UMLS:C1762617 - FACTA Search

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Inspiratory muscle strength in COPD could be reduced either because of mechanical disadvantage consequent to increased lung volume or because respiratory muscles share in generalized muscle weakness. To assess the relative contributions of these factors, we measured maximal inspiratory and expiratory pressures (Pimax, Pemax, cmH2O) at RV and TLC, respectively, in 32 patients with COPD. The TLC, RV, and diaphragm length index at RV (DLI, cm/cm height) were determined roentgenographically and compared with values from 22 normal subjects studied at comparable lung volume. Half the patients with COPD had normal and half had low values of Pemax, but both groups had similar values of TLC, RV, and DLI. In patients with COPD, Pimax correlated (p less than 0.001) with Pemax (r = 0.73) and DLI (r = 0.64). The slope of the Pimax-DLI relationship was essentially the same in both groups of patients with COPD as it was in the normal subjects. However, at any value of DLI, Pimax was in the normal range in patients with normal Pemax, but significantly lower in patients with low Pemax (p less than 0.001). Expressing Pimax as a combined function of Pemax and DLI yielded the highest correlation (r = 0.84, p less than 0.001), with Pemax explaining 46% and DLI explaining 35% of the variance in Plmax not explained by the other variable alone (p less than 0.001). The PaCO2 was elevated in 13 of 18 patients whose Pimax was less than 55 cm H2O, and inversely correlated with Pimax (r = -0.66, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Determinants of maximal inspiratory pressure in chronic obstructive pulmonary disease. 401 71

It has been suggested that low body weight may be associated with decreased respiratory muscle function in COPD, but the precise mechanism is not known. Since body compositional change inevitably accompanies body weight change, we decided to study the possible relationship between respiratory muscle strength and body composition in patients with COPD. We studied respiratory muscle strength, pulmonary function, and body composition in 24 Japanese male patients with COPD. Patients were divided into two groups according to their body weight (group A, body weight lower than 80% of ideal body weight vs group B, 80% or more) and a comparison was made together with age-matched controls (group C). Maximal inspiratory mouth pressure (PImax) and maximal expiratory mouth pressure (PEmax) were measured by a previously reported method. Body compositional analysis was performed using dual energy x-ray absorptiometry (DXA; Norland XR26). It showed significantly lower fat body mass (FAT), FAT/body weight%, and lean body mass (LEAN) in group A than those in group B. The PImax in group A was significantly lower than that in group B and C (44.2 +/- 13.8, 76.4 +/- 29.9, and 88.6 +/- 18.1 cm H2O, respectively). PEmax in group A was also significantly lower than that in group B and group C (61.9 +/- 20.1, 86.7 +/- 26.8, and 90.4 +/- 17.6 cm H2O, respectively). Both PImax and PEmax were significantly correlated with LEAN (r = 0.656, r = 0.591, p < 0.01, respectively) in patients with COPD. These results show that respiratory muscle strength is closely associated with body weight and lean body mass in patients with COPD. The present approach to compare respiratory muscle strength with lean body mass should be useful for studying the mechanism of respiratory muscle weakness in patients with COPD.
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PMID:Relationship between respiratory muscle strength and lean body mass in men with COPD. 775 Mar 11

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

Inspiratory muscle function has been shown to be related to general muscle weakness, weight loss, blood gas tensions, airway obstruction and hyperinflation. The aim of this study was to define (1) the factor that is the main determinant of the tension-time index of the inspiratory muscles (TTmus), and which this increases the risk of inspiratory muscle fatigue; and (2) whether a breathing strategy is adopted to avoid inspiratory muscle fatigue. Twenty-seven normal volunteers and 35 stable COPD outpatients (FEV1% predicted, range: 21-89%; and FRC/TLC, range: 49-77%) were studied. The TTmus was determined as follows: TTmus = PI/PImax.TI/Ttot, where Pi is the mean inspiratory pressure calculated from the mouth occlusion pressure (P0.1), PImax is the maximal inspiratory pressure, TI is the inspiratory time, and Ttot is the total time of the breathing cycle. COPD patients showed significantly lower PImax and higher P0.1, PI, PI/PImax, and TTmus than normal subjects. No patient had a TTmus value higher than the inspiratory muscle fatigue threshold of 0.33. The FEV1 was significantly correlated with TTmus and all its components in the patients. The FRC/TLC was also correlated with all components except PI. Body weight was only correlated with PImax. In a forward and backward stepwise regression analysis, FEV1 appeared to be the only significant factor explaining the variance of log (PI/PImax) and log (TTmus), whereas FRC/TLC was the principal determinant of PImax. In COPD patients, a non-linear relationship was found between TI and P0.1. A negative linear relationship was found between TI/Ttot and PI/PImax. In conclusion, although hyperinflation predominantly affected inspiratory muscle strength in a group of stable COPD patients with a wide range of severity, airway obstruction was the principal factor determining the magnitude of TTmus. In addition, in order to remain below the inspiratory muscle fatigue threshold, as the severity of airway obstruction increased, patients adopted a breathing strategy characterized by decreased TI/Ttot as inspiratory pressure demand increased.
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PMID:Tension-time index of inspiratory muscles in COPD patients: role of airway obstruction. 985 Mar 66

