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

Sleep-related breathing disorders, ranging from habitual snoring to the increased upper airway resistance syndrome to sleep apnea, are now recognized as major health problems. The majority of patients have excessive daytime sleepiness and tiredness. Neuropsychological dysfunction results in poor work performance, memory impairment, and even depression. Until recently, the coexistence of cardiovascular and cerebrovascular diseases with sleep-related breathing disorders was thought to be the result of shared risk factors, such as age, sex, and obesity. However, in the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic tone, and altered baroreflex control during sleep. Sleep apnea may lead to the development of cardiomyopathy and pulmonary hypertension. Early recognition and treatment of sleep-related breathing disorders may improve cardiovascular function.
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PMID:Sleep-related breathing disorders and cardiovascular disease. 1075 96

Obstructive sleep apnea syndrome (OSAS) is characterized by prolonged, generally partial, upper airway obstruction associated with hypoxemia and/or hypercapnia. Main etiological factors include hypertrophy of the tonsils and adenoids, craniofacial abnormalities with reduction in the upper airway caliber, abnormality of neural upper airway control, or a combination of these factors. Symptoms depend on age, but they always include snoring and breathing difficulties during sleep. Diagnosis of OSAS must be established early in order to prevent complications. It is suspected on history, physical examination and investigative confrontation such as nasofibroscopy and imaging. Polysomnography is the gold standard for diagnosis, scoring of the obstruction and distinction between primary snoring and obstructive breathing. Adenotonsillectomy is an effective therapy. For selected patients, craniofacial surgery may be helpful. Some children require continuous positive airway pressure or the nasopharyngeal tube. Tracheotomy is rarely indicated.
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PMID:[Obstructive sleep apnea syndrome in infants and children]. 1107 66

We experienced a family in whom sleep apnea syndrome (SAS) was recognized in six members and habitual snoring in seven members among 26 subjects of four generations. In all members with snoring, the disorder was noticed before the age of 20. Hypercapnic response study showed normal findings, and ultrafast magnetic resonance image of the upper airway revealed that the obstruction of the upper airway occurred at the velopharyngeal portion during apneic episodes in all SAS-afflicted subjects. In this family, the similar craniofacial structural abnormalities were thought to cause the aggregated occurrences of the disorders at young ages, and obesity was regarded as a contributor for the aggravated symptoms.
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PMID:Aggregated occurrence of sleep apnea syndrome in a family. 1142 63

This issue of Sleep and Breathing presents a section on sleep in COPD, a widespread disease consuming many health resources which is often diagnosed so late that little chance of reversibility remains. The early detection of the warning clinical signs can include sleep studies, mainly in the presence of arterial carbon dioxide levels higher than expected from pulmonary function tests. Two of the articles deal with hypercapnia and nocturnal hypoventilation in COPD; the third underlines the impact of tobacco smoking on snoring and on oxygen availability to tissues, showing a poor reliability of pulse oximetry in subjects with heavy smoking habits.
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PMID:Sleep disordered breathing and COPD. 1191 57

Obstructive sleep apnoea is a disease of increasing importance because of its neurocognitive and cardiovascular sequelae. Abnormalities in the anatomy of the pharynx, the physiology of the upper airway muscle dilator, and the stability of ventilatory control are important causes of repetitive pharyngeal collapse during sleep. Obstructive sleep apnoea can be diagnosed on the basis of characteristic history (snoring, daytime sleepiness) and physical examination (increased neck circumference), but overnight polysomnography is needed to confirm presence of the disorder. Repetitive pharyngeal collapse causes recurrent arousals from sleep, leading to sleepiness and increased risk of motor vehicle and occupational accidents. The surges in hypoxaemia, hypercapnia, and catecholamine associated with this disorder have now been implicated in development of hypertension, but the association between obstructive sleep apnoea and myocardial infarction, stroke, and congestive heart failure is not proven. Continuous positive airway pressure, the treatment of choice for obstructive sleep apnoea, reduces sleepiness and improves hypertension.
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PMID:Obstructive sleep apnoea. 1250 19

