Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cellular mechanism of muscle fatigue is still in debate. Opposite conclusions regarding the role of intracellular pH (pHi) in fatigue have been drawn from skinned fiber vs. isolated perfused muscle studies. Because these experiments are typically performed at different temperatures, we tested the hypothesis that temperature alters the effects of pH on force. Tetanic force of isolated mouse extensor digitorum longus was measured at temperatures between 13 and 25 degrees C in either normocapnia (5% CO2) or hypercapnia (25% CO2). Hypercapnia decreased pHi (monitored by 31P nuclear magnetic resonance spectroscopy) by the same amount at both 15 and 25 degrees C. However, inhibition of force by hypercapnia was greater at the lower temperature. A similar pattern of temperature-dependent inhibition of force by pH was observed in glycerinated fibers from rabbit psoas at maximum Ca2+ activation. We conclude that temperature differences are responsible for disparate conclusions on the role of pHi in muscle fatigue. Based on our results, we suggest that changes in pHi may have little or no role in the loss in force production associated with muscular fatigue at physiological temperatures.
 ...
PMID:Effect of intracellular pH on force development depends on temperature in intact skeletal muscle from mouse. 884 18

Weaning failure is, unfortunately, a rather common phenomenon for mechanically-ventilated patients (especially those with chronic obstructive pulmonary disease (COPD)), and the respiratory muscles play a pivotal role in its development. Weaning fails whenever an imbalance exists between the ventilatory needs and the neurocardiorespiratory capacity. This can happen if there is an increase in the energy demands of the respiratory muscles, a decrease in the energy available, a decrease in neuromuscular competence, or if the respiratory muscles pose an impediment to the heart and blood flow. The imbalance created will lead to weaning failure through the development of respiratory muscle fatigue, hypercapnia, dyspnoea, anxiety and organ dysfunction.
 ...
PMID:Respiratory muscles and weaning failure. 894 90

Impaired pulmonary gas exchange can result from lung parenchymal failure inducing oxygenation deficiency and fatigue of the respiratory muscles, which is characterized by hypercapnia or a combination of both mechanisms. Contractility of and coordination between the diaphragm and the thoracoabdominal respiratory muscles predominantly determine the efficiency of spontaneous breathing. Sepsis, cardiac failure, malnutrition or acute changes of the load conditions may induce fatigue of the respiratory muscles. Augmentation of spontaneous breathing is not only achieved by the application of different technical principles or devices; it also has to improve perfusion, metabolism, load conditions and contractility of the respiratory muscles. Intermittent mandatory ventilation (IMV) allows spontaneous breathing of the patient and augments alveolar ventilation by periodically applying positive airway pressure tidal volumes, which are generated by the respirator. Potential advantages include lower mean airway pressure (PAW), as compared with controlled mechanical ventilation, and improved haemodynamics. Suboptimal IMV systems may impose increased work and oxygen cost of breathing, fatigue of the respiratory muscles and CO2 retention. During pressure support ventilation (PSV), inspiratory alterations of PAW or gas flow (trigger) are detected by the respirator, which delivers a gas flow to maintain PAW at a fixed value (usually 5-20 cm H2O) during inspiration. PSV may be combined with other modalities of respiratory therapy such as IMV or CPAP. Claimed advantages of PSV include decreased effort of breathing, reduced systemic and respiratory muscle consumption of oxygen, prophylaxis of diaphragmatic fatigue and an improved extubation rate after prolonged periods of mechanical ventilation. Minimum alveolar ventilation is not guaranteed during PSV; thus, close observation of the patient is mandatory to avoid serious respiratory complications. Continuous positive airway pressure breathing (CPAP) maintains PAW above atmospheric pressure throughout the respiratory cycle, which may increase functional residual capacity and decrease the effort of breathing. CPAP has been conceptually designed for the augmentation of spontaneous breathing and requires the intact central and peripheral regulation of the respiratory system. Airway pressure release ventilation (APRV) improves alveolar ventilation by intermittent release of PAW, which is kept above atmospheric pressure by means of a high-flow CPAP system. The opening of an expiratory valve for 1-2 s induces a decreased PAW and lung volume, which increases rapidly to pre-exhalation values after closure of the valve due to the high gas flow within the circuit (90-100 1/min). APRV may improve haemodynamics and VA/Q distribution as compared with conventional mechanical ventilation. Biphasic positive airway pressure (BIPAP) is characterized by the combination of spontaneous breathing and time-regulated, pressure-controlled mechanical ventilation. During the respiratory cycle the ventilator generates two alternating CPAP levels, which can be modified with regard to time and pressure. As with APRV, alveolar ventilation is maintained even if the spontaneous breathing efforts of the patient cease, which improves the safety of both modes of respiratory therapy. The contribution of spontaneous breathing to total minute ventilation may be important, since a decreased shunt and improved VA/Q relationship have been observed in experimental non-cardiogenic lung oedema. These data give support to the concept that spontaneous breathing should be maintained and augmented in the setting of acute respiratory failure.
 ...
PMID:[Augmented spontaneous breathing]. 896 3

