Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with autonomic insufficiency and extrapyramidal signs (Shy-Drager syndrome) and sleep apnea syndrome (SAS) underwent hemodynamic studies. In comparison to patients with SAS and intact autonomic reflexes, systemic hypertension was absent and marked sinus arrhythmia during sleep was blunted. Cyclical pulmonary hypertension associated with frequent apneic episodes during sleep persisted, reflecting a minor role of autonomic reflexes in the generation of this abnormality. Autopsy confirmed the Shy-Drager syndrome and multiple areas of degeneration were observed in areas of the CNS outside the medullary respiratory centers, suggesting their importance in the origin of the respiratory abnormalities in SAS.
 ...
PMID:Sleep apnea syndrome in a patient with Shy-Drager syndrome. 62 49

Twelve patients with predominantly obstructive type sleep apnea underwent cardiac catheterization, hemodynamic monitoring, and arterial blood gas analysis during wakefulness and sleep. Abnormalities during wakefulness included systemic hypertension in four of 12, exercise-induced mild pulmonary hypertension in five of 12, and alveolar hypoventilation in one. During sleep nine patients had cyclic elevations of arterial pressure with each apneic episode, exceeding 200 mm Hg systolic in three of 12. Pulmonary artery pressures increased in 10 of 12, exceeding 60 mm Hg systolic in five. Marked degrees of hypoxemia (arterial P02, less than 50 mm Hg in eight of 12) and moderate hypercapnia with respiratory acidosis were associated with these hemodynamic changes. Cyclic upper airway obstruction during sleep may result in hypercapnia, acidosis, and pronounced hypoxemia, which can lead to hemodynamic abnormalities during sleep. Sustained pulmonary hypertension and possibly systemic hypertension may follow. Tracheostomy is an effective therapy and is recommended to symptomatic patients who have predominantly obstructive apnea but no relievable anatomic cause of upper airway obstruction.
 ...
PMID:Hemodynamics in sleep-induced apnea. Studies during wakefulness and sleep. 99 7

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.
 ...
PMID:Sleep apnoea: causes, consequences and treatment. 141 52

We describe a twentieth month old infant who had a pycnodysostosis syndrome. This malformation shows a loss of the normal mandible angle with generalized bone hyperdensification. The first produced and airway obstruction, with special relevance during sleeping hours. A polysomnography revealed an obstructive sleep apnea syndrome. The respiratory picture deteriorated with worsening of the airway obstruction, hypoxemia and finally pulmonary hypertension and cor pulmonale. A tracheostomy was performed, with resolution of the sleep apnea and pulmonary hypertension. The etiology, pathophysiologic consequences and surgical treatment of obstructive sleep apnea syndrome is reviewed.
 ...
PMID:[Pyknodysostosis: extreme cause of sleep apnea]. 150 55

Obstructive sleep apnea may contribute to the development of pulmonary hypertension and RVF primarily through pulmonary vasoconstriction secondary to hypoxia. Several recent studies indicate, however, that intermittent apnea-related hypoxia is not sufficient to cause sustained pulmonary hypertension. These studies have been consistent in showing that pulmonary hypertension and RVF are almost invariably seen in the presence of diurnal hypoxia. Sustained pulmonary hypertension, therefore, appears to be associated with sustained hypoxia as is the case in COPD. Patients with OSA who have hypoxia while awake are, as a rule, obese and have mild-to-moderate diffuse obstructive airways disease. Thus, most cases of pulmonary hypertension in association with OSA result from a combination of OSA, obesity, and diffuse obstructive airways disease, a so-called overlap syndrome. However, from the therapeutic viewpoint, it is apparent that treatment of OSA by NCPAP or tracheostomy, in such cases, is usually sufficient to reverse pulmonary hypertension and RVF. More recent work has provided strong evidence that OSA can play a role in the pathogenesis of LV heart failure in patients with CHF of otherwise unknown etiology. It is likely that this occurs through a combination of increased LV afterload related to exaggerated negative Pit swings during obstructive apneas, to intermittent hypoxia, and to chronically elevated sympathoadrenal activity. Reversal of OSA by NCPAP in these patients may relieve LV heart failure. These findings add a new dimension to our understanding of the pathophysiologic effects of OSA on the cardiovascular system by demonstrating that the LV is a structure that may suffer functional impairment secondary to the stresses imposed by OSA. Finally, it has now become apparent that CSR in patients with CHF can cause symptoms of a sleep apnea syndrome when associated with intermittent hypoxia and arousals from sleep. Reversal of CSR during sleep by NCPAP can lead to alleviation of these symptoms and possibly to reduced cardiac dyspnea and LV systolic function as well. Taken together, this suggests that much more extensive use of polysomnography may be warranted in the investigation of cardiovascular disease. The reasons are compelling: sleep apnea disorders are common and eminently treatable conditions whose reversal can result in improved right and left heart function and symptomatic improvement in patients with impaired myocardial function.
 ...
PMID:Right and left ventricular functional impairment and sleep apnea. 152 13

