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

We studied the power spectrum of the diaphragm electromyogram (EMG) at frequencies between 31 and 246 Hz in four young normal subjects and five patients with chronic obstructive lung disease (COPD). Diaphragm EMGs were analyzed during spontaneous breathing and maximum inspiratory efforts to determine the effect of signal-to-noise ratio on the power spectrum and if treadmill exercise to dyspnea was associated with diaphragm fatigue. We found that the centroid frequencies of the power spectra (fc) were strongly correlated (r = 0.93) with ratios of power at high frequencies to power at low frequencies (H/L) for all subjects. Of the two indices, H/L had the largest standard deviation expressed as a percentage of the mean. The mean values of both of these decreased significantly after exercise, fc from 100.2 to 97.3 and H/L from 1.07 to 0.97. Signal-to-noise ratios were higher in maximal inspiratory efforts and after exercise in normal subjects and higher in COPD patients. The signal-to-noise ratio was correlated negatively with fc and H/L, indicating that these indices of the shape of the power spectrum are influenced by signal strength and noise levels as well as muscle function. We conclude that the fc and H/L index similar qualities of the power spectrum, that they are partially determined by the signal-to-noise ratio, and that, in some cases, exercise to dyspnea is associated with apparently mild diaphragm fatigue.
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PMID:Power spectral analysis of the diaphragm electromyogram. 687 80

The mechanisms of chronic ventilatory failure in chronic obstructive pulmonary disease are complex. This paper analyses the diverse available information: mechanical factors and gas-exchange, fighter vs. non-fighter, the ventilatory pattern theory and the fatigue threshold theory. Finally we comment on the evidence supporting the new concept that hypercapnia may develop to avoid or prevent fatigue. Indeed, it is very likely that chronic CO2 retention in COPD may develop by mechanical disadvantages of the inspiratory muscles rather than impairment of ventilation-perfusion ratios. This opens a fascinating new research line on the neuromechanical control of breathing. When the respiratory effort is approaching the fatigue level, the respiratory muscles may elicit a negative feedback reflex, the muscle activity is depressed and hypercapnia develops. If this is so, chronic hypercapnia may be an index of imminent fatigue if increases in ventilation or work of breathing are required. Under this condition some degree of central diaphragm fatigue may help to protect the muscle from severe or limiting peripheral fatigue or even muscle injury. Finally, we comment on some therapeutic approaches such as ventilatory stimulants, training, rest and, specially, oxygen administration and the mechanisms involved in the PCO2 increases.
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PMID:[Causes of CO2 retention in patients with chronic obstructive lung disease]. 820 18

Among 182 episodes with ARF (PaCO2 > 50 torr) in 400 episodes of COPD patients who were admitted to Chulalongkorn Hospital during the period 1982 to 1986, despite conservative treatment, 66 developed severe acute respiratory failure requiring assisted ventilation. Patients with a history of chronic cough, pneumonia as a precipitating factor and more severe ARF on admission, as indicated by palpitation, headache, cyanosis, alteration of consciousness, cor-pulmonale and decompensated acidosis (pH < 7.30), were likely to require mechanical ventilation. Indications for mechanical ventilation were carbon dioxide narcosis (43 episodes), severe hypoxemia despite on a high FIO2 (one episode), various combination parameters of respiratory muscle fatigue, cardiovascular instability (22 episodes). The major complications of mechanical ventilation were pneumonia, sepsis, pneumothorax, UGI bleeding of 16, 8, 5 and 9 episodes, respectively. The average duration of assisted ventilation and hospitalization were 15.8 and 19.02 days, respectively. The mortality rate was 50 per cent in the mechanical ventilation group compared with 9.8 per cent in the non-mechanical ventilation group. Increased mortality rate was found in those with pneumonia as the precipitating factor (68.4 vs 14.3%, respectively, in comparing the two groups). Complications of mechanical ventilation, which included pneumonia, sepsis, fluid overload, hyponatremia and persistent acidosis, were high-risk factors for the non-surviving group.
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PMID:Mechanical and non-mechanical ventilation of respiratory failure in chronic obstructive pulmonary disease. 822 88

