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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied diaphragmatic muscle function during inspiratory flow resistive (IFR) loaded breathing in unanesthetized sheep. We measured the change in transdiaphragmatic pressure (dPdi) and arterial blood gas tensions and recorded diaphragmatic electromyogram (EMG) from electrodes implanted on the muscle. We found that, with IFR loads less than 150 cmH2O X l-1 X s, dPdi and the integrated EMG increased, reached a plateau, and were maintained at high levels. The centroid frequency (fc) of the EMG power spectrum did not consistently change. With IFR loads greater than 150 cmH2O X l-1 X s, O2 was administered to prevent hypoxia, cyanosis, and agitation. With these loads, dPdi increased severalfold above base line, reached a plateau, and then started to decrease. Arterial PCO2 increased sharply at the time when dPdi decreased. The integrated EMG (iEMG) and fc started to decrease gradually 10-20 min before dPdi started to decrease. We conclude that 1) the diaphragm is capable of generating large pressures for prolonged periods with no evidence of fatigue; 2) with very high IFR loads, mechanical failure of the diaphragm can occur in the unanesthetized awake sheep; 3) diaphragmatic fatigue is associated with acute hypercapnia and therefore failure of the entire respiratory pump; and 4) a decrease in iEMG and a concommitant shift in the power spectrum density towards lower frequencies precede the mechanical failure of the diaphragm.
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PMID:Diaphragmatic fatigue in unanesthetized adult sheep. 646 79

When the ventilatory muscles are unable to develop the required force as it occurs during fatigue, hypercapnic respiratory failure ensues. We present evidence that when the respiratory muscles work in a fatiguing load domain the central controllers respond at an early stage with tachypnea, while when the muscles fail bradypnea ensues which is followed by apnea. Although bradypnea and apnea in addition to muscle inability to develop force may reduce alveolar ventilation by virtue of reducing the total minute ventilation, tachypnea may also be followed by hypercapnia at constant total minute ventilation by virtue of a reduction in tidal volume (VT). Such a strategy will increase the ratio of dead space (VD) to tidal volume (VD/VT) and PCO2 will rise. It is argued that this mechanism could satisfactorily explain the high levels of CO2 in patients with chronic obstructive lung disease, as well as the CO2 retention at an early stage in acute cases of fatigue during, for example, the weaning period of a patient from the respirator. Bradypnea and apnea contribute to CO2 retention at a later stage, when the muscles are exhausted and total ventilation decreases. This sequence in frequency of breathing is explained as an advantageous strategy adopted for the respiratory muscles, because it allows the muscles to operate at an optimal length. It is also hypothesized that muscle afferents, probably via the small fibers III and IV and/or Golgi and tendon organs, are responsible for this interaction of CNS and respiratory muscles.
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PMID:Ventilatory muscle fatigue governs breathing frequency. 650 21

The use by West et al. of gases with different solubilities and of appropriate models has indicated that impairment of gas exchange in patients with chronic obstructive pulmonary disease and respiratory failure resulted essentially from altered ventilation/perfusion ratios. To understand why some patients do not appear to be capable of compensating this impairment and become hypercapnic, it is necessary to examine the other components of the respiratory system (control of ventilation, respiratory muscles) and their interactions. The measurement of occlusion pressure and of average inspiratory flow, and analysis of the timing of the respiratory cycle provides interesting information on the output of the control system and the efficiency of respiratory muscles. Electromyography of respiratory muscles also affords useful information on the degree of fatigue of these muscles. The use of this data should help to clarify the problem that has remained unanswered for many years: is the patient with hypercapnia someone who does not want to, or cannot, increase his ventilation? Other studies in the same group of patients during sleep have supplied evidence for the presence of numerous episodes of arterial oxygen desaturation with marked effects on the cardiovascular system. Pathophysiology should also consider this aspect of respiratory failure which occurs in the third of our lifetime devoted to sleep.
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PMID:[Physiopathology of chronic respiratory insufficiency]. 678 66

