaning period of a patient from the respirator. Bradypnea and apnea contribute to CO2 retention at a later stage, when the muscles are exhausted and total ventilation decreases. This sequence in frequency of breathing is explained as an advantageous strategy adopted for the respiratory muscles, because it allows the muscles to operate at an optimal length. It is also hypothesized that muscle afferents, probably via the small fibers III and IV and/or Golgi and tendon organs, are responsible for this interaction of CNS and respiratory muscles.
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PMID:Ventilatory muscle fatigue governs breathing frequency. 650 21

The clinicopathologic features of constrictive pericardial disease in 13 dogs were reviewed. The causes were infection (3 dogs), metallic foreign body (1 dog), and idiopathic (9 dogs). Owner complaints included abdominal enlargement, tachypnea, weakness or syncope, exertional fatigue, and weight loss. Ascites and jugular venous distention were consistently observed, whereas abnormalities of arterial pulses and heart sounds were variable and inconsistent. Diminished QRS voltages were common. Mild to moderate cardiomegaly, rounding of the cardiac silhouette, and variable and nonspecific angiographic findings were frequently observed. Cardiac catheterization consistently showed elevation and equilibration of atrial and ventricular diastolic pressures, but a prominent early diastolic (y) descent was uncommon. Fibrosis was confined to the parietal pericardium in 8 dogs, and included the epicardium in 5 dogs. Parietal pericardectomy was successful in relieving the syndrome in 6 of 10 dogs. Pulmonary thrombosis was the most common cause of early postoperative mortality.
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PMID:Constrictive pericardial disease in the dog. 670 98

We have previously shown that the chemosensitivity of the respiratory centers is well preserved in myotonic dystrophy but that the ventilatory output is reduced. The present study was designed to determine at which degree of ventilatory performance weakness and fatigability of the respiratory muscles are interfering with ventilation and which mechanical factors contribute to the tachypnea of patients with myotonic dystrophy at rest and during low ventilatory output. We studied 10 patients with the disease and 10 normal control subjects. The strength of respiratory muscles was assessed by measurements of maximal pressure-volume diagrams generated against airway occlusion. Performance was evaluated during 1-min maximal voluntary ventilation (1-min MVV) test, during 7-min 7% CO2 breathing and during quiet breathing. Occlusion pressure (P0.1) in patients at rest was slightly higher than in control subjects, and during CO2 breathing, it was similar to that of control subjects. Maximal static pressure was reduced in patients to an average of 35% of that of control subjects. During the 1-min MVV test, there was a 50% reduction in esophageal and transdiaphragmatic pressure output (Pes, Pdi) in patients, resulting in similar reduction in ventilation (VE) and patients had rapid cycles of alternating dominant thoracic and abdominal volume displacements (Vrc/Vabd) suggesting respiratory muscle fatigue. During the 3- to 4-fold increase in breathing drive induced by hypercapnia, pressure output and the Vrc/Vabd were identical in both groups. However, ventilation was reduced in patients who had tachypneic respiration. In patients, tachypnea was also observed during quiet breathing. This tachypnea was associated with higher impedance of the respiratory system (Zrs) in patients and identical impedance of the lung (ZL) in both groups. In addition, Pdi during tidal volume was significantly higher in patients. These data demonstrate that the ventilatory output in out patients was altered predominantly by weakness and fatigability of the respiratory muscles during high ventilatory performance and by increased impedance of the respiratory system at lower degrees of ventilation.
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PMID:Pathogenesis of respiratory insufficiency in myotonic dystrophy: the mechanical factors. 680 50

Twelve patients exhibiting difficulties during discontinuation of artificial ventilation permitted us to investigate physical examination techniques used in diagnosing inspiratory muscle fatigue. Diaphragmatic and intercostal electromyographic tracings, arterial blood gases, rate and depth of ventilation, and thoracoabdominal motion were monitored during spontaneous breathing. Six patients showed electromyographic evidence of inspiratory muscle fatigue. A sequence of events leading to respiratory acidemia emerged--namely electromyographic evidence of fatigue, accompanied or followed by an increased respiratory rate, in turn followed by alternation between abdominal and rib cage breathing (respiratory alternans), paradoxical inward abdominal motion during inspiration (abdominal paradox), and finally an increase in PaCO2 associated with a fall in minute ventilation and respiratory rate, and worsening of respiratory acidemia. The abnormalities of respiratory movements may be reliable clinical signs of inspiratory muscle fatigue, particularly when accompanied by tachypnea and hypercapnia.
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PMID:Clinical manifestations of inspiratory muscle fatigue. 681 17

A pediatric patient is reported who experienced fatal progressive pulmonary fibrosis as a complication of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) therapy. The patient received a cumulative dosage of 1.29 g (1.72 g/m2) over a two-year period as adjuvant therapy for a medulloblastoma. Two and one-half years after cessation of therapy, cough, tachypnea and fatigue were noted. Progressive pulmonary insufficiency developed. Pulmonary pathologic findings included interstitial fibrosis and alveolar dysplasia. Other cases of BCNU pulmonary toxicity are cited from the medical literature.
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PMID:Pulmonary fibrosis: a complication of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) therapy. 727 34