Two hundred seventy severely hypoxemic (PaO2 < or = 55 mm Hg: mean +/- SD = 48 +/- 6) COPD patients (232 men) were selected for long-term oxygen therapy (LTOT). They were old (mean = 66 +/- 8 years), with severe airflow limitation (FEV1 = 30 +/- 12 percent of predicted), some CO2 retention (PaCO2 = 47 +/- 9 mm Hg), and compensated respiratory acidosis. Eighteen percent of the patients presented some complicating pleuropulmonary diseases (pleural thickening, sequelae of tuberculosis, etc). Overall survival proportion was poor: 70, 50, and 43 percent at 1, 2, and 3 years, respectively. The Cox model showed that the factors which independently reduced survival were lower CO transfer coefficient, smaller intrathoracic gas volume, more severe bronchial obstruction, the fact that oxygen administration did not increase PaO2 above 65 mm Hg, increasing age, and the presence of chest wall abnormalities. When the patients were divided into three groups according to mortality risk, the mean clinical and functional profile of the high-mortality risk group was consistent with the prevalence of emphysematous lesions. Moreover, the best survivors fitted better into the "bronchitic" type; they showed a higher mean PaCO2, suggesting that some degree of hypoventilation could delay muscular fatigue and improve survival. The difference in the proportion of "emphysematous" and "bronchitic" patients is a possible explanation for the variability of the mortality rate reported in literature.
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PMID:Prognosis of severely hypoxemic patients receiving long-term oxygen therapy. 830 23

Many daily activities, from basic grooming to employment tasks, require adequate unsupported arm endurance (UAE). We developed an electromechanical device to measure UAE endurance. The purpose of this study was to standardize the instrument for two rates of arm motion, moderate and slow, in 18 normal adult subjects (FEVI = 3.7L +/- .78, FVC = 4.2L +/- .74, FEV1/FVC = 1.1 +/- .08). Exercise endurance limits, and the following metabolic, ventilatory, and sensation responses were determined at rest prior to exercise and at end-exercise limits for both rates of UAE:minute ventilation (Ve), tidal volume (VT), respiratory rate (RR), duty cycle (Ti/Ttot), oxygen uptake (VO2), carbon dioxide production (VCO2), inspiratory flow (VT/Ti), heart rate (HR), and visual analog scale measurements (VAS) of dyspnea (D), respiratory effort (RE), and arm fatigue (AF). Significance increases from baseline rest were shown at the endurance limits for both rates of UAE in: VO2, VCO2, Ve, VT, RR, VT/Ti, HR, VAS-D, VAS-RE, and VAS-AF. There were no changes in Ti/Ttot and SaO2 with UAE. Peak VO2, RR, Ve, VT/Ti, and VAS-D with moderate exercise were significantly greater than slow UAE; and there was a trend increase in peak HR for moderate as opposed to slow rate UAE. Despite these differences, the endurance time between the two rates of UAE were similar. These data provide standards against which UAE in COPD can be evaluated.
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PMID:Instrument development in the measurement of unsupported arm exercise endurance in normal adult subjects. 850 57

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 excessive load placed on inspiratory muscles when patients with COPD exercise could lead to fatigue and contribute to exercise limitation. Slowing of maximal relaxation rate (MRR) of skeletal muscle is an early index of the fatiguing process. We investigated whether inspiratory muscle MRR slows when patients with COPD walk to exhaustion. We studied nine well-trained and motivated patients with stable severe COPD (mean FEV1: 0.7 L, 28% predicted). Each subject performed sniff maneuvers before and after walking on a treadmill until they were forced to stop because of dyspnea. Esophageal (Pes), gastric, and transdiaphragmatic pressures were measured using balloon-tipped catheters. MRR was calculated as the percent Pes drop/10 ms. In the first minute after exercise there was a mean decrease of Pes MRR of 42% (range, 21 to 65%) (p < 0.01), which returned to baseline within 3 to 5 min. The fall in MRR indicates that the inspiratory muscles of patients with COPD walking to exhaustion are sufficiently heavily loaded to initiate the fatiguing process.
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PMID:Exhaustive exercise slows inspiratory muscle relaxation rate in chronic obstructive pulmonary disease. 856 33