Bronchial rupture is a rare but severe complication of intubation with a double-lumen tube. Cardinal symptoms are mediastinal and subcutaneous emphysema as well as pneumothorax. Larger injuries result in an air leak and the endtidal carbon dioxide decreases. The gas exchange may worsen drastically when mucosal prolapse or bronchial haemorrhagia lead to bronchial occlusion. Mediastinitis or sepsis can be the sequel of the opened mediastinum. If bronchial injury is suspected probably fibreoptic bronchoscopy is indicated. We report on a case of bronchial rupture due to overinflation of the endobronchial cuff or movement of the inflated cuff when repositioning the patient. The conservative therapy was successful in spite of the fact that surgical intervention is recommended in the literature following bronchial rupture. To avoid tracheobronchial injuries an adequate tubus size must be selected. The more flexible polyvinylchloride (PVC) tubes without a carinal hook should be preferred to the Carlens tube. An atraumatic intubation is promoted by leaving the stylet inside after the tip of the tube has passed the vocal cords. To identify the minimum occlusive pressure of the endobronchial cuff for lung isolation different methods are described and should be used. The cuff has to be deflated when the patient is repositioned and when one-lung-ventilation is not required. Tumours of the tracheobronchial tree and weakness of the bronchial wall caused by steroid hormone therapy or COPD may increase the risk of tracheobronchial laceration.
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PMID:[Diagnosis, procedures and conservative therapy of a bronchial rupture after intubation with double-lumen tube]. 1007 58

Pulmonary rehabilitation (PR) is an important tool in the treatment of COPD patients. It is now clearly established that PR improves exercise capacity, reduces symptoms and improves quality of life in COPD patients. There is further evidence that the programmes also improve survival and reduce medical consumption. Pulmonary rehabilitation programmes are multidisziplinary and consist of exercise training (endurance, power), chest physiotherapie, education, psychosocial and nutritional support. Patients with poor exercise capacity, peripheral muscle weakness, severe complaints and poor quality of life seem to profit most from in- and outpatients rehab programmes. The type of rehabilitation depends on the severity of symptoms, the competence of the rehab-team and the local possibilities.
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PMID:[Rehabilitation in COPD]. 1021 34

Exertional dyspnea is a most popular symptom in COPD patients often lead to exercise intolerance. Indeed the reduced activity in patient's daily life due to dyspnea may lead to deconditioning and peripheral muscle weakness. Bronchodilators and anti-inflammatory drugs are an important treatment to reduce symptoms and improve airflow limitation but not improve deconditioning. Impairment of exercise tolerance is a common problem in patients with COPD and therefore exercise training is an important component of all pulmonary rehabilitation programs. It is now clearly established that exercise training reduce dyspnea, improve exercise tolerance and improve activities of daily living (ADL) and health related quality of life (QOL). Oxygen therapy during exercise are often considered in the COPD patients with exercise induced hypoxemia.
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PMID:[The efficacy and practice of exercise training in patients with chronic obstructive pulmonary disease (COPD)]. 1049 3

If chronic hypercapnia in patients with severe COPD occurs as a consequence of respiratory muscle (RM) weakness or fatigue, we would expect that ventilatory muscle recruitment (VMR) and exercise performance in stable hypercapnic patients would differ from those in eucapnic patients. We evaluated exercise performance and RM function at rest and during exercise in 19 eucapnic (PCO(2) 40 +/- 3 mm Hg), and 13 hypercapnic (PCO(2) 52 +/- 10 mm Hg) patients with severe COPD. A metabolic cart was used to determine V E, V O(2), V CO(2), and HR. Gastric (Pg) and esophageal (Ppl) balloons were used to measure Pg, Ppl, and Pdi. Ventilatory muscle recruitment pattern (VMR) was partitioned using end-inspiratory and end-expiratory Pg and Ppl. Hypercapnic patients had lower FEV(1) (0.60 +/- 0.24 versus 0.95 +/- 0.31 L, p < 0.001), MVV (28 +/- 11 versus 41 +/- 13 L, p < 0.001), resting PO(2) (61 +/- 11 versus 70 +/- 11 mm Hg, p < 0.001), peak PO(2) (60 +/- 20 versus 75 +/- 22 mm Hg, p < 0.005), and V E(max) (24 +/- 10 versus 32 +/- 12 L/min, p < 0.001). Patients in both groups had similar FRC (5.7 +/- 1.6 versus 5.0 +/- 1.5 L), V O(2)max (0.58 +/- 0.30 versus 0.76 +/- 0.32 L/min), Watts (45 +/- 48 versus 71 +/- 59), V E/MVV (88 +/- 33 versus 79 +/- 14), and HRmax (117 +/- 17 versus 128 +/- 18 beats/min). PI(max) (67 +/- 28 versus 65 +/- 32 cm H(2)O) and PE(max) (98 +/- 34 versus 96 +/- 40 cm H(2)O) were also similar in both groups. VMR (DeltaPg/DeltaPpl) at rest (-0.28 +/- 0.51 versus 0 +/- 0.35) and during exercise (0.4 +/- 0.2 versus 0.39 +/- 0.15) was equally affected in both groups. We conclude that exercise capacity and ventilatory muscle recruitment are similarly impaired in eucapnic and hypercapnic patients with severe COPD. These findings make inability of the lung to increase ventilation and not respiratory muscle dysfunction a more attractive explanation for CO(2) retention in stable hypercapnic patients.
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PMID:Respiratory muscle recruitment and exercise performance in eucapnic and hypercapnic severe chronic obstructive pulmonary disease. 1071 37

