Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Panic attacks during sleep are analysed in terms of a hyperventilation theory of panic disorder. The theory assumes that panic attacks during sleep are a manifestation of severe chronic hyperventilation, a dysfunctional state in which renal compensation has led to a relatively steady state of diminished bicarbonate. Reductions in respiration during deep non-REM sleep lead to respiratory acidosis which triggers hyperventilatory hypocapnea and subsequent panic. A probability model designed to predict when during sleep panic attacks are likely to occur is supported by relevant data from studies of sleep and panic attacks. Implications for treatment are discussed.
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PMID:Panic attacks during sleep: a hyperventilation-probability model. 314 36

We have carried out sequential studies of respiration and sleep state, from two weeks to two years of age in a girl with congenital central hypoventilation. When awake her minute ventilation (VE) and blood gases are normal, and when asleep she shows hypoventilation, with progressive hypoxia, hypercarbia and respiratory acidosis, most marked in NREM sleep. There has been no consistent change in VE (expressed as ml/kg/min) with age, awake or asleep, and she remains ventilator dependent when asleep. Growth and development are normal. We report a trial of almitrine bismesylate at the age of 21 months. A dose of 1.5 mg/kg/day orally for eight days produced minimal changes in VE, but when given 2.6 mg/kg/day for a further seven days there was a significant increase in VE in both NREM (27% increase) and in REM sleep (30% increase). These changes were accompanied by substantial improvements in blood gases, with PaCO2 less than 50 mmHg and PaO2 greater than 60 mmHg throughout a four hour study period asleep, off the ventilator, in air. After stopping almitrine bismesylate VE and blood gas values returned to pretreatment values. Almitrine bismesylate may be of value as an alternative to artificial ventilation in this condition.
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PMID:Almitrine bismesylate in congenital central hypoventilation. 642 94

Long-term exposure to elevated ambient CO2-levels is a common condition for living in a closed environment such as a spacecraft. In this study, the cardio-respiratory system response to CO2-levels of 0.7% and 1.2% was assessed. The response was investigated during non-REM sleep when the sensitivity of the respiratory system to ambient CO2 is low and only subject to the metabolic respiratory drive. Four subjects were exposed to 0.7% and 1.2% CO2 for 23 d each. Respiration rate and heart rate were determined for the first two phases of slow wave sleep. In addition, the occurrence of central apneas was assessed. Data were analyzed by a repeated measure ANOVA. As a response to CO2 exposure two dynamic effects were observed. Heart rate increased initially with a peak between the second and the sixth night. Over the period of the exposure, respiration rate and heart rate decreased steadily. At least two mechanisms with different time constants must be considered for this dynamic behavior: an uncompensated respiratory acidosis, followed by a phase of relative compensation. At the end of the 23-d exposure, equilibrium in the physiological state had not been reached. Though the experiment did not show severe effects from CO2, it is too early to state that a long-term exposure does not have any consequences for health and well-being.
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PMID:Joint NASA-ESA-DARA Study. Part three: cardiorespiratory response to elevated CO2 levels during sleep. 959 21

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