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)

Sleep deprivation is common in acutely ill patients because of their underlying disease and can be compounded by aggressive medical care. While sleep deprivation has been shown to produce a number of psychological and physiologic events, the effects on respiration have been minimally evaluated. We therefore studied resting ventilation and ventilatory responses to hypoxia and hypercapnia before and after 24 h of sleeplessness in 13 healthy men. Hypoxic ventilatory responses (HVR) were measured during progressive isocapnic hypoxia, and hypercapnic ventilatory responses (HCVR) were measured using a rebreathing technique. Measures of resting ventilation, i.e., minute ventilation, tidal volume, arterial oxygen saturation, and end-tidal gas concentrations, did not change with short-term sleep deprivation. Both HVR and HCVR, however, decreased significantly after a single night without sleep. The mean hypoxic response decreased 29% from a slope of 1.20 +/- 0.22 (SEM) to 0.85 +/- 0.15 L/min/% saturation (p less than 0.02), and the slope of the HCVR decreased 24% from 2.07 +/- 0.17 to 1.57 +/- 0.15 L/min/mmHg PCO2 (p less than 0.01). These data indicate that ventilatory chemosensitivity may be substantially attenuated by even short-term sleep deprivation. This absence of sleep could therefore contribute to hypoventilation in acutely ill patients.
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PMID:Sleep deprivation and the control of ventilation. 641 47

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

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

Insomnia is common in many patients with chronic obstructive pulmonary disease (COPD). The causes of insomnia are sleep induced pathophysiological effect of COPD itself, COPD comorbidities and the presence of coexisted obstructive sleep apnea. Sleep has profound adverse effects on respiration and gas exchange in patients with COPD. There are several mechanisms underlying oxygen desaturation during sleep. They include decreased functional residual capacity, decreased ventilatory responses to hypoxia and hypercapnia, impaired respiratory mechanical effectiveness, respiratory muscle fatigue, decreased respiratory drive, and increased upper airway resistance. COPD comorbidities include DM, cardiovascular diseases, osteoporosis, depression, and GERD. The coexistence of COPD and sleep apnea-hypopnea syndrome has been denominated "overlap syndrome".
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PMID:[Chronic obstructive pulmonary disease (COPD)]. 1976 34

We present the case of a 48-year-old woman suffering from fatal familial insomnia (FFI)--a rare prion disease--who developed Biot's breathing and secondary respiratory failure during the early stages of the illness. Once hypercapnia was detected a trial of nocturnal noninvasive ventilation (NIV) was offered with important improvement of arterial blood gases (ABG), and subjective good quality of sleep. To our knowledge, this is the first report in the medical literature of the use of NIV in the management approach of this devastating disease. Its impact on the prognosis and survival of these patients, however, is yet to be elucidated.
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PMID:Biot's breathing in a woman with fatal familial insomnia: is there a role for noninvasive ventilation? 2134 52

Obstructive sleep apnea (OSA) is a nocturnal breathing disorder that is associated with cognitive impairment. The primary determinants of cognitive deficits in OSA are thought to be sleep disruption and blood gas abnormalities. Cognitive impairment is also seen in other disorders that are characterised primarily by sleep disturbance (e.g., sleep restriction/deprivation, insomnia) or hypoxia/hypercarbia (e.g., chronic obstructive pulmonary disease (COPD)). Assessment of the cognitive deficits observed in these other disorders could help better define the mechanisms underlying cognitive deficits in OSA. This study utilised meta-review methodology to examine the findings from systematic reviews and meta-analyses of the effects of untreated OSA, COPD, insomnia, and sleep deprivation on cognitive function in adults, compared with norms or controls. Eighteen papers met inclusion criteria: seven in OSA, two in insomnia, five in COPD, and four in sleep deprivation. OSA and COPD were both accompanied by deficits in attention, memory, executive function, psychomotor function, and language abilities, suggesting that hypoxia/hypercarbia may be an important determinant of deficits in these domains in OSA. Both OSA and sleep deprivation studies were accompanied by deficits in attention and memory, suggesting that short-term sleep disturbance in OSA may contribute to deficits in these domains. Visuospatial deficits were unique to OSA, suggesting the contribution of a mechanism other than sleep disturbance and hypoxia/hypercarbia to this problem. Our findings suggest that the cognitive deficits associated with untreated OSA are multidimensional, with different physiological disturbances responsible for differing cognitive problems.
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PMID:Cognitive deficits in obstructive sleep apnea: Insights from a meta-review and comparison with deficits observed in COPD, insomnia, and sleep deprivation. 2876 May 49

Sleep disorders like obstructive sleep apnea syndrome, periodic limb movements in sleep syndrome, insomnia and narcolepsy-cataplexy are all associated with an increased risk of cardiovascular diseases. These disorders share an impaired autonomic nervous system regulation that leads to increased cardiovascular sympathetic tone. This increased cardiovascular sympathetic tone is, in turn, likely to play a major role in the increased risk of cardiovascular disease. Different stimuli, such as intermittent hypoxia, sleep fragmentation, decrease in sleep duration, increased respiratory effort, and transient hypercapnia may all initiate the pathophysiological cascade leading to sympathetic overactivity and some or all of these are encountered in these different sleep disorders. In this manuscript, we outline the different pathways leading to sympathetic over-activity in different sleep conditions. This augmented sympathetic tone is likely to play an important role in the development of cardiovascular disease in patients with sleep disorders, and it is further hypothesized to that sympathoexcitation contributes to the metabolic dysregulation associated with these sleep disorders.
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PMID:Sleep biology updates: Hemodynamic and autonomic control in sleep disorders. 2957 32