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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An awakening has taken place over the last 25 years to the science of sleep disorders. Foremost amongst these, both in the medical world and the public eye, has been Sleep Apnoea Syndrome (SAS). The prevalence is thought to be the order of 1-2%. Males are eight times more commonly affected than females, although after the menopause the gap narrows considerably. Sleep apnoea occurs in children, usually in relation to large tonsils and adenoids, but in adult life patients usually present between the age of 40 and 60 and the prevalence increases with age. Numerous apnoeas or hypopnoeas during the night's sleep result in disordered sleep architecture and unrefreshing sleep. This is usually accompanied by night-long snoring which may lead to marital discord and even complaints from neighbours. Symptoms on waking may be a headache and a feeling of not being refreshed by sleep. Sleepiness during the day can interfere with work and social activities and may produce risks to the patient and others if it occurs while operating dangerous machinery or driving. Over a longer time scale SAS results in intellectual and memory deterioration, a higher incidence of ischaemic heart disease, hypertension, polycythemia and pulmonary hypertension. Right heart failure is particularly likely if there is chronic airflow obstruction contributing to a low arterial oxygen level. Asystolic periods and tachyarrhythmias may occur during apnoeic periods. The increased mortality of SAS relates to coronary and cerebrovascular disease and arrhythmias. Sudden death occurs with greater frequency in patients with SAS, mainly at night.
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PMID:Sleep apnoea: causes, consequences and treatment. 141 52

The Pickwickian syndrome can be divided into two primary breathing disorders, which can affect patients alone or in combination: sleep apnea syndrome (SAS) and obesity hypoventilation syndrome (OHS). Between 1980 and 1990, 126 patients with respiratory insufficiency underwent gastric surgery for morbid obesity, 12.5% of the entire series. These patients weighed more (164 +/- 36 vs 135 +/- 25 kg, P less than 0.0001) and were more often men (62% vs 14%, P less than 0.001) than those without pulmonary dysfunction. Sixteen had OHS alone, 65 had SAS alone, and 45 had both. Of those with OHS, 38 have been followed for 5.8 +/- 2.4 y since surgery and 29 are currently asymptomatic. In the 12 patients in whom arterial blood gases were available greater than 5 y since surgery, the PaO2 increased from 54 +/- 10 to 68 +/- 20 mm Hg (P less than 0.0001) and PaCO2 fell from 53 +/- 9 to 47 +/- 11 mm Hg (P = 0.05). Of the 110 patients with SAS, 57 were available for follow-up an average of 4.5 +/- 2.3 y since surgery and 38 were completely asymptomatic, 15 had mild SAS, and 4 had both SAS and OHS. In 40 patients with pre- and post-weight reduction sleep polysomnograms, the sleep apnea index fell from 64 +/- 39 to 26 +/- 26 (P less than 0.0001). Although respiratory insufficiency of obesity patients had a higher operative mortality than did patients without pulmonary dysfunction (2.4% vs 0.2% after gastric bypass), weight loss was associated with significant improvements in sleep apnea, arterial blood gases, pulmonary hypertension, left ventricular dysfunction, lung volumes, and polycythemia.
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PMID:Long-term effects of gastric surgery for treating respiratory insufficiency of obesity. 173 36

Oxyhemogloblin affinity (P50 at pH 7.4, PaCO2 = 40 mm Hg, temperature = 37 degrees C) and 2,3-DPG concentration were assessed in 15 nonsmokers (14 men and one woman 46 to 63 yr of age) with sleep apnea syndrome (SAS) and in 10 normal subjects (eight men and two women 22 to 48 yr of age). In patients with SAS, mean nocturnal apnea index was 46 +/- 20/h, and mean nocturnal SO2 was 86 +/- 6% versus 94.6 +/- 1.8% during the daytime. Daytime mean P50 of the patients was 28.5 +/- 1.2 mm Hg versus 27.1 +/- 0.3 mm Hg in the normal subjects (p less than 0.05). Daytime mean 2.3-DPG was 1.23 +/- 0.25 moles DPG/mole hemoglobin versus 0.80 +/- 0.15 (p less than 0.05). Significant correlations were found in patients between P50 and mean nocturnal SO2 (r = -0.62, p less than 0.01) and between P50 and 2,3-DPG (r = 0.68, p less than 0.01). The measurements were repeated in five patients after surgical or positive-pressure treatment. P50 and 2,3-DPG both decreased and returned to normal values. In conclusion, the oxyhemoglobin dissociation curve is shifted to the right in patients with SAS and there is an increase in 2,3-DPG. These could be protective mechanisms against the development of polycythemia, pulmonary hypertension, and cor pulmonale.
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PMID:Decreased oxyhemoglobin affinity in patients with sleep apnea syndrome. 190 Apr 1

