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

A prospective evaluation of the prevalence of CO2 retention and its relationship to lung mechanics and inspiratory muscle strength was carried out in 311 clinically stable patients with chronic obstructive pulmonary disease (COPD). Of these patients 32.8% had hypercapnia (PaCO2 greater than or equal to 43 mm Hg). PaCO2 was directly related to lung resistance (RL; r = 0.53) and inversely related to FEV1 (r = 0.53) and to an expression of the dead space/tidal volume ratio (1 - VD/VT) (r = 0.48). RL was found to be a major determinant of the mean intrathoracic pressure swing developed during inspiration (PI) at rest (r = 0.85). Maximal inspiratory pressure (PImax) was found to improve the predictive value for PaCO2 of several mechanical loads, with RL/PImax the best predictor (r = 0.57). The prevalence of hypercapnia increased from virtually 0 to 100% with increases in the RL/PImax value and was higher in the obese subjects at intermediate RL/PImax values, probably because of the burden placed on the respiratory muscles by chest wall mass loading. Our results show that chronic alveolar hypoventilation is likely to develop in COPD patients who have a combination of high inspiratory loads and inspiratory muscle weakness. hypercapnia may be one strategy available to avoid overloading of the inspiratory muscles leading to fatigue and possible irreversible failure.
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PMID:Inspiratory muscle dysfunction and chronic hypercapnia in chronic obstructive pulmonary disease. 202 40

Three patients with respiratory muscle weakness developed sleep fragmentation due to nonobstructive apnea and hypopnea. In two patients in whom inspiratory muscle electromyogram was recorded, the apneas and hypopneas were terminated only by arousal and excessive recruitment of accessory muscles. Nocturnal rocking bed ventilatory support resulted in immediate improvement in sleep fragmentation and inhibited arousal-associated phasic accessory muscle activation, resulting in improvement in daytime hypercapnia and subjective sleepiness. Sleep fragmentation may occur more commonly than generally appreciated in neuromuscular disease patients who are independent of daytime ventilatory support. The use of nocturnal rocking bed is an effective noninvasive method of reversing sleep fragmentation and daytime sequelae when obstructive apnea is absent.
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PMID:Nocturnal rocking bed therapy: improvement in sleep fragmentation in patients with respiratory muscle weakness. 279 14

We report a study of an adult with a maltase acid deficiency myopathy. A restrictive respiratory syndrome due to respiratory muscle weakness is associated with paralysis of other muscular groups. In 1982 the patient presented with an alveolar hypoventilation, and mechanical ventilation was required after acute respiratory failure. The patient has received nocturnal mechanical ventilation by tracheostomy at home for 5 years. His clinical status gradually improved in parallel to amelioration of his respiratory condition. Functional respiratory tests improved: initial hypoxia-hypercapnia disappeared, vital capacity increased. The possible mechanisms underlying the improvement are discussed. Increase in pulmonary compliance is an argument to explain the functional improvement observed. Ventilatory response to carbon dioxide was abnormal whereas the ventilatory response to exercise and maxima minute ventilation test were normal. Results are consistent with a respiratory control impairment. The role of mechanical ventilation is difficult to assess in the improvement we observed.
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PMID:Adult maltase acid deficiency myopathy: treatment with long-term home mechanical ventilation. 305 36

The functional anatomy of the respiratory muscles has been reviewed. The diaphragm has been emphasized, since this is the most important inspiratory muscle, but the view has been presented that the intercostal, scaleni, and other accessory inspiratory muscles become increasingly important as airflow obstruction leads to hyperinflation. As work increases, the demand for energy and hence blood flow to those muscles has to increase. In spite of a large reserve there are situations in which demands may outstrip supply. This leads to local metabolic changes that result in muscle fatigue. We are now capable of detecting this change as alterations in EMG or in the ability to generate pressures. The latter leads to a decrease in the capacity of the respiratory pump to exchange gas, ultimately resulting in hypercapnia and hypoxemia. The true importance of respiratory muscle fatigue and its differentiation from weakness in patients with severe CAO requires more analysis. It is intuitively appropriate to address the overall decrement in the ability to maintain adequate ventilatory work at low energy cost with the different therapeutic modalities thought to be beneficial. A combination of a decrease in the load imposed on the respiratory muscles, an improvement in the contractility of those muscles, and, when there is absolute need, the resting of the fatigued muscles should result in a better chance to lead a meaningful life and perhaps to improve survival in these patients.
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PMID:Respiratory muscle function. 353 72

Severe nocturnal hypoxemia may occur in patients with respiratory muscle weakness caused by neuromuscular disorders. Negative pressure ventilators may be partially effective in these patients but can cause upper airway obstructive apneas. We examined the effectiveness of positive pressure ventilation through a nose mask in preventing nocturnal hypoxemia and compared it with negative pressure systems. We reasoned that nasal positive pressure would provide stability for the upper airway. Five patients with neuromuscular disorders underwent a series of all-night sleep studies under control conditions, negative pressure ventilation, and positive pressure ventilation through a comfortable nose mask. Sleep staging and respiratory variables were monitored during all studies. Daytime awake lung function, respiratory muscle strength, and arterial blood gases were also measured. The severe hypoxemia and hypercapnia that occurred under control conditions were prevented by positive pressure ventilation through a nose mask. Negative pressure ventilation improved NREM ventilation in all patients, but did not prevent severe oxyhemoglobin desaturation, which occurred during REM sleep. Negative pressure ventilation appears to contribute to upper airways obstruction during REM sleep as evidenced by cessation of air flow, reduced chest wall movements, falls in arterial oxyhemoglobin saturation, and hypercapnia. With treatment, daytime PaO2 improved from a mean of 70 to 83 mm Hg, and PaCO2 decreased from a mean of 61 to 46 mm Hg. We conclude that nasally applied positive pressure ventilation is a highly effective method of providing nocturnal assisted ventilation because it stabilizes the oropharyngeal airway.
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PMID:Treatment of respiratory failure during sleep in patients with neuromuscular disease. Positive-pressure ventilation through a nose mask. 354 13