We have previously shown that the chemosensitivity of the respiratory centers is well preserved in myotonic dystrophy but that the ventilatory output is reduced. The present study was designed to determine at which degree of ventilatory performance weakness and fatigability of the respiratory muscles are interfering with ventilation and which mechanical factors contribute to the tachypnea of patients with myotonic dystrophy at rest and during low ventilatory output. We studied 10 patients with the disease and 10 normal control subjects. The strength of respiratory muscles was assessed by measurements of maximal pressure-volume diagrams generated against airway occlusion. Performance was evaluated during 1-min maximal voluntary ventilation (1-min MVV) test, during 7-min 7% CO2 breathing and during quiet breathing. Occlusion pressure (P0.1) in patients at rest was slightly higher than in control subjects, and during CO2 breathing, it was similar to that of control subjects. Maximal static pressure was reduced in patients to an average of 35% of that of control subjects. During the 1-min MVV test, there was a 50% reduction in esophageal and transdiaphragmatic pressure output (Pes, Pdi) in patients, resulting in similar reduction in ventilation (VE) and patients had rapid cycles of alternating dominant thoracic and abdominal volume displacements (Vrc/Vabd) suggesting respiratory muscle fatigue. During the 3- to 4-fold increase in breathing drive induced by hypercapnia, pressure output and the Vrc/Vabd were identical in both groups. However, ventilation was reduced in patients who had tachypneic respiration. In patients, tachypnea was also observed during quiet breathing. This tachypnea was associated with higher impedance of the respiratory system (Zrs) in patients and identical impedance of the lung (ZL) in both groups. In addition, Pdi during tidal volume was significantly higher in patients. These data demonstrate that the ventilatory output in out patients was altered predominantly by weakness and fatigability of the respiratory muscles during high ventilatory performance and by increased impedance of the respiratory system at lower degrees of ventilation.
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PMID:Pathogenesis of respiratory insufficiency in myotonic dystrophy: the mechanical factors. 680 50

Twelve patients exhibiting difficulties during discontinuation of artificial ventilation permitted us to investigate physical examination techniques used in diagnosing inspiratory muscle fatigue. Diaphragmatic and intercostal electromyographic tracings, arterial blood gases, rate and depth of ventilation, and thoracoabdominal motion were monitored during spontaneous breathing. Six patients showed electromyographic evidence of inspiratory muscle fatigue. A sequence of events leading to respiratory acidemia emerged--namely electromyographic evidence of fatigue, accompanied or followed by an increased respiratory rate, in turn followed by alternation between abdominal and rib cage breathing (respiratory alternans), paradoxical inward abdominal motion during inspiration (abdominal paradox), and finally an increase in PaCO2 associated with a fall in minute ventilation and respiratory rate, and worsening of respiratory acidemia. The abnormalities of respiratory movements may be reliable clinical signs of inspiratory muscle fatigue, particularly when accompanied by tachypnea and hypercapnia.
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PMID:Clinical manifestations of inspiratory muscle fatigue. 681 17

A new method for the detection and recording of the oculocardiac reflex (OCR) is described and applied to 49 healthy infants and children (six months to nine years old) undergoing strabismus surgery under halothane anaesthesia with spontaneous ventilation. Eighty-one extraocular muscles were studied. Square wave stimuli (abrupt and sustained tractions) were definitely more reflexogenic than slow slope stimuli (very gradual, progressive and gentle tractions). Vagal escape, as well as fatigue of the OCR, are graphically documented and analysed. In this series, using well-defined and controlled tractions, the medial rectus was not more reflexogenic than the other extraocular muscles. Hypercapnia was an important adjuvant factor of the OCR. Controlled ventilation is recommended. The routine use of intravenous anticholinergic drugs is briefly discussed. Prevention of the OCR, and prophylaxis of cardiac arrhythmias during strabismus surgery, now seem to be placed on a more rational basis.
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PMID:The oculocardiac reflex: a graphic and statistical analysis in infants and children. 687 77

