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

Benzodiazepine have been shown to suppress ventilatory responses to hyperoxic hypercapnia (HCVR) and isocapnic HVR when taken parenterally. Most patients would, however, prefer to take an oral rather than parenteral preparation but the effect of oral benzodiazepine on these ventilatory responses has not been well studied. We therefore studied the effect of oral midazolam (7.5 mg) and diazepam (5 mg) both given orally on resting ventilation and respiratory drive, as assessed by HCVR and HVR. Flumazenil, a specific benzodiazepine antagonist, was administered intravenously to reverse the effect. A mental alertness-drowsiness index in five grades, from 1 (awake and alert) to 5 (asleep), was used to assess the sedation effect. Six normal male subjects, (aged 31 +/- 1.6 yrs) (mean +/- SD), participated in the study. Mean resting ventilation, and ventilatory response to HCVR and HVR were not significantly altered by these drugs when taken orally. Flumazenil also had not significant effect on HCVR and HVR. However the mental alertness-drowsiness index rose from 1 to 2.83 with oral midazolam and reversed to 1.25 with flumazenil. Similarly, this index increased from 1 to 2.25 after oral diazepam and reversed to 1.42 after flumazenil. In conclusion, we found that even though oral midazolam and diazepam produced a significant sedation effect, which was reversed with flumazenil, the drugs had no effect on ventilation at rest and the ventilatory responses to hypoxia and hypercapnia.
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PMID:The effect of oral midazolam and diazepam on respiration in normal subjects. 842 93

We report on a 45-year old woman with daytime sleepiness, polycythemia, hypoxemia and hypercapnia, admitted to hospital on three occasions in a 10 month period for acute respiratory failure. Polysomnography demonstrated apneas of central type, testing of the respiratory drive suggested central alveolar hypoventilation and magnetic resonance imaging showed an Arnold-Chiari malformation with syringomyelia. The originality of this case is the absence of any neurologic sign, respiratory failure being the sole manifestation of the Arnold-Chiari malformation.
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PMID:[Isolated respiratory insufficiency in Arnold-Chiari malformation]. 892

A 13-year-old boy with juvenile-onset acid alpha glucosidase deficiency was reported. Proximal muscle weakness including respiratory muscles and scoliosis progressed since nine year of age. He developed nocturnal dyspnea and daytime somnolence at age 13. His arterial blood gas analysis showed hypoxemia (PO2 54.1 mmHg) and hypercapnia (PCO2 72.3 mmHg), and spirometry showed significantly decreased vital capacity (% VC 21%). He was treated with nocturnal NIPPV employing a device for delivering bilevel positive airway pressure (Bi-PAP). Nocturnal dyspnea and daytime somnolence rapidly disappeared with nocturnal ventilatory support. Daytime arterial PO2 and PCO2 improved after the therapy, namely 74.8 mmHg and 64.1 mmHg respectively. We conclude that NIPPV is a noninvasive and effective therapy for respiratory failure in patients with chronic progressive neuromuscular disorder including acid alpha glucosidase deficiency.
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PMID:[Chronic respiratory failure in a case with juvenile-onset acid alpha-glucosidase deficiency; successful therapy with nasal intermittent positive pressure ventilation (NIPPV)]. 898 97

A 57-yr-old man with idiopathic central apnea is reported. He presented at our hospital complaining of excessive daytime sleepiness. Polysomnography, including esophageal pressure monitoring, confirmed central sleep apnea with an apnea index of 27/h. He had mild non-insulin-dependent diabetes mellitus (NIDDM) but no signs of diabetic neuropathy or other background diseases. The ventilatory responses to hypoxia and hypercapnia tested while he was awake indicated increased respiratory chemosensitivity. We applied nasal continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BPAP) in an attempt to compare the possible difference in therapeutic efficacy. Although nasal CPAP completely reversed central apnea, nasal BPAP adversely affected both apnea length and frequency in an applied pressure-dependent manner. Arterial blood gas analyses while he was being treated indicted alveolar hypoventilation with CPAP and hyperventilation with BPAP. Additionally, administration of a mixed gas containing 5% CO2 through a face mask had a significant effect on the disappearance of central apnea in this patient. These findings support the theory that the arterial PCO2 level is critical in generating idiopathic central apnea and that nasal CPAP therapy may be effective in eliminating central apnea by raising the PaCO2.
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PMID:Continuous versus bilevel positive airway pressure in a patient with idiopathic central sleep apnea. 910 99

