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

We describe a case of prolonged severe hypercapnia with respiratory acidosis occurring during an episode of near-fatal asthma in an 8-year-old boy, followed by complete recovery. After admission to the intensive care unit, despite treatment with maximal conventional bronchodilatative therapy, the clinical picture deteriorated with evident signs of respiratory muscle fatigue. The child was sedated, intubated and mechanically ventilated. Magnesium sulphate, ketamine and sevoflurane were gradually introduced together with deep sedation, curarization and continuous bronchodilatative therapy. Ten hours after admission, arterial pCO2 reached 39 kPa (293 mmHg), pH was 6.77 and pO2 8.6 kPa (65 mmHg). Chest radiograph showed severe neck subcutaneous emphysema, with signs of mediastinal emphysema. No episode of haemodynamic instability was seen despite severe prolonged hypercapnia lasting more than 14 h. Oxygenation was maintained and successful recovery followed without neurological or cardiovascular sequelae. This case shows the cardiovascular and neurological tolerance of a prolonged period of supercarbia in a paediatric patient. The most important lesson to be learned is the extreme importance of maintaining adequate tissue perfusion and oxygenation during an asthma attack. The second lesson is that when conventional bronchodilators fail, the intensivist may resort to the use of drugs such as ketamine, magnesium sulphate and inhalation anaesthesia. In this context deep sedation and curarization are important not only to improve oxygenation, but also to reduce cerebral metabolic requirements.
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PMID:Hypercapnia: what is the limit in paediatric patients? A case of near-fatal asthma successfully treated by multipharmacological approach. 1564 71

Noninvasive positive pressure ventilation in patients with stable chronic obstructive pulmonary disease. The role of non-invasive positive pressure ventilation (NIPPV) is well documented in patients with restrictive thoracic diseases like kyphoscoliosis, tuberculosis sequelae or neuromuscular disease. There is also a good evidence for the use of NIPPV in acute respiratory failure in patients with an exacerbation of COPD. The application of NIPPV in patients with chronic respiratory failure is growing, but there is less evidence than in restrictive disorders. NIPPV can unload the respiratory muscles in patients with chronic hypercapnic COPD and so alleviates fatigue of the respiratory pump, but improvement in the maximal inspiratory pressure (Pi (max)) is small or even absent. An improvement of sleep quality has also postulated, there was an increase in total sleep time and sleep effectiveness when using higher inspiratory pressure. An increase of the walking distance was shown in short term studies, only. In most studies, there was an increase in quality of life as a main topic. Mortality was unchanged in the two long-term randomised controlled studies. Current data suggest a possible role of NIPPV in patients with severe hypercapnia. A high effective inspiratory pressure and a ventilator mode with a significant reduction in the work of breathing should be choosen. NIPPV should be started in hospital, a close reassessment must be performed. Patients who accepted NIPPV in the first weeks had a good compliance for long-term use.
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PMID:[Noninvasive mechanical ventilation in patients with stable severe COPD]. 1521 36