Physiological studies performed 1 week after initiation of thyroid replacement showed persistence of significant respiratory muscle weakness in a patient presenting with hypothyroidism and hypercapnia. Repeat studies 12 months later demonstrated return of respiratory muscle strength to normal. Earlier reports on respiratory failure in hypothyroidism had postulated a critical role for respiratory muscle weakness in the genesis of hypercapnia. Since hypercapnia was rapidly reversed despite the persistence of severe respiratory muscle weakness, this explanation may not be always correct. It appears than in our patient thyroid replacement had its primary effect on the respiratory control system.
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PMID:Reversible respiratory muscle weakness in hypothyroidism. 362 Mar 25

Abnormal ventilatory function is common in patients with neuromuscular disorders. This report describes depressed ventilatory response to both hypoxia and hypercapnia, as well as arterial oxygen desaturation during sleep in a family with congenital myopathy. The index patient also had an abnormal ventilatory response to metabolic acid loading. There was clinical evidence of proximal muscle weakness, and a muscle biopsy specimen was consistent with myopathy. The reduction in ventilatory drive, however, could not be explained solely by ventilatory muscle weakness. This report describes a distinct familial syndrome of congenital myopathy and abnormal ventilatory response to hypercapnia and hypoxia. All affected family members had unique facial features, proximal muscle weakness, and impaired ventilatory responses. The combination of impaired ventilatory drive and reduced ventilatory muscle strength leaves patients particularly vulnerable, and heightened awareness of this association is important in the treatment of these patients.
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PMID:Abnormal ventilatory chemosensitivity and congenital myopathy. 366 6

A 52-year-old woman presented with increasing pain, weakness, and paraesthesiae of four months' duration in the lower limbs. She suffered from chronic obstructive airways disease and hypertension. Neurological examination revealed wasting of the quadriceps muscles, weakness of the lower limbs, and absent ankle jerks. The sensory examination was normal. Full blood count, ESR, biochemical, immunological, and viral studies, urinary heavy metal assays, and cerebrospinal fluid examination were normal. Nerve conduction studies were consistent with a sensorimotor neuropathy, and electromyographic sampling was consistent with acute denervation. A sural nerve biopsy showed axonal degeneration and segmental demyelination. One month after admission, she developed carbon dioxide retention. Her weakness spread to affect the upper limbs, and she could not be resuscitated after a cardiac arrest three months after admission. General autopsy examination revealed bronchopneumonia. Neuropathological examination showed a lymphocytic infiltrate in the nerve roots of the cauda equina, the lumbosacral plexus, and the sural and vagal nerves. Increased cellularity and collagen were evident in these nerves. A diagnosis of chronic inflammatory polyneuropathy was made. The neuropathology of this entity is discussed.
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PMID:Neuropathological findings in a case of chronic inflammatory polyneuropathy. 384 15

Respiratory muscle weakness is considered to be a factor in the inability to wean from mechanical ventilation. To assess this possibility, the present study examined the mechanical behavior of the diaphragm by measuring the change in transdiaphragmatic pressure (delta Pdi) during weaning. Nine "T-piece" weanings were carried out in seven patients with prior weaning failure and were terminated with the development of hypercapnia, hypoxemia, or severe tachypnea. Serial measurements of delta Pdi during these weans revealed that (1) in no case was there a decrease in delta Pdi at termination of weaning, and (2) in the subgroup of patients whose weaning failed because of hypercapnia, the increase in arterial carbon dioxide tension (mean increase of 12 mm Hg) was associated with a significant increase in delta Pdi, from the beginning (21.1 +/- 12.1 cm H2O) to the end (24.8 +/- 13.4 cm H2O) of the trial (p less than 0.05). We conclude that failure to wean in these patients, in particular the development of carbon dioxide retention, was not due to failure of the diaphragm as a pressure generator.
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PMID:Diaphragmatic strength during weaning from mechanical ventilation. 393 89

We studied 53 patients with proximal myopathy to determine at what level of muscle weakness hypercapnic respiratory failure is likely, and which tests of pulmonary function or respiratory muscle strength would best suggest this development. Respiratory muscle strength was determined from maximal static efforts and in half the patients, both inspiratory and expiratory muscle strengths were less than 50% of normal. In the 37 patients without lung disease respiratory muscle weakness was accompanied by significant decreases in vital capacity, total lung capacity, and maximum voluntary ventilation; by significant increases in residual volume and arterial carbon dioxide tension (PaCO2); and greater likelihood of dependence on ventilators, atelectasis, and pneumonia. Hypercapnia was particularly likely when respiratory muscle strength was less than 30% of normal in uncomplicated myopathy, and when vital capacity was less than 55% of the predicted value in any patient.
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PMID:Respiratory muscle and pulmonary function in polymyositis and other proximal myopathies. 641 85


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