We studied 134 patients with Steinert's myotonic dystrophy (MD) in order to determine the prevalence of chronic hypercapnia, the level of muscle weakness and forced expiratory volume at which hypercapnic respiratory failure is likely to occur, and how clinical assessment might help predict hypercapnic respiratory failure. Subjects were divided into five classes with a muscular disability rating scale (MDRS): 0 = no clinical impairment (n = 9), I = minimal signs of impairment (n = 11), II = distal weakness (n = 41), III = moderate proximal weakness (n = 62), and IV = nonambulatory (n = 11). The prevalence of hypercapnia (PaCO2 > or = 43 mm Hg) was found to be 0%, 27%, 29%, 45% and 55% for MDRS 0 to 4, respectively (p = 0.03). A multiple regression analysis limited to clinical data showed that daytime hypersomnolence was a significant cofactor with the MDRS (p = 0.01) in predicting PaCO2 (r = 0.40). Among respiratory parameters, FVC, respiratory muscle strength (RMS), and maximal inspiratory pressure against occluded airways (PImax) were found to be predictors of nearly equal strength, explaining 16%, 15%, and 14% of the PaCO2 variance, respectively. In multiple regression analysis, sex, daytime sleepiness, and the expected/observed FVC ratio for a given RMS were found to be significant cofactors with PImax in predicting PaCO2 (r = 0.51). It is concluded that respiratory insufficiency should be suspected in MD patients with proximal weakness or daytime sleepiness. The likelihood of hypercapnia also increases with volume restriction and respiratory muscle weakness. Our study suggests that the combination of inspiratory muscle weakness and loading plays a predominant role in the pathogenesis of chronic alveolar hypoventilation in MD patients. The occurrence of daytime hypersomnolence suggests that other factors, such as low central ventilatory drive or sleep apnea, might play an additional role.
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PMID:Relationship between chronic hypercapnia and inspiratory-muscle weakness in myotonic dystrophy. 923 Jul 37

Apnea and hypopnea during sleep are often viewed as different expressions of the same sleep-related breathing disorder. In our point of view, both symptoms are two different entities which can occur in the same patient. We discuss the hypothesis that sleep apnea is a disorder associated with recurrent arousals and chronic activation of the sympathetic nervous system, leading to daytime sleepiness and disturbances in the autonomic system. Hypoventilation results from reduced alveolar ventilation and is associated with hypercapnia. In rare cases it is caused by genuine disorders of the breathing center, like Odine's curse. In most cases, hypoventilation is secondary to an underlying disease and a strategy of the body, to avoid respiratory muscle failure. Treatment trials of hypoventilation of the respiratory muscles by stimulating the breathing center failed to be beneficial. However, unloading treatment with long-term oxygen and/or home mechanical ventilation improves arterial blood gases, physical activity and prognosis.
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PMID:How important is the differentiation between apnea and hypopnea? 938 Sep 56

Under urethane anesthesia, animals exhibit patterns of cortical activity similar to those seen in wake, drowsiness and slow-wave sleep in unanesthetized animals. In the present study, hypoxic and hypercapnic ventilatory reflexes were examined in unanesthetized and urethane-anesthetized golden mantled ground squirrels in states with similar EEG profiles. Synchronized EEG patterns occurred less frequently in both unanesthetized and anesthetized animals during hypoxic (10% O2) and hypercapnic (5% CO2) exposure. Breathing frequency fell significantly during sleep in animals breathing all gas mixtures, while the relative ventilatory sensitivity to hypoxia and hypercapnia increased during sleep. Urethane-anesthetized animals also showed significant falls in breathing frequency and ventilation and increases in relative ventilatory sensitivity to hypoxia and hypercapnia as they moved into states with synchronized EEG patterns. These data suggest that the brain activity states observed under urethane anesthesia mimic sleep/wake in terms of their effect on respiratory function and that changes in breathing pattern and the enhancement of ventilatory responses in states with a synchronized EEG is not due solely to changes in levels of behavioural stimuli.
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PMID:Cortical activation states in sleep and anesthesia. II: respiratory reflexes. 969 85