Sleep hypoventilation is common in hypercapnic chronic obstructive pulmonary disease (COPD) and may contribute to daytime hypercapnia. The contributions of respiratory drive and respiratory mechanics to alterations in minute ventilation VI during sleep in this group have not been assessed. We assessed VI, breathing pattern, upper airway and total lung resistance (UAR, RL), intraoesophageal diaphragmatic EMG (EMGoes), intrinsic positive end-expiratory pressure (PEEPi), dynamic compliance (Cdyn), pressure-time product of oesophageal pressure (PTPoes), tension-time index of the diaphragm (TTIdi), end-expiratory lung volume (EELV) and respiratory drive (assessed as the slope of Poes versus time in the isovolumetric interval before PEEPi is overcome). Measurements were made in wakefulness and non-rapid eye movement (NREM) sleep, on 76%N2/24%O2 and on 76%He/24%O2 (heliox). Satisfactory data for analysis were obtained in 10 patients; five had measurements on heliox. VI fell from (mean (S.E.M.)) 8.84(0.46) to 6.64(0.91 l min(-1), P = 0.011) between wakefulness and stage II sleep, due to a fall in tidal volume. No changes were seen in PEEPi, Cdyn, EELV, PTPoes, TTIdi, EMGoes or respiratory drive. UAR increased (3.11(0.8) to 10.24(2.96) cm H2O l(-1) s (P=0.013) but RL was unchanged. UAR was reduced on heliox (5.20(1.67) to 3.45(1.35) cm H2O l(-1) s, P=0.049) but VI during sleep did not increase. PTPoes (350.2(51.0) to 259.4(46.3) cm H2O s min(-1), P=0.016), TTIdi (0.13(0.02) to 0.10(0.02) P=0.04), and respiratory drive (20.48(4.69) to 15.02(4.57) cm H2O s(-1), P=0.01) were all reduced. This suggests respiratory drive alters to maintain a preset VI in sleep, irrespective of load, at least while the fatigue threshold of respiratory muscles is not exceeded.
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PMID:Changes in respiration in NREM sleep in hypercapnic chronic obstructive pulmonary disease. 1523 77

There is significant controversy over the effects of hypercapnia on the human newborn brain. Previous studies have shown that 1 h of an arterial CO2 pressure (Paco2) of 80 mm Hg alters brain cell membrane Na+K+-ATPase enzyme activity in the cerebral cortex of newborn piglets. The present study tests the hypothesis that hypercapnia (either a Paco2 of 65 or 80 mm Hg) results in decreased energy metabolism and alters neuronal nuclear enzyme activity and protein expression, specifically Ca++/calmodulin-dependent kinase (CaMK) IV activity, phosphorylation of cAMP response element binding protein (CREB), and expression of apoptotic proteins in cortical neuronal nuclei of newborn piglets. Studies were performed in 20 anesthetized normoxic piglets ventilated at either a Paco2 of 65 mm Hg, 80 mm Hg, or 40 mm Hg for 6 h. Energy metabolism was documented by ATP and phosphocreatine (PCr) levels. Results show ATP and PCr levels were significantly lower in the hypercapnic groups than the normocapnic. CaMK IV activity, phosphorylated CREB density, and Bax protein expression were all significantly higher in the hypercapnic groups than the normocapnic group. Bcl-2 protein was similar in all three groups, making the ratio of Bax/Bcl-2 significantly higher in the hypercapnic groups than in the normocapnic group. We conclude that hypercapnia alters neuronal energy metabolism, increases phosphorylation of transcription factors, and increases the expression of apoptotic proteins in the cerebral cortex of newborn piglets and therefore may be deleterious to the newborn brain.
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PMID:Hypercapnia-induced modifications of neuronal function in the cerebral cortex of newborn piglets. 1558 83

The efficiency of the respiratory system presents significant limitations on the body's ability to perform exercise due to the effects of the increased work of breathing, respiratory muscle fatigue, and dyspnoea. Respiratory muscle training is an intervention that may be able to address these limitations, but the impact of respiratory muscle training on exercise performance remains controversial. Therefore, in this study we evaluated the effects of a 12-week (10 sessions week(-1)) concurrent inspiratory and expiratory muscle training (CRMT) program in 34 adolescent competitive swimmers. The CRMT program consisted of 6 weeks during which the experimental group (E, n = 17) performed CRMT and the sham group (S, n = 17) performed sham CRMT, followed by 6 weeks when the E and S groups performed CRMT of differing intensities. CRMT training resulted in a significant improvement in forced inspiratory volume in 1 s (FIV1.0) (P = 0.050) and forced expiratory volume in 1 s (FEV1.0) (P = 0.045) in the E group, which exceeded the S group's results. Significant improvements in pulmonary function, breathing power, and chemoreflex ventilation threshold were observed in both groups, and there was a trend toward an improvement in swimming critical speed after 12 weeks of training (P = 0.08). We concluded that although swim training results in attenuation of the ventilatory response to hypercapnia and in improvements in pulmonary function and sustainable breathing power, supplemental respiratory muscle training has no additional effect except on dynamic pulmonary function variables.
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PMID:Effects of concurrent inspiratory and expiratory muscle training on respiratory and exercise performance in competitive swimmers. 1594 67

