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)

36 night sleep recordings were carried out on 15 patients suffering from myotonia dystrophica. 9 of these patients complained of diurnal hypersomnia. 10 patients had a disturbance of night sleep with a reduction of REM sleep sometimes associated with interruption of the recording with an increase in the light stages of sleep or alternatively with an increase of REM sleep with a reduction in the latency period of the first paradoxical sleep or with narcoleptic elements. 13 patients had abnormally early abolition of chin EMG activity, almost on falling asleep. 11 cases had pathological apnoeic episodes during sleep and in 9 of the 10 patients who underwent respiratory function studies there was a restrictive airways defect. In addition 9 had frank hypoxia without hypercapnia and 4 a right to left shunt. 3 clinically unaffected patients but with affected relatives were also investigated, 2 were found to have sleep disturbances 1 of which was associated with early abolition of tone.
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PMID:[Disturbances of wakefulness, sleep and respiratory function in Steinert's disease]. 92 30

Abnormal physical exhaustion and fatigue are often simply regarded as a natural consequence of pulmonary diseases. Apart from factors not specifically related to pulmonary diseases (e.g. consequences of infections or malignant diseases of the lungs), increased work of breathing due to impaired lung/thoracic cage mechanics, the effects of chronic hypoxia and hypercapnia, the consequences of disturbed sleep and psychosocial factors are mainly responsible for the impaired physical fitness and the fatigue in association with lung diseases. A careful case history including psychosocial aspects and a thorough physical examination are essential for an efficient diagnostic evaluation. Tests of pulmonary function not only in the awake patient at rest, but also during sleep or adequate physical exercise can reveal the causes of impaired physical performance and fatigue related to lung diseases.
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PMID:[Pulmonary causes of abnormal fatigability]. 175 70

The prevalence of reported sleep disturbances in a general population is high. Many of the complaints are the result of sleep-related breathing disorders, due mainly to the occurrence of obstructive and central apnoeas. Obstructive sleep apnoea is a fully described and well-recognized entity. Central sleep apnoea (CSA) however, has been poorly studied. There is accumulating evidence that central sleep apnoea should be considered as the end of a spectrum. Instability in the breathing pattern is the main underlying mechanism and is due to the interaction of many factors. Breathing during sleep is dependent on metabolic control and the activity of the respiratory muscles. Decreased chemical drive and/or failing respiratory muscle function are associated with CSA and usually also with ongoing hypoventilation during wakefulness, characterized by chronic daytime hypercapnia. Central respiratory drive can also be inhibited by upper airway reflexes. Mostly, however, CSA occurs as the hallmark of unstable breathing during sleep brought about by an overall increase in loop gain (especially in light sleep stages) and the unmasking of a CO2 threshold. Arousal following central apnoeas acts as an amplification of the instability. Micro electroencephographic (EEG) arousals are often observed as a consequence of CSA. They are responsible for sleep fragmentation and hypersomnolence during the day. The daytime hypersomnolence and complaints of awakenings during sleep in patients with CSA can be striking. CSA can occur in specific pathologies, such as chronic heart failure and (post-traumatic) brain lesions, that are associated with irregular breathing. Treatment strategies are remarkably few in number. Use of nasal ventilation and the inhalation of CO2 are mainly of theoretical interest, since patients do not often tolerate these more invasive therapies. Drug treatment, especially with acetazolamide, is easier to perform. Stimulation of upper airway reflexes, by less invasive methods, seems to be promising for the near future.
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PMID:Central sleep apnoea, pathogenesis and treatment: an overview and perspective. 748 5

The two broad categories of sleep apnea syndrome are associated with obstructive or mixed events on the one hand, and central events on the other. The pathogenesis of both seems to involve periodic reduction in respiratory drive, although obstructive apneas may also involve an anatomic abnormality of the upper airway. Patients with obstructive sleep apnea syndrome most commonly exhibit resuscitative snoring and daytime sleepiness. Snoring is generally less prominent in the central sleep apnea syndromes; those with daytime hypercapnia generally complain of daytime sleepiness, whereas those without hypercapnia complain of disturbed sleep. The overnight polysomnogram is the preferred method of diagnosing both disorders.
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PMID:Sleep apnea syndromes: overview and diagnostic approach. 802 35