Sleep-related breathing disorders (SRBDs) represent a spectrum of abnormalities that range from simple snoring to upper airway resistance syndrome to sleep apnea. The clinical presentation may include obesity, snoring, neuropsychological dysfunction, and daytime hypersomnolence and tiredness. The acute hemodynamic alterations of obstructive sleep apnea include systemic and pulmonary hypertension, increased right and left ventricular afterload, and increased cardiac output. Earlier reports attributed the coexistence of SRBDs with cardiovascular diseases to the shared risk factors such as age, sex, and obesity. However, recent epidemiologic data confirm an independent association between SRBDs and the different manifestations of cardiovascular diseases. Possible mechanisms may include a combination of intermittent hypoxia and hypercapnia, repeated arousals, sustained increase in sympathetic tone, reduced baroreflex sensitivity, increased platelet aggregation, and elevated plasma fibrinogen and homocysteine levels. The strength of the association, its pathogenesis, and the impact of treatment of SRBDs on the health outcome of patients with cardiovascular diseases are issues to be addressed in future studies.
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PMID:Cardiovascular consequences of sleep-related breathing disorders. 1235 Feb 42

Acute confusional syndrome, or delirium, is a transitory mental state characterized by the fluctuating alteration of awareness and attention levels. We present the case of a patient with acute confusional syndrome associated with obstructive sleep apnea syndrome (OSAS) aggravated by metabolic acidosis induced by oral acetazolamide treatment.A 70-year-old man with no history of neurological disease was referred with a clinical picture consistent with acute confusional syndrome presenting between midnight and dawn. During the admission examination infectious, toxic, and neurologic causes, or those related to metabolic or heart disease were ruled out. Arterial blood gases measured during one of the nighttime episodes of acute confusional syndrome showed mild hypoxia and hypercapnia with mixed acidosis. Signs and symptoms suggestive of OSAS had been developing over the months prior to admission, with snoring, sleep apnea, and moderate daytime drowsiness. Polysomnography demonstrated severe OSAS with an apnea-hypopnea index of 38. Mean arterial oxygen saturation was 83%; time oxygen saturation remained below 90% was 44%. The attending physician ordered the withdrawal of oral acetazolamide, which was considered the cause of the metabolic component of acidosis. Treatment with continuous positive airway pressure was initiated at 9 cm H2O, after a titration polysomnographic study. The patient continued to improve.OSAS, for which very effective treatment is available, should be included among diseases that may trigger acute confusional syndrome.
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PMID:[Acute confusional syndrome associated with obstructive sleep apnea aggravated by acidosis secondary to oral acetazolamide treatment]. 1516 96

The problems children have in sleeping are manifold; the gamut of disorders that have been described ranges from simple, occasional snoring with no accompanying complications, through the syndrome of increased blockage of the upper airways to the obstructive sleep apnea-hypopnea syndrome (OSAHS) where respiratory difficulties accompanied by hypoxemia, hypercapnia and structural sleep difficulties. Mouth breathing and chronic snoring occur frequently in children, with the incidence of snoring, identical for both sexes, varying between 3.2 and 27%. Difficulties in sleeping begin between the ages of the 3 and 9, peaking between 3 and 6. These results demonstrate, in a general way, the disparity between growth of the adenoids and tonsils, and upper airway growth. A differential diagnosis between the various pathological possibilities is based on the observed clinical signs and symptoms, analysis of cephalometric radiographs, polysomnography, a nocturnal cardio-respiratory polygraph and a video film taken during sleep. Snoring is the most characteristic sign of OSAHS in children. We do not yet have available any synthetic study that would sum up results of studies of sleep disorders in children. Nevertheless, we can define obstructive sleep apnea in children as the partial or total cessation of nose and mouth breathing for a period double that of the normal respiratory cycle. Classical treatment of children who suffer from severe respiratory difficulties during sleep, after identification of the etiology of the problem, consists of surgical removal of the adenoids or tonsils and, in certain, continuous positive pressure to assist breathing. The authors of this article have worked with 137 patients between the ages of 6 and 9, 77 of whom were chronic snorers with an average age of 7 years 6 months. The average age of the control group of 60 children was 7 years 2 months. We collected clinical data, medical histories, and distributed a questionnaire to determine individual sleep and vigilance behavior of each child in the sample. To complete our evaluation, we made a cephalometric analysis of facial type, antero-postero skeletal pattern, upper airways, and hyoid bone position. The symptom that we encountered most frequently in young chronic snorers was agitated and uneasy sleep, sometimes accompanied by bed-wetting and cervical hyperextension. We often found daytime symptoms of hyperactivity and personality or behavioral problems. Hypertrophy of the adenoids, the adenoidal fascia, and the tonsils were also frequent clinical signs. The cephalometric analyses often showed the patients to be of the dolichocephalic facial type, often with the mandible rotated posteriorly. The children were as likely to be classified as Class II owing to retrognathic mandibles as to be Class III owing to maxillary deficiencies or mandibular excess. At the level of the upper airways, it appears that the development of snoring can be explained by a reduction in the dimensions of the upper pharynges accompanied by an increase in the dimensions of the middle and lower pharynges.
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PMID:[Chronic snoring and obstructive sleep apnea-hypopnea syndrome in children]. 1530 72