Carbon monoxide poisoning usually results from inhalation of exhaust fumes from motor vehicles, smoke from fires or fumes from faulty heating systems. Carbon monoxide has a high affinity for hemoglobin, with which it forms carboxyhemoglobin. The resulting decrease in both oxygen-carrying capacity and oxygen release can lead to end-organ hypoxia. The clinical presentation is nonspecific. Headache, dizziness, fatigue and nausea are common in mild to moderate carbon monoxide poisoning. In more severe cases, tachycardia, tachypnea and central nervous system depression occur. When carbon monoxide intoxication is suspected, empiric treatment with 100 percent oxygen should be initiated immediately. The diagnosis is confirmed by documenting an elevated carboxyhemoglobin level. Hyperbaric oxygen therapy is recommended in patients with neurologic dysfunction, cardiac dysfunction or a history of unconsciousness.
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PMID:Carbon monoxide intoxication. 769 50

Growth in children with congenital heart disease (CHD) is often compromised. For several decades, investigators have tried to identify the factors affecting growth in children with CHD. Cardiac malformations are undoubtedly responsible for malnutrition, which may range from mild undernutrition to severe failure to thrive (FTT). Malnutrition may then significantly undermine the outcome of corrective surgical operations and postoperative recovery. Mechanisms linking CHD to malnutrition may be related either to decreased energy intake and/or to increased energy requirements. Decreased energy intake can involve deficiencies of specific nutrients, or insufficient total caloric intake. Increased respiratory rate accompanying congestive heart failure may be responsible for increased energy requirements. Different types of cardiac malformations and consequent interventions may have different effects on growth and require diverse strategies. Most treatment strategies aim to facilitate "catch-up" growth, providing extra calories and protein that exceed the Recommended Dietary Allowance for age. However, there is no generally accepted set of guidelines that define appropriate caloric intake for catch-up growth. We attempt to identify the most important causes of malnutrition and highlight the most effective nutrition strategies for children with CHD.
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PMID:Children with congenital heart disease: a nutrition challenge. 781 52

The demographics and natural clinical history of canine congenital subaortic stenosis (SAS) were evaluated by retrospective analysis of 195 confirmed cases (1967 to 1991), 96 of which were untreated and available for follow-up evaluation. Of these, 58 dogs had left ventricular outflow systolic pressure gradients available for assessment of severity. All 195 dogs were used for demographic analysis. Breeds found to be at increased relative risk included the Newfoundland (odds ratio, 88.1; P < .001), Rottweiler (odds ratio, 19.3; P < .001), Boxer (odds ratio, 8.6; P < .001), and Golden Retriever (odds ratio, 5.5; P < .001). Dogs with mild gradients (16 to 35 mm Hg) and those that developed infective endocarditis or left heart failure were diagnosed at older ages than those with moderate (36 to 80 mm Hg) and severe (> 80 mm Hg) gradients. Of 96 untreated dogs, 32 (33.3%) had signs of illness varying from fatigue to syncope; 11 dogs (11.3%) developed infective endocarditis or left heart failure. Exercise intolerance or fatigue was reported in 22 dogs, syncope in 11 dogs, and respiratory signs (cough, dyspnea, tachypnea) in 9 dogs. In addition, 21 dogs (21.9%) died suddenly. Sudden death occurred mainly in the first 3 years of life, primarily but not exclusively, in dogs with severe obstructions (gradient, > 80 mm Hg; odds ratio, 16.0; P < .001). Infective endocarditis (6.3%) and left heart failure (7.3%) tended to occur later in life and in dogs with mild to moderate obstructions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The natural clinical history of canine congenital subaortic stenosis. 788 29

The purpose of this study was to determine whether the tachypneic breathing pattern of constant work rate, heavy exercise (CWE) is unique to CWE or whether it represents the usual pattern of the respiratory control system at high levels of ventilation (VI). We compared breathing pattern in ten healthy subjects (age 20-29 years) during CWE and maximal incremental exercise (MIE) on a bicycle ergometer. Work rate was constant at 76% of maximum work rate in CWE and progressively increased by 25 watts/minute until exhaustion during MIE. Breathing pattern was examined at matched levels of VI equivalent to 80% and about 100% of maximum VI during CWE (97.1 and 121.4 L.min-1, respectively). Exercise duration (mean+standard deviation) was 13 +/- 6 and 12 +/- 1 min during CWE and MIE, respectively (P = NS). Tidal volume (VT) fell by an average of 0.20 L towards the end of CWE, but was maintained relatively high and constant towards the end of MIE. At high, but not lower, matched levels of VI breathing pattern during CWE was significantly more rapid and shallow than that during MIE. The tachypnoea of CWE did not correlate with the progressive rise in VI, oxygen uptake or cardiac frequency during CWE. We conclude that (1) CWE is associated with a tachypneic influence that is absent or less during incremental exercise; this tachypnea is most marked at the end of CWE. (2) The tachypnoea of CWE is not part of a generalized rate accelerating process during CWE. The mechanism(s) underlying the tachypnoea are unclear but it may be related to inspiratory muscle fatigue, pulmonary oedema, and/or altered respiratory mechanics.
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PMID:Differential ventilatory control during constant work rate and incremental exercise. 793 15


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