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

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

A central apnea is a disorder characterized by apneic events during sleep with no associated ventilatory effort. Central sleep apnea syndrome is characterized by repeated apneas during sleep resulting from loss of respiratory effort. Although the etiology of central apnea remains obscure in most cases, current investigations into breathing control system during sleep and association with certain diseases have pointed out possible mechanisms. Ventilation during sleep is highly dependent on the nonbehavioral control system. As a result, any diseases affecting this control system could influence the breathing patterns while the patient is asleep. As our results show, most patients with central sleep apnea and without congestive heart failure had quantifiable abnormalities like diminished carbon dioxide response curves. Neurological diseases affecting the brainstem are able to produce breathing pattern disorders in sleep. Well-known neurological diseases such as arteriosclerosis in the elderly, infarctions, tumors, hemorrhage, accidents with damage of this region, encephalitis, poliomyelitis or other infectious diseases may cause central apnea during sleep, even if in wakefulness no abnormalities of breathing patterns are present. Apneas cause hypoxemia, hypercapnia and increased sympathicotonia. This may result in development of pulmonary artery hypertension or systemic hypertension. Published results demonstrate that medical treatment is ineffective in these patients. Implantation of a diaphragm pacing device is an invasive measure, the efficacy of the diaphragm pacing has not been proven by long-term trials, however. Mechanical ventilation was shown to be the most efficient treatment. A therapeutic procedure using a timed n-BiPAP device is able to normalize blood gases during sleep. The n-BiPAP prevented the development of severe pulmonary artery hypertension during sleep.
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PMID:Central sleep apnea. 904 68

Central sleep apnea hypopnea syndrome (CSAHS) and sleep hypoventilation syndrome (SHVS) are two distinct clinical syndromes with clearly defined diagnostic criteria. It is important to distinguish between normo/hypocapnic and hypercapnic CSAHS prior to treatment. Nasal continuous positive airway pressure is currently considered the primary treatment of choice for normo/hypocapnic CSAHS. The initial management of hypercapnic CSAHS and SHVS should include identification of any treatable causes and discontinuation of any sedative medications. Medroxyprogesterone may be effective in the long term management of these patients. If pharmacologic therapy fails, assisted ventilation should be considered. Assisted ventilation during the night is usually sufficient to improve hypercapnia and hypoxemia both at night and during the day. Assisted ventilation is usually best administered through a tight fitting nasal mask.
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PMID:Central Sleep Apnea and Hypoventilation Syndrome. 1112 58

Central sleep apnea syndrome (CSAS) is a disorder characterized by repeated apneic events during sleep with no associated ventilatory effort. CSAS is classified as either hypercapnic or non-hypercapnic. In the hypercapnic form of CSAS, increases in PaCO(2) generally result from reductions in ventilation or outright apneas due to an underlying depression of respiratory drive. Hypercapnic CSAS is common in central hypoventilation syndromes which may be primary (idiopathic) or secondary to other disorders that cause damage to the respiratory center. Non-hypercapnic CSAS is not associated with either a primary reduction in respiratory drive or respiratory muscle weakness. Non-hypercapnic CSAS can be a primary disorder or can occur secondary to high altitude, other medical illnesses such as congestive heart failure and central nervous system disease.
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PMID:[Central sleep apnea syndrome]. 1514 16

Heart failure is a highly prevalent disorder, with significant economic impact, and is associated with excess morbidity and mortality. One factor that may contribute to the progressively declining course of heart failure is the occurrence of recurrent episodes of apnea and hypopnea. There are two major kinds of sleep-related breathing disorders: obstructive and central sleep apnea. In patients with heart failure, in contrast to the general population, central sleep apnea is the most common form of sleep-related breathing disorder. Episodes of apnea, hypopnea, and the subsequent hyperpnea cause sleep disruption, arousals, hypoxemia-reoxygenation, hypercapnia/hypocapnia, and changes in intrathoracic pressure. These pathophysiologic consequences of sleep-related breathing disorders have deleterious effects on the cardiovascular system, and may be even more pronounced in the setting of established heart failure and coronary artery disease. Therefore, sleep apnea in heart failure should be treated. Central sleep apnea may be treated with nocturnal supplemental nasal oxygen, theophylline, or nasal-positive pressure devices, such as nasal continuous positive airway pressure (CPAP). The treatment of choice for obstructive sleep apnea is nasal CPAP. Although long-term controlled trials of the effect of treatment of sleep apnea on mortality in patients with heart failure are still pending, treatment of sleep apnea, both obstructive and central, does result in a decrease in sympathetic activity and an improvement in systolic function, which are known surrogates of mortality. Therefore, diagnosis and treatment of sleep-related breathing disorders may increase survival of patients with heart failure.
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PMID:Prevalence and treatment of breathing disorders during sleep in patients with heart failure. 1600 60

Charcot-Marie Tooth disease (CMT) encompasses several inherited peripheral motor-sensory neuropathies and is one of the most common inherited neuromuscular diseases. Charcot-Marie-Tooth disease can be associated with several disorders that may be encountered by the pulmonary physician, including restrictive pulmonary impairment, sleep apnea, restless legs, and vocal cord dysfunction. Restrictive pulmonary impairment has been described in association with phrenic nerve dysfunction, diaphragm dysfunction, or thoracic cage abnormalities. Central sleep apnea may be associated with diaphragm dysfunction and hypercapnia, whereas obstructive sleep apnea has been reported as possibly due to a pharyngeal neuropathy. Restless legs and periodic limb movement during sleep are found in a large proportion of patients with CMT2, a type of CMT associated with prominent axonal atrophy. Vocal cord dysfunction, possibly due to laryngeal nerve involvement, is found in association with several CMT types and can often mimic asthma. There may be special therapeutic considerations for the treatment of those conditions in individuals with CMT. For instance, bi-level positive airway pressure may be more appropriate than continuous positive airway pressure (CPAP) for the treatment of sleep apnea in the individual with concomitant restrictive pulmonary impairment. The prominence of peripheral neuropathy as a cause of the restless legs syndrome in CMT may justify treatment with neuropathic medications as opposed to the more commonly recommended dopaminergic agents. The risk of progression to bilateral vocal cord dysfunction in CMT and the risk of aspiration with laryngeal neuropathy may limit the therapeutic options available for vocal cord paralysis.
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PMID:Disorders of pulmonary function, sleep, and the upper airway in Charcot-Marie-Tooth disease. 1729 38