The chest and abdomen impedance respirographs (IRG), including the one dimensional IRG and the two dimensional IRG were designed and produced by applying the principle of bioelectrical impedance. Using IRG the non-synchronized chest and abdomen respiratory motions occurring in diaphragmatic fatigue were measured. The results showed that all 203 normal controls showed synchronized style of chest and abdomen respiratory motions. In 189 COPD patients 117 (61.9%) showed non-synchronized respiratory motions which could be further divided into three types: type I showed complete contra-directional respiratory movements of chest and abdomen respiration, with M > 24 % and alpha angel > 120 degrees; type II showed staggered peak of the chest and abdomen motion curves (13% < M < 24%), 50 degrees < alpha angle < 120 degrees; type III showed double peaks of abdomen trace in the one dimensional IRG and "8"-shaped double circles on the two dimensional IRG, (M < 13%, 50 degrees < alpha angle < 120 degrees. When compared with trans-diaphragmatic pressure (Pdi) and diaphragm myoelectricity frequency spectrum, the rates of conformity were 81.8% and 90%, respectively, suggesting that IRG could be reliably used for diagnosing diaphragmatic fatigue. This technique is simple, easy to use, cheap and pain-free.
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PMID:Application of electrical impedance principle in the diagnosis of diaphragm fatigue. 873 30

We designed and performed the chest and abdomen impedance respirograph (IRG), which included the one dimentional IRG and the two dimentional IRG, by applying the principle of bioelectrical impedance. Using IRG, we measured the non-synchronized chest and abdomen respiratory motions occurring in the diaphragmatic fatigue. The results showed that all 203 normal control subjects showed synchronized pattern of chest and abdomen respiratory motions. In 189 COPD patients 117 (61.9%) showed non-synchronized respiratory motions which could be further divided into three types: type I showed complete contradirectional movements of respiration, M > 24% and alpha angle > 120 degrees; type II showed staggered peak of the chest and abdomen motion curves, 13% < M < 24%, 50 degrees < alpha angle < 120 degrees; type III showed double peaks in the one dimentional IRG and 8-shaped double circles in the two dimentional IRG, M < 13%, alpha angle > 40 degrees. When compared with Pdi and diaphragm myoelectricity frequency spectrum the rates of accordance were 81.8% and 90%, respectivity, suggesting that IRG could be reliably used to diagnose diaphragmatic fatigue. This technique is simple, easy, cheap and non-invasive. It is, therefore, worth to be widely recommanded for clinical investigation.
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PMID:[Investigation of the application of electrical impedance principle for the diagnosis of diaphragm fatigue]. 876 84

Mechanical ventilation via a tracheal tube is an invasive measure whose complications may prevent recovery from respiratory failure. Today, noninvasive positive pressure ventilation via mouthpiece or mask is an economically and medically successful alternative for the treatment of chronic respiratory failure and acute exacerbation of COPD, respectively. Within certain limits, noninvasive ventilation may take over inspiratory work of breathing as well as elevate mean airway pressure and inspiratory oxygen concentration. This does not at all question the absolute indications to maintain a patent airway by tracheal intubation. Clinical applications of noninvasive ventilation within these limits are acute exacerbation of COPD, congestive heart failure with pulmonary edema or atelectasis. Respiratory muscle fatigue, cardiogenic and septic shock, severe pneumonia and ARDS are still absolute indications for invasive ventilation. Table 1 specifies 12 disadvantages and endpoints of noninvasive mechanical ventilation.
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PMID:[Contra: noninvasive ventilation in acute respiratory insufficiency]. 923 64


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