We studied 20 patients with obstructive sleep apnea syndrome (OSAS) prospectively, before and after administering continuous positive airway pressure through a nasal mask (CPAPn) at night for 10 months, with the aim of determining the effects of ventilatory pattern of long-term treatment with CPAPn in OSAS patients. The following data were collected for all patients: anthropometric variables, lung function test results, arterial gasometric readings at rest, oxygen alveolar-arterial differential [Dif(A-a)O2)], central respiratory function variables at rest and during hypercapnic stimulus. Mean duration (range) of treatment with CPAPn was 12.5 (10-18) months. We observed a significant increase in PaO2 (p = 0.01) and a decrease in PaCO2 (p = 0.02) with slight variations in body weight and no changes in lung mechanics or in Dif(A-a)O2. The ventilatory pattern at rest showed an increased in VE and in respiratory frequency (p = 0.0003 and p = 0.033, respectively) with non significant changes in VT. The VT/Ti ratio increased (p = 0.015) and P0.1 decreased slightly (p = 0.025). We found no significant changes in the CO2 response slopes of VE or P0.1. In conclusion, CPAPn improves hypoxemia and hypercapnia in OSAS patients, above all by increasing baseline basal ventilation. The exact mechanisms implicated are poorly understood, but our data suggest a certain direct or indirect effect on respiratory muscles, reducing muscle fatigue, thus favoring greater availability during sleep.
 ...
PMID:[Long-term effects of nasal continuous positive airway pressure on ventilatory patterns of patients with obstructive sleep apnea syndrome]. 928 May 59

We previously reported that patients with spinal muscular atrophy do not lose muscle strength over time as measured quantitatively. However, we noted that many patients with spinal muscular atrophy suffer from what they call fatigue. We wondered if we could measure fatigue during a single maximal voluntary contraction, whether fatigue might increase with time, independent of muscle strength, and whether increasing fatigue might correlate with loss of function in some patients. We measured fatigue during a single maximal voluntary contraction in a cohort of patients having spinal muscular atrophy using quantitative strength testing. We included only patients with spinal muscular atrophy aged 5 years or older, so they could follow instructions regarding muscle contraction, and who were followed for at least 2 years. Seventy-six children with spinal muscular atrophy and 24 untrained individuals, aged 5 to 57 years (mean, 16.8 years), were studied. There was no discernible abnormal fatigue in patients with spinal muscular atrophy compared to untrained controls using our methodology. Thus, spinal muscular atrophy may not be associated with fatiguability. Moreover, spinal muscular atrophy does not appear to cause progressive muscle fatigue with age or loss of function. It is possible that fatigue was undetectable by our methods. An alternative explanation is that what patients describe as fatigue may be caused by factors outside the neuromuscular system. Such factors may include chronic respiratory insufficiency with hypoventilation and carbon dioxide retention as well as chronic malnutrition and negative nitrogen balance.
 ...
PMID:Muscle fatigue in spinal muscular atrophy. 937

Although fatigue of the inspiratory muscles has been well documented, its prevalence in patients with chronic obstructive pulmonary disease (COPD) and its influence on mortality are unknown, because of the lack of a simple, clinically available diagnostic test. The hypothesis and experimental evidence relating inspiratory muscle dysfunction to the development of hypercapnia and hypercapnic ventilatory failure are reviewed. Since a poor prognosis in COPD is associated with carbon dioxide retention, inspiratory muscle weakness and/or fatigue may have an association with survival in these patients.
 ...
PMID:Inspiratory muscle dysfunction as a cause of death in COPD patients. 940 71