The diagnosis of obstructive sleep apnea is frequently made by taking a meticulous history coupled with a high index of suspicion. Snoring and hypersomnolence are clinical features common to individuals with sleep apnea. Since snoring is said to be a "disease of listeners," it is not uncommon that bed partners reported an increased incidence of depression and marital displeasure. It is for this reason that the spouse or bed partner should be interviewed, since the patient may not be aware of any sleeping problems. Physicians should also be alert to complaints of excessive daytime somnolence, because studies have shown that patients with obstructive sleep apnea are at increased risk for automobile crashes. It has been estimated that approx 58,000 motor vehicle accidents involving people with sleep apnea will occur in the US each yr. By proper diagnosis and treatment, the physician is in a unique position to prevent at least some of the automobile accidents that result from falling asleep while driving. Polysomnography is the only definitive way to obtain a diagnosis of sleep apnea. This allows the physician not only to diagnosis the disorder, but also helps in the evaluation of the severity of the syndrome and selection of therapy. An ENT evaluation is also important in ruling out anatomic disorders that can cause upper airway obstruction. Certain factors, such as alcohol and sedative ingestion, may aggravate the condition in a person predisposed to sleep apnea, and subtle changes, such as unexplained hypertension, polycythemia, and cor pulmonale, should lead one to investigate the possibility of sleep apnea as the etiology.
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PMID:Diagnosis of obstructive sleep apnea. 229 95

Sleep apnea syndromes have been identified only relatively recently. Their most frequent form is characterized by a sleep-related upper airway obstruction resulting in apneas which may repeat themselves up to several hundred times during a night's sleep. Their mean duration is about 30 to 40 seconds, but some apneas last over one minute. Breathing resumption requires an arousal, which may be clearly identified on the EEG but usually goes unnoticed by the patient. The most immediate consequence are hypoxemia and sleep fragmentation. There may be associated arrhythmias and hemodynamic changes, especially in the pulmonary circulation. The predominant clinical signs are snoring (during the breathing resumption between the apneas) and daytime somnolence due to sleep fragmentation. In addition to the risks of work and traffic accidents, these patients run a long-term risk of cardiovascular accidents. About 20% develop pulmonary hypertension, a contributing factor to right heart failure. About 50% are hypertensive, which combined with a frequently observed polycythemia, makes them vulnerable to ischemic accidents. The treatment is based upon the use of continuous positive airway pressure (CPAP) during sleep. In case of failure, surgical alternatives may be considered.
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PMID:[Sleep apnea syndromes]. 253 41

Morbid obesity is not infrequently associated with severe respiratory impairment. In our experience approximately 10 per cent of morbidly obese patients who underwent gastric surgery had severe respiratory impairment. Respiratory insufficiency of obesity can be divided into two primary breathing disorders: the obstructive sleep apnea syndrome (SAS) and the obesity hypoventilation syndrome (OHS). In its most severe form, when both SAS and OHS are present, it is called the Pickwickian syndrome. In our series 59 morbidly obese patients with respiratory insufficiency secondary to obesity underwent gastric surgery for weight reduction. Fourteen had OHS, 19 had SAS and 26 had both. Of these, two patients died of postoperative complications and one died at five weeks with an inconclusive autopsy, totalling an operative mortality rate of 3.4 per cent and a total mortality of 5.1 per cent. In our overall experience morbidly obese patients lost 67 per cent of excess weight after gastric procedures. In conclusion, surgically induced weight loss will markedly improve or correct respiratory insufficiency secondary to obesity. It will improve arterial oxygenation, minimize CO2 retention, expand lung volumes, correct polycythemia, and reduce apnea frequency. The magnitude of changes in these variables is clinically significant. Therefore, respiratory insufficiency of obesity should be considered a major indication for an aggressive approach to weight reduction. The jejunoileal bypass and unbanded gastroplasty operations have an unacceptable incidence of complications or failure, respectively. There is a high degree of recidivism following dietary programs. Sweets eaters will not do well with a gastroplasty procedure. Gastric bypass for individuals addicted to sweets or the vertical banded gastroplasty for "gorgers" are currently our procedures of choice and are associated with the average loss of two thirds of excess weight and correction of breathing problems associated with morbid obesity.
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PMID:Pulmonary function in morbid obesity. 331 3