Sleep plays a large role in patients with heart failure. In normal subjects, sleep is usually in a supine position with reduced sympathetic drive, elevated vagal tone and as such a relatively lower cardiac output and minute ventilation, allowing for recuperation. Patients with heart failure may not experience the same degree of autonomic activity change and the supine position may place a large strain on the pulmonary system. More than half of all heart failure patients have one of two types of sleep apnea: either obstructive or central sleep apnea. Some patients have both types. Obstructive sleep apnea is likely to be a cause of heart failure due to large negative intrathoracic pressures, apnea related hypoxemia and hypercapnia, terminated by an arousal and surge in systemic blood pressure associated with endothelial damage and resultant premature atherosclerosis. Reversal of obstructive sleep apnea improves blood pressure, systolic contraction and autonomic dysfunction however mortality studies are lacking. Central sleep apnea with Cheyne Stokes pattern of respiration (CSA-CSR) occurs as a result of increased central controller (brainstem driving ventilation) and plant (ventilation driving CO2) gain in the setting of a delayed feed back (i.e., low cardiac output). It is thought this type of apnea is a result of moderately to severely impaired cardiac function and is possibly indicative of high mortality. Treatment of CSA-CSR is best undertaken by treating the underlying cardiac condition which may include with medications, pacemakers, transplantation or continuous positive airway pressure (CPAP). In such patients CPAP exerts unique effects to assist cardiac function and reduce pulmonary edema. Whether CPAP improves survival in this heart failure population remains to be determined.
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PMID:Sleep in heart failure. 1911 Jan 35

Central sleep apnea is highly prevalent in association with heart failure, some neurological diseases and chronic opioids use. There are two main categories of central sleep apnea respectively related with different underlying conditions. Some hypocapnic patients exhibit respiratory control system instability and central apnea occurs when PaCO(2) falls below the threshold for apnea during sleep. The other group are patients with chronic hypercapnia mainly in the context of neuromuscular disorders or obesity hypoventilation syndrome. All these patients should be assessed by recording blood gases, polysomnography and ventilatory responses to CO(2). Cardiologic assessment should include pro-brain natriuretic factor (pro-BNP) and cardiac echography whereas neurological examination requires brain imaging and/or electromyography. Ventilatory supports used for treating central sleep apnea are non-invasive ventilation and servo-assisted ventilation in hypercapnic and hypocapnic patients respectively.
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PMID:[Management of central sleep apnea]. 1978 53

Central sleep apnea (CSA) describes a group of conditions in which cessations in air flow occur without respiratory effort. In contrast, obstructive sleep apnea patients have ongoing respiratory effort during respiratory events. However, considerable overlap exists in the pathogenesis and clinical presentation of obstructive sleep apnea and CSA. A good working knowledge of the mechanisms underlying CSA is important for optimal clinical care. In general, CSA can be classified into those with excessive drive (eg, Cheyne-Stokes breathing) versus those with inadequate drive (eg, sleep hypoventilation syndrome). One critical factor contributing to the cessation of air flow during sleep is the concept of the apnea threshold, such that a P(aCO(2)) value below a certain level will lead to cessations in breathing. P(aCO(2)) can fall below the chemical apnea threshold when drive is excessive (eg, robust chemosensitivity) or when hyperventilation is occurring (eg, following arousal). Another important factor is the loss of the so-called wakefulness drive to breathe, such that some rise in P(aCO(2)) is likely to occur at the onset of sleep. A variety of factors contribute to this rise, including upper-airway collapse and diminished chemosensitivity (particularly during rapid-eye-movement sleep). In patients with low central drive, this further loss of drive at sleep onset can lead to marked hypercapnia in some cases. The treatment of CSA is also reviewed in some detail, including a role for positive airway pressure (eg, bi-level positive airway pressure in hypoventilation patients) and optimization of medical therapy (eg, in Cheyne-Stokes breathing). A paucity of research exists in this area, emphasizing the opportunities for young investigators who are interested in this field.
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PMID:What is central sleep apnea? 2079 99

Central sleep apnea (CSA) results from a reduction in lack of output from the central respiratory generator in the brainstem, manifesting as apneas and hypopneas without discernible efforts. CSA can lead to hypercarbia, arrhythmias, pulmonary hypertension, and heart failure. Indeed, the patient may develop a disturbed breathing during sedation procedures. We report a patient who was diagnosed with CSA and had been on continuous positive airway pressure (CPAP) therapy for 5 years. He was referred for multiple tooth extractions under sedation owing to severe gag reflex and phobic anxiety disorder. The treatment was completed uneventfully under N(2)O and sevoflurane inhalation accompanied by midazolam and ketamine induction. The role of sedative, analgesic, and anesthetic agents as a precipitating factor for CSA is of particular concern. The combined administration of midazolam, ketamine, sevoflurane, and N(2)O/O(2) is a useful and safe option for patients requiring sedation.
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PMID:Dental treatment of a patient with central sleep apnea and phobic anxiety under sedation: report of a case and clinical considerations. 2308 86


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