The development of fatigue was investigated in the diaphragm of anaesthetized, tracheostomized, spontaneously breathing cats during restricted air flow. Ventilation, transdiaphragmatic pressure (Pdi), integrated electrical activity of diaphragm (Edi) and phrenic nerve (Eph) were measured simultaneously and expressed as a percentage of values at unloaded breathing. Inspiratory loads were 60, 70 and 80% of Pdi max. The Pdi max was measured by airway occlusion at functional residual capacity. The duration of loads was 40-60 min. The diaphragmatic fatigue developed only during heavy inspiratory loading (80% Pdi max). During the first 10 min of heavy load Pdi, Edi and Eph increased to 905 +/- 60%, 248 +/- 20% and 229 +/- 24%, respectively (P < 0.01), and then began to fall gradually. Ventilation declined to 39 +/- 3% after 60 min of heavy load (P < 0.01), resulting in acute hypercapnia and hypoxia. Initial fatigue appeared as a decrease in Pdi (to 781 +/- 63%) and parallel decline in Edi (to 233 +/- 21%) after 30 min of load (P < 0.05). Phrenic nerve activity did not change during this stage. These data suggest a peripheral basis of diaphragmatic fatigue, related to disorders in neuromuscular transmission. After 60 min of heavy load, Pdi fell to 675 +/- 49%, Edi declined to 209 +/- 28% and Eph decreased to 189 +/- 25%. We interpret the decrease in phrenic nerve activity as a weakening of central inspiratory drive and development of the central component of diaphragmatic fatigue in the last stage.
 ...
PMID:Central and peripheral components of diaphragmatic fatigue during inspiratory resistive load in cats. 940 88

The purpose of this study was to determine the relationship between intrathoracic pressure (delta ITP) and diaphragm shortening (DS) during the development of diaphragm fatigue. Fatigue of the diaphragm was produced by having rats breath 15% CO2 in O2. Diaphragm shortening increased significantly to 178% of control during the first 5 min of hypercapnia and then decreased to 86% of control at approximately 80 min. Twenty minutes after terminating hypercapnia, DS increased to 115% of the prehypercapnic value. delta ITP increased to 199% of control following 5 min of hypercapnia and continued to increase, reaching 267% of control at the end of the hypercapnic period. Twenty minutes later, delta ITP was 147% of control. These results illustrate that during increased respiratory work, DS can decrease while intrathoracic pressure remains increased. These findings suggest that intrathoracic pressure may not always reflect the contractile status of the diaphragm. These findings are consistent with other studies indicating that as the diaphragm fatigues, accessory respiratory muscle activity increases to maintain delta ITP.
 ...
PMID:Diaphragm shortening and intrathoracic pressure during hypercapnia in rats. 951 16

1. Given the importance of the ventilatory 'pump' muscles, it would not be surprising if they were endowed with both sensory and motor specializations. The present review focuses on some unexpected properties of the respiratory muscle system in human subjects. 2. Although changes in blood gas tension were long held not to influence sensation directly, studies in subjects who are completely paralysed show that increases in arterial CO2 levels elicit strong sensations of respiratory discomfort. 3. Stretch reflexes in human limb muscles contain a monosynaptic spinal excitation and a long-latency excitation. However, inspiratory muscles show an initial inhibition when tested with brief airway occlusions during inspiration. This inhibition does not depend critically on input from pulmonary or upper airway receptors. 4. Human inspiratory muscles (including the diaphragm) have been considered to fatigue during inspiratory resistive loading. However, recent studies using phrenic nerve stimulation to test the force produced by the diaphragm show that carbon dioxide retention (hypoventilation) and voluntary cessation of loading occur before the muscles become overtly fatigued.
 ...
PMID:Human respiratory muscles: sensations, reflexes and fatiguability. 978 13

Noninvasive long-term ventilation is consensually advocated when daytime hypercapnia > 6 kPa at steady state in chronic restrictive pulmonary syndromes. Several mechanisms can cause the occurrence of hypercapnia in these diseases. They may involve impairment of lung mechanics or airway function and cough, ventilation-perfusion mismatching, blunted central ventilatory drive or respiratory muscle fatigue. These abnormalities may occur while awake or during sleep. From a practical point of view, imperative ventilation, a palliative technique that aims to supply respiratory muscle weakness, and preventive ventilation, aimed at delaying respiratory handicap, should be distinguished between. The latter is offered to patients who do not fulfil any criteria for mechanical ventilation. Otherwise, the underlying disease markedly influences both pathophysiology and outcome. This implies that the available modes of ventilatory support should be assessed in each disease. Several findings have been published about Duchenne's muscular dystrophy. Mechanical ventilation, usually using noninvasive methods, is offered to patients with either hypercapnia or a forced vital capacity < 20% of the predicted value. Nevertheless, based on our experience, deterioration of the restrictive syndrome should be followed by a tracheostomy. By contrast, early ventilation, offered to patients free of symptoms and whose forced vital capacity are within 20-50% pred and with normal arterial blood gas levels, achieves no benefit.
 ...
PMID:Is early noninvasive mechanical ventilation of first choice in stable restrictive patients with chronic respiratory failure? 1021 81


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>