Sleep apnoea syndromes are a frequent disease, with an incidence of more than 1% in the adult population, a strong male predominance, and a maximal frequency between 40 and 60 years. Their clinical manifestations are dominated by snoring and daytime sleepiness, at times associated with morning headaches, intellectual deficiency, sexual impotence. Obesity, hypertension and polycythemia are not uncommon. These patients are at risk for accidents due to sleepiness, sudden death due to sleep apnoea-related cardiac arrhythmias, ischemic attacks related to hypertension and polycythemia and right heart failure secondary to pulmonary hypertension and alveolar hypoventilation. The most frequent form of sleep apnoea syndromes include obstructive and mixed apnoeas. Their mechanism involves both anatomic factors (upper airway narrowing) and functional factors (defective activation of upper airways dilatory muscles) which lead to upper airway occlusion upon inspiration during sleep. Two therapeutic strategies are possible: a surgical one, uvulopalatopharyngoplasty, the efficacy of which is inconstant and unpredictable and nasal continuous positive airway pressure, which is constantly efficacious but constraining. Central sleep apnoea syndromes are rare, less clearly defined and more difficult to treat.
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PMID:[Sleep apnea syndromes in adults]. 332 Dec 51

In the 24 months after a sleep breathing laboratory opened in a general hospital, 48 patients thought to have a primary sleep breathing disorder were referred for study. Evaluation of breathing during sleep was most useful in those having excessive daytime sleepiness or unexplained polycythemia. The sleep apnea syndrome was documented in 19 of 24 patients with excessive daytime sleepiness. Of 15 patients with unexplained polycythemia, ten were found to have severe hypoxemia during sleep. This experience suggests that facilities for evaluation of sleep breathing disorders should be available in larger medical centers.
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PMID:Diagnosis of sleep breathing disorders in a general hospital. Experience and recommendations. 708 18

This study addresses the hypothesis that patients with obstructive sleep apnea, who exhibit recurrent episodes of oxygen desaturation at night, have higher hematocrit levels than nonapneic control subjects. We prospectively studied 624 patients referred to the sleep disorders center at St. Michael's Hospital because of suspicion of sleep apnea. All patients had nocturnal polysomnography and measurements of hematocrit level, hemoglobin value, WBC count, and platelet count. Smoking history and awake oxygen saturation (SaO2) was recorded in all of them. Nocturnal oxygenation was assessed using three indices: lowest nocturnal SaO2 (LoSaO2), mean nocturnal SaO2 (MnSaO2) and percent of total sleep time spent at SaO2 lower than 85 percent (TST85%). Patients with TST85% in the lowest quartile (TST85% = 0) had minimally lower hematocrit levels than patients with TST85% in the highest quartile (8 < or = TST85% < or = 90): 0.41 +/- 0.03 vs 0.40 +/- 0.02 in female subjects and 0.45 +/- 0.05 vs 0.43 +/- 0.05 in male subjects, respectively (p < 0.05). Multiple linear regression analysis revealed that MnSaO2, age, and pack-years of smoking were significant predictors of hematocrit level, but they accounted for only 9 percent of the variability in hematocrit level (multiple R2 = 0.087; p < 0.05). We conclude that intermittent nocturnal hypoxemia during episodes of apnea does not lead to clinical polycythemia, but is associated with minor elevations in hematocrit value. These small elevations are unlikely to be useful as markers of hypoxic stress associated with sleep apnea.
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PMID:Hematocrit levels in sleep apnea. 808 60

Polycythaemia, peripheral oedema formation and hypertension have classically been described in association with obstructive sleep apnoea (OSA). However, there is very limited information about blood volume in OSA and how it changes during long-term treatment with nasal continuous positive airway pressure (nCPAP). Plasma (PV) and red-cell volumes (RCV), 24-h ambulatory blood pressure (BP), 24-h natriuresis and morning plasma aldosterone, renin activity and atrial natriuretic peptide in 11 men with a mean age of 47 y (range 37-55), apnoea index (AI) of 55 (22-106), body mass index of 36 (30-43) and seated BP of > or = 140/90 mmHg without any medication were measured. BP-measurements were repeated after 3 weeks and all measurements after 3 mo of nCPAP treatment. Aldosterone and 24-h mean heart rates decreased during treatment. Twenty-four-h BP decreased after 3 weeks but that decrease did not persist after 3 mo of treatment. There was a relationship between changes in night-time mean BP and PV and aldosterone. The haematocrit declined in every patient. No significant changes were found in the mean PV or RCV. They were in all instances lower than has earlier been described for normal, non-obese subjects. These data also suggest that OSA causes divergent individual disturbances in blood volume homeostasis which can be corrected by nCPAP.
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PMID:Effect of nasal CPAP treatment on plasma volume, aldosterone and 24-h blood pressure in obstructive sleep apnoea. 895 8


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