Alveolar hypoventilation associated with neuromuscular disease can occur in acute and chronic forms. In the acute form, progressive weakness of respiratory muscles leads to rapid reduction in vital capacity followed by respiratory failure with hypoxemia and hypercarbia. Symptoms are those of acute respiratory failure, including dyspnea, tachypnea, and tachycardia. In the chronic form, impairment of the respiratory muscles affects mechanical properties of the lungs and chest wall, decreases the ability to clear secretions, and eventually may alter the function of the central respiratory centers. Symptoms include orthopnea, fatigue, disturbed sleep, and hypersomnolence. Treatment and outcome of the disease's chronic form are dependent on the underlying clinical cause of the alveolar hypoventilation. For chronic but stable diseases such as old polio, quadriplegia, or kyposcoliosis, mechanical support of minute ventilation can reverse symptoms. For chronic and progressive disease such as muscular dystrophy and amyotrophic lateral sclerosis, mechanical support of minute ventilation provides only symptomatic relief and is usually associated with deterioration to the point of complete ventilator dependency for survival. For the chronic progressive forms of alveolar hypoventilation, there is currently a need for quality randomized controlled clinical trials to define physiologic indicators and appropriate timing for mechanical support of minute ventilation.
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PMID:Neuromuscular disease and hypoventilation. 1057 Jul 36

Because the circadian rhythms of oxygen consumption (VO(2)) and body temperature (T(b)) could be contributed to by differences in thermogenesis and because hypoxia depresses thermogenesis in its various forms, we tested the hypothesis that hypoxia blunts the normal daily oscillations in VO(2) and T(b). Adult rats were instrumented for measurements of T(b) and activity by telemetry; VO(2) was measured by an open-flow method. Animals were exposed to normoxia (21% O(2)), hypoxia (10.5% O(2)), and normoxia again, each 1 wk in duration, in either a 12:12-h light-dark cycle ("synchronized") or constant light ("free running"). In this latter case, the period of the cycle was approximately 25 h. In synchronized conditions, hypoxia almost eliminated the T(b) circadian oscillation, because of the blunting of the T(b) rise during the dark phase. On return to normoxia, T(b) rapidly increased toward the maximum normoxic values, and the normal cycle was then reestablished. In hypoxia, the amplitude of the activity and VO(2) oscillations averaged, respectively, 37 and 56% of normoxia. In free-running conditions, on return to normoxia the rhythm was reestablished at the expected phase of the cycle. Hence, the action of hypoxia was not on the clock itself but probably at the hypothalamic centers of thermoregulation. Hyperoxia (40% O(2)) or hypercapnia (3% CO(2)) had no significant effects on circadian oscillations, indicating that the effects of hypoxia did not reflect an undifferentiated response to changes in environmental gases. Modifications of the metabolism and T(b) rhythms during hypoxia could be at the origin of sleep disturbances in cardiorespiratory patients and at high altitude.
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PMID:Hypoxic depression of circadian rhythms in adult rats. 1065 99

Chronic obstructive pulmonary disease (COPD) is a common medical disorder, which causes considerable morbidity and mortality. Given the chronic and symptomatic nature of the disease, the patient is often seen in the physician's office with complaints of dyspnea. However, more than 50% of COPD patients also have sleep complaints characterised by longer latency to falling asleep, more frequent arousals and awakenings, and/or generalised insomnia. Sleep disturbance tends to be more severe with advancing disease and substantially reduces the COPD patients' quality of life. In approaching the COPD patient who complains of insomnia it is important to take a complete sleep history. Having characterised the degree and duration of the problem, medical management of the underlying COPD must first optimise oxygen saturation while minimising the effects of many of the medications used for COPD. While aerosol therapies may be systemically absorbed and contribute to sleep disruption, anticholinergics, such as ipratropium bromide, are the least likely to do so and indeed have been shown to improve sleep quality in this population. Many of the traditional sedatives and hypnotics have been used in the COPD population including benzodiazepines, imidazopyridines, pyrazolopyrimidines and, less commonly, antidepressants and phenothiazines. Clinical trials support the role of numerous agents in treating insomnia in this population but do not always provide reassurance that these therapies can be used safely, particularly in the patient with severe COPD with hypercarbia. Benzodiazepines are among the most commonly employed agents, but case reports and series continue to describe adverse pulmonary events. Although the newer pyridine derivatives also have the potential to worsen pulmonary function, they appear less likely to do so. Data to date are limited with the tricyclic antidepressants and phenothiazines, although they appear to be very well tolerated from a respiratory point of view. Since sleep disturbances are often long-standing and associated with maladaptive behaviours towards sleep, cognitive/behavioural approaches are often useful and are more effective in the long-term than are hypnotics. When prescription of a sedative is to be made, extra caution is required for those patients at increased risk of adverse respiratory effects, such as those with advanced disease and hypercarbia in whom pharmacological therapy is often best avoided. Selection of the various options will depend upon the degree of underlying disease and the patient's specific complaints of insomnia. Finally, it is important to remember that while most hypnotics work in an acute setting, the long-term management will require an integrated approach.
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PMID:Management of insomnia in patients with chronic obstructive pulmonary disease. 1255 60