Plasma levels of amino acids were measured by ion-exchange, high-pressure liquid chromatography in 30 ambulatory patients with chronic obstructive pulmonary disease (COPD; mean +/- SD: age 64 +/- 13 y and forced expiratory volume in 1 s [FEV1] 0.85 +/- 0.25 L) and 30 age- and sex-matched healthy control subjects with regard to nutritional status, resting energy expenditure (REE), and pulmonary function. The ratio of branched-chain amino acids to aromatic amino acids was significantly (P < 0.001) decreased in COPD patients and was significantly correlated with percentage of ideal body weight (r = 0.403, P < 0.05), percentage of arm-muscle circumference (r = 0.492, P < 0.01), and %FEV1 (r = 0.467, P < 0.05). Plasma levels of alanine and cysteine were decreased, whereas levels of glutamine, aspartic acid, serine, and ornithine were elevated in COPD patients as opposed to control subjects. The ratio of resting energy expenditure to predicted resting energy expenditure was negatively correlated with the ratio of branched-chain to aromatic amino acids (r = -0.716, P < 0.01), percentage of arm-muscle circumference (r = -0.770, P < 0.05), %FEV1 (r = -0.839, P < 0.01), and the maximal inspiratory pressure (r = -0.803, P < 0.001). Underweight COPD patients also exhibited a greater degree of hyperinflation (percentage of residual volume = 205 +/- 15 for underweight patients and 156 +/- 8 for normal-weight patients). In conclusion, a decrease in plasma levels of branched-chain amino acids in relation to hypermetabolism, possibly resulting from the severity of COPD and respiratory muscle weakness, and various disturbances in plasma amino-acid levels were found in underweight COPD patients.
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PMID:Plasma levels of amino acids and hypermetabolism in patients with chronic obstructive pulmonary disease. 1124 Mar 35

Chronic obstructive pulmonary disease, COPD is a highly prevalent disorder of increasing medical and socio-economical importance. It is characterized by irreversible airflow obstruction. Besides airflow obstruction also other features are present. One of these is respiratory muscle weakness. Inspiratory muscle weakness is caused by hyperinflation and by generalized muscle weakness causing both respiratory and peripheral muscle dysfunction. The expiratory muscles partake in this generalized muscle weakness. Hyperinflation shortens the inspiratory muscles although in chronic hyperinflation sarcomere adaptation occurs. Generalized muscle weakness is caused by deconditioning, malnutrition, electrolyte disturbances, cardiac failure, systemic inflammation and treatment with corticosteroids causing steroid-induced myopathy. The latter disease was studied intensively both in patients and in animal models of disease. The major findings were that microscopically a myopathic pattern was present associated with generalized fiber atrophy. This is in contrast to classical belief that the atrophy would be confined to type IIx fibers. We noted severe down-regulation of the IGF-I mRNA expression, without important changes in the expression of the binding proteins. This may be responsible for the observed muscle atrophy and the myopathy. The latter is likely to be caused by a simultaneous upregulation of the ubiquitin protease pathway attacking structural proteins. Presently, we study the relationship between local and systemic cytokine expression and respiratory and peripheral muscle dysfunction in COPD patients. Respiratory and peripheral muscle dysfunction have significant consequences for COPD patients. Both respiratory and peripheral muscle dysfunction are associated with reduced exercise tolerance and reduced quality of life. Both are independent determinants of survival, in addition to the degree of airflow obstruction as measured by FEV1. Finally, also the utilization of health care resources appeared to be related to respiratory and peripheral muscle weakness. Treatment of respiratory and peripheral muscle weakness in COPD patients is possible. Respiratory and peripheral muscle training have been shown to produce beneficial effects. Nutritional intervention and anabolic steroids are only useful in combination with muscle training. Systemic administration of growth hormone and IGF-I only produces small effects. In animal models, local administration of IGF-I and transfer of the IGF-I gene transfer appear more promising for the future. Lung volume reduction surgery, LVRS, improves the force-generating capacity of the inspiratory muscles, presumably because of the geometrical alterations it causes in these muscles. It does not appear to improve intrinsic inspiratory muscle function.
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PMID:Respiratory muscles in COPD: regulation of trophical status. 1181 11

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