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

The current techniques of respiratory gas-exchange monitoring during stress testing in patients with congestive heart failure have provided new physiopathologic and clinical data. The "breath-by-breath" measurement of oxygen consumption and carbon dioxide production and the evaluation of the relationship between these parameters and respiratory volumes, allow to determine both ventilatory and metabolic responses during exercise, thus giving a precise estimate of the effective cardiopulmonary functional capacity. The demonstration of peripheral vascular and metabolic abnormalities by these techniques have provided new insights into the mechanism of dyspnea and fatigue in patients with heart failure. Although the relationship between respiratory and metabolic parameters and hemodynamics has been extensively studied, its mechanisms are still unclear. Moreover, controversy still exists as to the link between functional capacity and prognosis. Finally, recent studies on the cardiopulmonary adaptations to exercise training in patients with left ventricular dysfunction, have clearly demonstrated clinical and hemodynamic improvement after conditioning. These data, if confirmed, may provide a new approach in the management of patients with this disorder.
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PMID:[Monitoring of respiratory exchange during ergometric test in patients with heart failure: current aspects and prospects]. 219 41

Continuous monitoring of important respiratory indices has the potential for predicting catastrophes and for providing an opportunity for the timely institution of lifesaving measures. Pulmonary gas exchange can be assessed by indices derived from arterial blood gas measurements, but these are limited by their invasive and intermittent nature. Intra-arterial electrodes that provide a continuous recording of blood gases are under development and appear very promising. Specially designed pulmonary artery catheters permit continuous recording of mixed venous O2 saturation, whereas continuous, non-invasive recordings of arterial oxygenation can be obtained with pulse oximetry and transcutaneous electrodes. A satisfactory method of monitoring CO2 tension does not exist. Measurements of respiratory drive can be obtained at the bedside, but their clinical usefulness remains unknown. Assessment of respiratory muscle strength is helpful in determining the need for mechanical ventilation, but a practical method of diagnosing respiratory muscle fatigue remains elusive. Recordings of the airway pressure waveform, calculation of thoracic compliance, and detailed examination of the pattern of breathing are helpful in assessing pulmonary mechanics. Although respiratory monitoring provides much useful information, it does not substitute for careful bedside examination.
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PMID:Respiratory monitoring during mechanical ventilation. 219 1

Mechanical ventilation in 75 out of 560 status asthmaticus episodes during a five-year period (1984-1988) at Chulalongkorn Hospital were analyzed. There were 58 patients with an average age of onset of first asthmatic attack of 18.5 years and an average age when requiring mechanical ventilation of 33 years, which is significantly younger than among those who did not require assisted ventilation. At the time of intubation, four patients were in sudden unexpected arrest and 19 patients were urgently ventilated because of respiratory muscle fatigue or carbon dioxide narcosis; the remaining 52 patients required elective mechanical ventilation. The arterial blood gas of 52 patients revealed a pH of 7.11 +/- 0.66, PaCO2 of 58.0 +/- 5.5 mmHg, and HCO3 of 15.0 +/- 5.8 mEg/L. Controlled mechanical ventilation was maintained for a mean of 38.68 hours. Fifty-one patients required intravenous diazepam (average dose = 24.3 mg) and 37 required morphine (average dose = 11.1 mg) for good syncronization in controlling mechanical ventilation. Pneumothorax was the most common complication with four, nine and one episodes occurring prior to, during and after assisted ventilation, respectively. Four, one and two patients developed the complications of pneumonia, atelectasis of the left lung due to mucous plugging and upper gastrointestinal hemorrhage, respectively. There were six patients who died of complications: four of brain anoxia, one of pneumothorax and another of unexplained cause.
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PMID:Mechanical ventilation in status asthmaticus: experience with 75 episodes. 223 Jun 27

Central neurogenic hyperventilation (CNH), for which there is no effective therapy, can eventually result in respiratory fatigue and death. This report describes a patient with CNH due to a brainstem anaplastic astrocytoma who also exhibited disturbances of sleep and ocular motor function. The CNH responded clinically to morphine sulfate and methadone. Analysis of ventilatory response to CO2 before and after morphine demonstrated a depression of ventilatory response (49 to 53% of baseline) and occlusion pressure response (35 to 50% of baseline) to CO2, with a requirement for high doses of naloxone (10 mg IV) to reverse the effect. Polysomnography revealed sustained hyperventilation, elevated O2 saturation, and low end-tidal CO2 throughout all stages of non-rapid eye movement (NREM) sleep, and absence of rapid eye movement (REM) sleep. Ocular motor evaluation disclosed absence of horizontal and reflexive saccades with compensatory head thrusts. Correlation of the clinical and physiologic data with the MRI abnormalities suggested that the lesion responsible for CNH in this patient might reside in the medial tegmental parapontine reticular formation. Since recurrent episodes of hyperventilation responded in a sustained fashion to IV and oral opiates, this treatment may warrant consideration in other patients with CNH.
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PMID:Central neurogenic hyperventilation: pharmacologic intervention with morphine sulfate and correlative analysis of respiratory, sleep, and ocular motor dysfunction. 223 27