Obstructive sleep apnea syndrome is caused by upper airway collapse during inspiration, causing intermittent hypoxemia, hypercapnia, acidosis, sympathetic nervous system activation, and arousal from sleep. Nighttime blood pressure is higher, but unexpectedly, daytime hypertension occurs. The prevalence of hypertension is very high and the incidence of hypertension increases as the number of apneic and hypopneic events per hour rises. Obesity is a major predisposing factor for the development of obstructive sleep apnea. Daytime sleepiness, snoring, and breathing pauses are important symptoms to elicit from the patient or sleep partner. Resistant hypertension is an important clue. Overnight polysomnography is required for diagnosis. Weight loss, avoidance of nocturnal sedatives, cessation of evening alcohol ingestion, and avoidance of the supine position during sleep are initial therapeutic actions in mild obstructive sleep apnea syndrome. Continuous positive airway pressure is the treatment of choice for patients unable to find relief from lifestyle changes. Blood pressure modestly improves with treatment.
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PMID:Obstructive sleep apnea syndrome. 1702 91

Obstructive sleep apnea (OSA) syndrome is a disorder characterized by repetitive episodes of upper airway obstruction that occur during sleep. Associated features include loud snoring, fragmented sleep, repetitive hypoxemia/hypercapnia, daytime sleepiness, and cardiovascular complications. The prevalence of OSA is 2-3% and 4-5% in middle-aged women and men, respectively. The prevalence of OSA among obese patients exceeds 30%, reaching as high as 50-98% in the morbidly obese population. Obesity is probably the most important risk factor for the development of OSA. Some 60-90% of adults with OSA are overweight, and the relative risk of OSA in obesity (BMI >29 kg/m(2)) is >or=10. Numerous studies have shown the development or worsening of OSA with increasing weight, as opposed to substantial improvement with weight reduction. There are several mechanisms responsible for the increased risk of OSA with obesity. These include reduced pharyngeal lumen size due to fatty tissue within the airway or in its lateral walls, decreased upper airway muscle protective force due to fatty deposits in the muscle, and reduced upper airway size secondary to mass effect of the large abdomen on the chest wall and tracheal traction. These mechanisms emphasize the great importance of fat accumulated in the abdomen and neck regions compared with the peripheral one. It is the abdomen much more than the thighs that affect the upper airway size and function. Hence, obesity is associated with increased upper airway collapsibility (even in nonapneic subjects), with dramatic improvement after weight reduction. Conversely, OSA may itself predispose individuals to worsening obesity because of sleep deprivation, daytime somnolence, and disrupted metabolism. OSA is associated with increased sympathetic activation, sleep fragmentation, ineffective sleep, and insulin resistance, potentially leading to diabetes and aggravation of obesity. Furthermore, OSA may be associated with changes in leptin, ghrelin, and orexin levels; increased appetite and caloric intake; and again exacerbating obesity. Thus, it appears that obesity and OSA form a vicious cycle where each results in worsening of the other.
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PMID:Abdominal fat and sleep apnea: the chicken or the egg? 1859 60


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