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death, affecting 14 million adults in the United States. Symptoms related to sleep disturbances are common in moderate to severe COPD, particularly in elderly patients, in the form of morning tiredness and early awakenings. One major cause of morbidity in this population is abnormalities in gas exchange and resultant hypoxemia. Sleep has profound adverse effects on respiration and gas exchange in patients with COPD. There are several mechanisms underlying nonapneic oxygen desaturation during sleep. They include decreased functional residual capacity, diminished ventilatory responses to hypoxia and hypercapnia, impaired respiratory mechanical effectiveness, diminished arousal responses, respiratory muscle fatigue, diminished nonchemical respiratory drive, increased upper airway resistance, and the position of baseline saturation values on the oxyhemoglobin dissociation curve. Smoking cessation, bronchodilation, and pulmonary rehabilitation are cornerstones of treatment of COPD. Improvement in lung mechanics and gas exchange should lead to better sleep quality and health status.
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PMID:Sleep in chronic obstructive pulmonary disease. 1605 23

Hypoxia or hypercapnia impairs diaphragmatic contractility and induces fatigue. However, little is known about the combined effect of hypoxic and hypercapnic acidosis (HHA) on diaphragmatic fatigue. In this study, a gas mixture (21% O2, 12% CO2 and 67% N2) was used to produce HHA-induced rat diaphragmatic fatigue. Force-frequency relationships and twitch characteristics including peak twitch tension (PTT), time to peak tension (TPT), half relaxation time (1/2RT), maintaining tension (MT) and direct-muscle-stimulation tension (MST) were measured in diaphragm preparations from male SD rats. The HHA gas mixture attenuated force at all frequencies (5-120 Hz) and decreased PTT, MT and MST significantly. Aminophylline, a positive control drug, blocked the negative inotropic effect of HHA in a dose-dependent manner. Moreover, salmeterol, a long-acting beta2-adrenoceptor agonist, inhibited the harmful effect of HHA at high frequencies (40-120 Hz), but without effect on MT and MST. These results suggest that an in vitro HHA-induced rat diaphragmatic fatigue model could be established by aerating with the gas mixture, which may be an optimal model to screen effective drugs for diaphragmatic fatigue. Furthermore, salmeterol may play a protective role in HHA-induced impairment.
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PMID:An in vitro rat diaphragmatic fatigue model induced by combined hypoxic and hypercapnic acidosis and the effect of salmeterol. 1631 Mar 75

Rosiglitazone is a peroxisome proliferator active receptor. gamma agonist, which increases insulin sensitivity in adipose tissue, muscle, and liver. Rosiglitazone is a member of the thiazolidinedione group, and because of its significantly positive effect on glycemic control, it is especially preferred in type 2 diabetic patients with a high cardiovascular disease risk. This drug, because of its decreasing effect on insulin resistance, is used alone or combined with type 2 diabetic drugs. A 73-year-old female patient was admitted to the emergency department with dyspnea, pink frothing phlegm, cyanosis, and tiredness. She was lethargic, uncooperative, and had no orientation. In arterial blood gases, hypoxemia and hypercapnia were found. She was taken to the general intensive care unit, and oxygen was applied via mask. The patient had a history of 10 years of diabetes mellitus, hypertension, and atherosclerotic cardiac disease, and she was using rosiglitazone for the past 6 weeks. Her chest x-ray was taken, and acute pulmonary edema was diagnosed. In her last echocardiography, which was performed 1 year before, no signs indicating cardiac failure and pleural effusion could be found. Therefore, it was concluded that pulmonary edema occurred as a complication of rosiglitazone use. After stabilizing the patient's vital signs, blood glucose levels, and lactate levels, medical treatment of diabetes mellitus was rearranged, and she was discharged on the seventh day after her admittance. In a patient with diabetes mellitus who has been admitted to the intensive care unit because of acute pulmonary edema, for differential diagnosis, use of rosiglitazone should be kept in mind during the determination of treatment. Therefore, the authors aim to discuss the effect of rosiglitazone on creating acute pulmonary edema with a case report presentation.
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PMID:Acute pulmonary edema due to rosiglitazone use in a patient with diabetes mellitus. 1669 44