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death, affecting 14 million adults in the United States. Symptoms related to sleep disturbances are common in moderate to severe COPD, particularly in elderly patients, in the form of morning tiredness and early awakenings. One major cause of morbidity in this population is abnormalities in gas exchange and resultant hypoxemia. Sleep has profound adverse effects on respiration and gas exchange in patients with COPD. There are several mechanisms underlying nonapneic oxygen desaturation during sleep. They include decreased functional residual capacity, diminished ventilatory responses to hypoxia and hypercapnia, impaired respiratory mechanical effectiveness, diminished arousal responses, respiratory muscle fatigue, diminished nonchemical respiratory drive, increased upper airway resistance, and the position of baseline saturation values on the oxyhemoglobin dissociation curve. Smoking cessation, bronchodilation, and pulmonary rehabilitation are cornerstones of treatment of COPD. Improvement in lung mechanics and gas exchange should lead to better sleep quality and health status.
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PMID:Sleep in chronic obstructive pulmonary disease. 1605 23

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death, affecting 14 millions adults in the United States. Symptoms related to sleep disturbances are common in individuals with moderate to severe COPD, particularly in the elderly, which is commonly manifested as morning fatigue and early awakenings. One major cause of morbidity in this population is abnormalities in gas exchange and resultant hypoxemia as they can lead to elevated pulmonary pressures, dyspnea and in severe cases right ventricular overload and failure. Sleep has profound adverse effects on respiration and gas exchange in patients with COPD. There are several mechanisms underlying nonapneic oxygen desaturation during sleep. They include decreased functional residual capacity, diminished ventilatory responses to hypoxia and hypercapnia, impaired respiratory mechanics, diminished arousal, respiratory muscle fatigue, diminished nonchemical respiratory drive, increased upper airway resistance, and the starting point of baseline saturation values while awake on the oxyhemoglobin dissociation curve. Smoking cessation, bronchodilation, inhaled steroids in those with a reversible component and pulmonary rehabilitation are corner stones of treatment of COPD. The goals of therapy for the clinician should be to improve lung mechanics as well as gas exchange ultimately leading to better sleep quality and health status.
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PMID:Chronic obstructive pulmonary disease and sleep: the interaction. 1721 94

The exact effect of opioid analgesics on sleep is to be determined. Although literature data are sporadically reported, the aim of this review is to summarize the already known effects of such medications on sleep. A variety of effects, both positive and negative, has been suggested, when opioids are used for pain treatment, but in the absence of pain as well. Although often thought to promote restful sleep, the reality is much more complicated. Sleep disturbances and alterations of sleep quantity and quality have been reported. In addition, their sedative effects have been relatively well established and opioids can cause respiration to slow and become irregular, leading to hypercapnia and hypoxia. As a result, their usage has been linked to irregular or ataxic breathing (Biot's breathing) and their use has been associated with both central and obstructive sleep apnea. One could estimate that central apnea is a common complication of such chronic therapy, affecting between 30% and 90% of patients. Thus, sleep disturbances can be induced or deteriorated. On the other hand, extended release opioid formulations have been suggested to improve sleep due to no analgesic gaps and less walking because of breakthrough pain. Furthermore, several reports have shown significantly improved sleep quantity and adequacy, with reduced sleep disturbances. Still, as no prospective trials on the effect of opioid therapy on sleep are available and evidence is scarce, definitive conclusions cannot be drawn. Future studies with their effect on sleep as primary end-point are needed to draw permanent conclusions.
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PMID:Non-analgesic effects of opioids: opioids' effects on sleep (including sleep apnea). 2274 42


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