This report describes a patient with primary alveolar hypoventilation who, after 2 yr of successful treatment with nocturnal oxygen, developed severe hypoxemia and hypercapnia during sleep, morning headaches, and daytime fatigue. Sleep studies demonstrated prolonged periods of hypoventilation and apnea without evidence of upper airway occlusion. Therefore, a phrenic nerve stimulator was implanted to allow pacing of the diaphragm during sleep. However, diaphragm pacing was accompanied by paradoxical movement of the rib cage and upper airway occlusion during sleep, and was unsuccessful in maintaining adequate ventilation. Therefore, the patient underwent a tracheostomy after which diaphragm pacing maintained adequate nocturnal ventilation; however, paradoxical movement of the rib cage persisted. The induction of upper airway occlusion as a result of diaphragm pacing, in contrast to the absence of occlusion during spontaneous breathing, highlights the importance of the normal temporal coordination of inspiratory activation of the upper airway muscles and diaphragm. The findings have important implications for the pathogenesis of obstructive sleep apneas in general.
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PMID:Upper airway occlusion induced by diaphragm pacing for primary alveolar hypoventilation: implications for the pathogenesis of obstructive sleep apnea. 697 4

The effects of oxygenation and hypercapnia on diaphragmatic function and central drives were assessed during the development of respiratory failure in anesthetized unbound spontaneously breathing rabbits. Oxygenation significantly altered endurance times, whereas hypercapnia had no effect. Isolated high-frequency contractile fatigue of the diaphragm was found in hyperoxic animals; all other animals had no evidence of contractile fatigue. Oxygenation and hypercapnia did not significantly alter the response of breathing frequency or duty cycle to loading. In all animals, there was a falloff in the intensity of central drive before apnea, with intensity of central drive remaining submaximal throughout loading. Oxygenation significantly altered the time and/or load at which drive intensity fell off, although critical blood gas levels were not associated with the falloff in intensity. We conclude that oxygenation influences the development of respiratory failure during inspiratory loading but does not directly explain the alterations is central drive. On the other hand, hypercapnia has no direct effect on respiratory muscle function or central drives during loading to respiratory failure. When the effects of hypoxemia are obviated by hyperoxia, high-frequency contractile fatigue may occur.
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PMID:Effects of oxygenation and hypercapnia on diaphragmatic function and central drive during respiratory failure. 764 10

Persons with sleep apnea syndromes experience 10 or more episodes per hour of sleep during which airflow ceases for more than 10 seconds. Sleep apnea syndromes are classified as obstructive, central or mixed: obstructive when the respiratory muscles continue to contract but airflow is not obtained, central when respiratory effort is not present, and mixed when elements of both obstructive and central apnea are present. Approximately 4 percent of adult men and 2 percent of adult women are believed to have these conditions. In addition to having symptoms such as snoring, headaches, depression, decreased libido and fatigue, patients with sleep apnea are at risk for a range of severe complications secondary to recurrent hypoxia and hypercapnia during sleep. Diagnosis may require an overnight polysomnogram in addition to the history, a physical examination and a laboratory assessment. Less cumbersome diagnostic modalities are being developed. Treatment options include weight reduction, change in sleeping position, avoidance of sedatives, use of continuous positive airway pressure and surgical treatment.
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PMID:Adult sleep apnea syndromes. 765 25

Chronic obstructive pulmonary disease (COPD) have several pathophysiological characteristics in common, the main one being an increased airways resistance (raw). It is the result of bronchial abnormalities and reduced parenchymal elasticity, and is influenced by lung volume. Raw decreases with increasing lung volume, and increases with decreasing lung volume. Such expiratory events are generally compensated on the inspiratory side. Inspiration is shortened to prolong expiration, and breathing takes place at higher lung volume to take benefit of the higher lung recoil. This inspiratory load is associated to an increased inspiratory drive, and contributes to put inspiratory muscles at disadvantage. However, with time, adaptative changes take place that restore their force at a shorter length. Chronic fatigue, often suspected in this setting, is therefore not currently demonstrated. Bronchial and parenchymal abnormalities lead to ventilation-perfusion mismatch, that contribute to hypoxemia and hypercapnia through deadspace and shunt effects. Hypercapnia can also correspond in part to protective mechanisms, if the energy requirements for its maintenance are too high.
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PMID:[Physiopathology of COPD (steady-state)]. 765 65


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