Respiratory failure as a result of overload and/or reduced capacity of the respiratory muscles is the most common cause of unsuccessful weaning and the need for long term mechanical ventilation. Chronic obstructive pulmonary disease (COPD) is the most common underlying cause leading into long term mechanical ventilation. The most important clinical parameter for fatigue of the respiratory muscles is the rapid shallow breathing index. Other essential factors which impact weaning failure, are the underlying diseases (e. g. neuromuscular disease or heart failure), micro- and macro aspiration, malnutrition, anemia and obesity. A protocol based strategy to discontinue mechanical ventilation and the use of weaning predictors are helpful. Nonetheless the experienced physician is irreplacable in the weaning process. Reconditioning of the respiratory muscles is the main focus during weaning after long term mechanical ventilation and all therapeutic measures should be targeted to unload the fatiguing respiratory muscles. With the widely used assisted ventilation modes, the inspiratory work of breathing is still significantly increased. Only controlled mechanical ventilation (pressure- or volume controlled), which may also be applied to unsedated patients when individually adapted, offers the best possible relief and recovery of the respiratory muscles. Additional strategies, such as the balancing of anemia, reduction of the respiratory drive with i. e. morphine derivates, oxygen therapy during spontaneous-breathing trials and supine position for patients with obesity contribute to the recovery. Particularly patients with chronic lung diseases with hypercapnia benefit from the use of non invasive ventilation (NIV) after extubation to prevent postextubation failure and even after tracheostomy. However, NIV should only be applied under close monitoring and in cooperative patients, always considering the limits of the method. Dying under mechanical ventilation in the end stage illness is still a challenge for all involved persons. In the end stage of their disease for some patients it is possible to discontinue mechanical ventilation so they can spend the last period of their lives on a normal ward or even at home.
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PMID:[Difficult weaning]. 1704 78

The mechanisms underlying acute respiratory failure induced by respiratory loads are unclear. We hypothesized that, in contrast to a moderate inspiratory resistive load, a severe one would elicit central respiratory failure (decreased respiratory drive) before diaphragmatic injury and fatigue. We also wished to elucidate the factors that predict endurance time and peak tracheal pressure generation. Anesthetized rats breathed air against a severe load ( approximately 75% of the peak tracheal pressure generated during a 30-s occlusion) until pump failure (fall in tracheal pressure to half; mean 38 min). Hypercapnia and hypoxemia developed rapidly ( approximately 4 min), coincident with diaphragmatic fatigue (decreased ratio of transdiaphragmatic pressure to peak integrated phrenic activity) and the detection in blood of the fast isoform of skeletal troponin I (muscle injury). At approximately 23 min, respiratory frequency and then blood pressure fell, followed immediately by secondary diaphragmatic fatigue. Blood taken after termination of loading contained cardiac troponin T (myocardial injury). Contrary to our hypothesis, diaphragmatic fatigue and injury occurred early in loading before central failure, evident only as a change in the timing but not the drive component of the central respiratory pattern generator. Stepwise multiple regression analysis selected changes in mean arterial pressure and arterial Pco(2) during loading as the principal contributing factors in load endurance time, and changes in mean arterial pressure as the principal contributing factor in peak tracheal pressure generation. In conclusion, the temporal development of respiratory failure is not stereotyped but depends on load magnitude; moreover respiratory loads induce cardiorespiratory, not just respiratory, failure.
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PMID:Cardiorespiratory failure in rat induced by severe inspiratory resistive loading. 1713 35


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