A 64-year-old man with multiple system atrophy complained of daytime sleepiness, fatigue, and snoring. Neurological examination revealed severe autonomic failure, mild cerebellar ataxia and akinesia. Daytime blood gas analysis showed respiratory acidosis with hypoxia and hypercapnia. MR imaging of the brain showed atrophy of the pons, cerebellum and bilateral frontal lobes. Although paralysis of the vocal cord abduction was not found by laryngoscopy during daytime examination, polysomnography (PSG) showed heavy snoring with paradoxical respiration associated with severe desaturation during sleep as well as reduced slow wave sleep and REM sleep. He was diagnosed as having sleep-related upper airway obstructive breathing disorder probably due to Gerhardt syndrome. Tracheostomy was considered, but we performed nasal CPAP therapy during sleep because this therapy is non-invasive and would not impair his daily life. After nasal CPAP therapy, daytime sleepiness, fatigue, and snoring with desaturation improved, and PSG showed increased slow wave sleep. These results demonstrate that nasal CPAP therapy improves the quality of sleep and should be considered in patients with early stages of multiple system atrophy who exhibit sleep-related breathing disorders.
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PMID:[Effective nasal CPAP therapy for heavy snoring and paradoxical respiration during sleep in a case of multiple system atrophy]. 1034 49

The obstructive sleep apnea syndrome is characterized by the occurrence of cyclic snoring and frequent apneic episodes during sleep, with consequent hypoxia and hypercapnia. Obstructive sleep apnea syndrome is associated with excess daytime sleepiness, depression, and an increased incidence of ischemic cardiopathy, cardiac arrhythmias, systemic hypertension and brain infarction. Hypoglossal motoneurons, which innervate extrinsic and intrinsic muscles of the tongue, play a key role in maintaining the patency of the upper airway and in the pathophysiology of obstructive sleep apnea syndrome. Based on data obtained by using extracellular recording techniques, there is a consensus that hypoglossal motoneurons cease to discharge during rapid eye movement sleep, because they are disfacilitated. Since other somatic motoneurons are known to be postsynaptically inhibited during rapid eye movement sleep, we sought to determine, by the use of intracellular recording techniques during cholinergically induced rapid eye movement sleep, whether postsynaptic inhibitory mechanisms act on hypoglossal motoneurons. We found that, during this state, a powerful glycinergic premotor inhibitory system acts to suppress hypoglossal motoneurons. This finding opens new avenues for the treatment of obstructive sleep apnea syndrome, and provides a foundation to explore the neural and pharmacological control of respiration-related motoneurons during rapid eye movement sleep.
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PMID:Hypoglossal motoneurons are postsynaptically inhibited during carbachol-induced rapid eye movement sleep. 1061 91

Complaints of poor sleep are very common in people with chronic respiratory disorders. In patients with chronic obstructive pulmonary disease (COPD), poor sleep may be due to many causes, including cough, excess mucous production, and frequent arousals from sleep caused by hypercapnia, as well as secondary to medications used to manage the lung disease. Patients with obstructive sleep apnea (OSA) also complain of excessive daytime sleepiness and fatigue due to poor-quality sleep, although the mechanism of sleep disruption is somewhat different from that in patients with COPD. Although benzodiazepines are often the drugs of choice for the management of insomnia, caution is suggested with the use of these agents in patients with chronic obstructive respiratory disease due to the reduction in upper airway muscle tone and blunting of the arousal response to hypercapnia. However, controlled trials with short-acting benzodiazepine receptor antagonists, including triazolam, zolpidem, and zaleplon, suggest that these agents may be safely used in selected patients who have mild to moderate COPD without daytime hypercapnia. Less data are available on the use of these agents for patients with OSA, but a preliminary trial using zaleplon suggests that respiratory function is not adversely affected in patients with mild to moderate OSA. Studies are needed to further define the benefit-risk ratio of the use of benzodiazepine receptor agonists for the management of insomnia in patients with chronic obstructive lung disease.
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PMID:Perspectives on the management of insomnia in patients with chronic respiratory disorders. 1075 6


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