The effect of acute hypercapnia on skeletal muscle contractility and relaxation rate was investigated. The contractile force of fresh and fatigued quadriceps femoris (QF) and adductor pollicis (AP) was studied in normal humans by use of electrical stimulation. Maximum relaxation rate from stimulated contractions was measured for both muscles. Acute hypercapnia led to a rapid substantial reduction of contraction force. The respiratory acidosis after 9% CO2 was breathed for 20 min [mean venous blood pH 7.26 and end-tidal PCO2 (PETCO2) 65.1 Torr] reduced 20- and 100-Hz stimulated contractions of QF to 72.8 +/- 4.4 and 80.0 +/- 5.1% of control values, respectively. After 8 and 9% CO2 were breathed for 12 min, AP forces at 20- and 50-Hz stimulation were also reduced. Twitch tension of AP was reduced by a mean of 25.5% when subjects breathed 9% CO2 for 12 min [mean arterialized venous blood pH (pHav) 7.25 and PETCO2 66 Torr]. Over the range of 5% (pHav 7.38 and PETCO2 47 Torr) to 9% CO2, there was a linear relationship between twitch tension loss and pHav, arterialized venous blood PCO2, and PETCO2. Acute respiratory acidosis (mean PETCO2 61 Torr) increased the severity of low-frequency fatigue after intermittent voluntary contractions of AP. At 20 min of recovery, twitch tension was 63.2 +/- 13.4 and 46.8 +/- 16.4% of control value after exercise breathing air and 8% CO2, respectively. Acute hypercapnia (mean PETCO2 65.1 and 60.5 Torr) did not alter the maximum relaxation rate from tetanic contractions of fresh QF and from twitch tensions of AP.
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PMID:Effect of acute hypercapnia on limb muscle contractility in humans. 226 73

Factors contributing to maximal incremental and short-term exercise capacity were measured before and after 12 wk of high-intensity endurance training in 12 old (60-70 yr) and 10 young (20-30 yr) sedentary healthy males. Peak O2 uptake in incremental cycle ergometer exercise increased from 1.60 +/- 0.073 to 2.21 +/- 0.073 (SE) l/min (38% increase) in the old subjects and from 2.54 +/- 0.141 to 3.26 +/- 0.181 l/min (29%) in the young subjects. Peak cardiac output, estimated by extrapolation from a series of submaximal measurements by the CO2 rebreathing method, increased by 30% (from 12.7 to 16.5 l/min) in the old subjects, associated with a 6% increase (from 126 to 135 ml/l) in arteriovenous O2 difference; in the young subjects there were equal 14% increases in both variables (18.0 to 20.5 l/min and 140 to 159 ml/l, respectively). Submaximal mean arterial pressure and cardiac output were lower posttraining in the old subjects; total vascular conductance and cardiac stroke volume increased. Although peak power at the start of a short-term maximal isokinetic test did not change, total work accomplished in 30 s at a pedaling frequency of 110 revolutions/min increased in both groups, from 11.2 to 12.6 kJ and from 15.7 to 16.9 kJ in the old and young, respectively; fatigue during the 30-s test was less, and postexercise plasma lactate concentrations were lower. In older subjects, increases in aerobic power after high-intensity endurance training are at least as large as in younger subjects and are associated with increases in vascular conductance, maximal cardiac output, and stroke volume.
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PMID:High-intensity endurance training in 20- to 30- and 60- to 70-yr-old healthy men. 227 73

We studied the effect of aminophylline on twitch tension (TT) and intracellular pH (pHi) in isolated rat diaphragm strips that were fatigued, hypercapnic, or hypoxic. Superfused muscles were directly stimulated at 0.5 Hz. The pHi was measured from distribution volumes of dimethyl-oxazolidinedione. Fatigue was induced by intermittent tetanic stimulation. Hypercapnia and hypoxia were produced by altering superfusate carbon dioxide tension (PCO2) or oxygen tension (PO2). Aminophylline (1.0 mmol.l-1) reversed the twitch decay seen during fatigue or hypercapnic acidosis, and caused partial recovery of twitch depression during hypoxia. Muscle fatigue was not due to an intracellular acidosis. Both hypercapnia and hypoxia lowered pHi. Aminophylline did not alter pHi in unstimulated muscles, but caused a significant fall in pHi in stimulated muscles that were fatigued or hypoxic. High dose aminophylline improved twitch tension in diaphragm strips that were fatigued, acidotic, or hypoxic. Twitch potentiation was not due to an intracellular alkalosis. Aminophylline lowered pHi in stimulated muscle, and thus, theoretically, could sometimes be harmful in the treatment of muscle fatigue.
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PMID:The effect of aminophylline on function and intracellular pH of the rat diaphragm. 228 69

Changes in blood gases, ions, lactate, pH, hemoglobin, blood temperature, total body metabolism, and muscle metabolites were measured before and during exercise (except muscle), at fatigue, and during recovery in normal and acetazolamide-treated horses to test the hypothesis that an acetazolamide-induced acidosis would compromise the metabolism of the horse exercising at maximal O2 uptake. Acetazolamide-treated horses had a 13-mmol/l base deficit at rest, higher arterial Po2 at rest and during exercise, higher arterial and mixed venous Pco2 during exercise, and a 48-s reduction in run time. Arterial pH was lower during exercise but not in recovery after acetazolamide. Blood temperature responses were unaffected by acetazolamide administration. O2 uptake was similar during exercise and recovery after acetazolamide treatment, whereas CO2 production was lower during exercise. Muscle [glycogen] and pH were lower at rest, whereas heart rate, muscle pH and [lactate], and plasma [lactate] and [K+] were lower and plasma [Cl-] higher following exercise after acetazolamide treatment. These data demonstrate that acetazolamide treatment aggravates the CO2 retention and acidosis occurring in the horse during heavy exercise. This could negatively affect muscle metabolism and exercise capacity.
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PMID:Effects of acetazolamide on metabolic and respiratory responses to exercise at maximal O2 uptake. 231 72

Whilst the sequelae of extensive tuberculous infections generally manifest as an overall respiratory failure, characterised by a rise in the alveolar arterial gradient for oxygen and often CO2 retention, we report some observations on six patients with significant pleural and parenchymal tuberculosis; these patients presented with a restrictive syndrome associated with an apparently isolated alveolar hypoventilation. In four of these patients an effort test showed that there was adequate adaptation to alveolar ventilation on effort. In one patient measurement of PO.1 in a resting state and then during the course of a test of CO2 responsiveness revealed an absence of any response to CO2. On the basis of these results, we propose that in certain subjects suffering from significant sequelae of tuberculous disease the major functional abnormalities can be expressed as alveolar hypoventilation. This latter is not necessarily followed by a mechanical overload leading to an eventual fatigue of respiratory muscles but rather to a disorder of the regulation of ventilation. The basic mechanism of such an anomaly remains undetermined.
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PMID:[Isolated alveolar hypoventilation as a tubercular sequellae]. 232 Jul 85

A 35-year-old furniture refinisher came to the occupational medicine clinic with complaints of upper respiratory irritation, fatigue, and lightheadedness occurring on a daily basis after using a methylene chloride-containing paint stripper. Determinations of blood carboxyhemoglobin (COHb) on three occasions showed an apparently linear elevation of COHb as a function of hours worked on the day of sampling. COHb levels predicted from spot industrial hygiene measurements were in close concordance with those observed in the patient, indicating the potential usefulness of COHb monitoring in estimating airborne exposure levels. Methylene chloride (or dichloromethane) is an organic solvent that has found wide use as a degreaser, paint remover, aerosol propellant, and a blowing agent for polyurethane foams, and as a solvent in food processing, photographic film production, and plastics manufacturing. Discovery of its unusual metabolic fate--conversion to carbon monoxide in vivo--has earned the compound a special place in the solvent toxicology literature. Demonstration of oncogenicity in experimental animals has occasioned a reconsideration of exposure limits, with emphasis upon stricter controls. In some workplaces, conditions prevail in which controls are inadequate to prevent even acute toxicity, much less long-term exposure risks.
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PMID:Methylene chloride intoxication in a furniture refinisher. A comparison of exposure estimates utilizing workplace air sampling and blood carboxyhemoglobin measurements. 234 62


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