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.
 ...
PMID:Long-term effects of gastric surgery for treating respiratory insufficiency of obesity. 173 36

This case report describes 3 patients with Down syndrome and obstructive breathing problems, ages: 5 months, 15 months, and 22 years. The youngest one had normal cardiopulmonary function at birth, but soon developed a pulmonary hypertension. The next had a severe atrioventricular defect and additional pulmonary hypertension and there was little hope for her to survive heart surgery. The oldest one had had apneas since childhood with increasing severity, but was regarded as having normal heart function. All 3 were operated to relieve their breathing obstruction. The 5-month-old boy improved only slightly after an initial UPPP and had to be tracheotomized, which solved his problems. The tracheotomy could be removed when he was one year. The 15-month-old girl was cured of her breathing problems through an A + T and survived her heart surgery one month later. Tonsillectomy and UPPP was performed on the oldest patient. Following surgery, he had an episode of life-threatening bleeding and developed a DIC syndrome, and was critically ill for 18 days. After he recovered, his sleep apnea had improved. Once a myxoedema was diagnosed and treated, he made further progress. These cases stress the significance of early recognition of sleep apnea in children with Down syndrome and the importance of a careful preoperative investigation in collaboration with cardiologists.
 ...
PMID:Down syndrome and sleep apnea--a therapeutic challenge. 183 Nov 85

Sleep apnea syndrome is responsible for repeated and sometimes deep arterial oxygen desaturations occurring during apneas, followed by episodes of transient pulmonary hypertension (PH). In chronic obstructive pulmonary disease (COPD) patients with respiratory insufficiency, a worsening of hypoxemia occurs during sleep, due to alveolar hypoventilation and/or ventilation-perfusion mismatching. This hypoxemia is also responsible for pulmonary hypertensive dips due to pulmonary hypoxic vasoconstrictiveness. But there is presently no evidence that sleep-related and transient PH may lead to daytime and permanent PH, in either sleep apnea syndrome or COPD. In fact permanent PH seems to be related, in most cases, to the presence of daytime (permanent) hypoxemia.
 ...
PMID:[Pulmonary artery hypertension and hypoxemia in sleep]. 185 26

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.
 ...
PMID:Decreased oxyhemoglobin affinity in patients with sleep apnea syndrome. 190 Apr 1

In order to study the frequency and the mechanisms of daytime pulmonary hypertension (PH) in obstructive sleep apnoea syndrome (OSAS) lung function tests, blood gas analysis and right-heart catheterization were performed in 46 consecutive patients. OSAS was assessed by polysomnography. 9 patients only (20%) had PH (mean pulmonary artery pressure (Ppa) greater than or equal to 20 mmHg). Patients with PH had lower daytime PaO2 (60.8 +/- 7.6 vs. 76.2 +/- 9.4 mmHg; p less than 0.001), higher daytime PaCO2 (44.8 +/- 4.2 vs. 38.0 +/- 4.0 mmHg; p less than 0.001), lower forced vital capacity (FVC) and forced expiratory volume (FEV1) (p less than 0.001), but the severity of OSAS was not different whether PH was present or not (apnoea index: 62 +/- 34 hour in the PH group vs. 65 +/- 40 hour, apnoea + hypopnoea index 102 +/- 33 hour in the PH group vs. 86 +/- 36 hour, lowest sleep SaO2: 59 +/- 21% in the PH group vs. 66 +/- 18%). There were significant correlations between Ppa and: daytime PaO2 (r = -0.61; p less than 0.001), PaCO2 (r = 0.55; p less than 0.001), FEV1 (r = -0.52; p less than 0.001) but not between Ppa and apnoea index, apnoea + hypopnoea index, lowest sleep SaO2. PH and daytime hypoxaemia were associated either with chronic airway obstruction or with severe obesity.
 ...
PMID:Frequency and mechanism of daytime pulmonary hypertension in patients with obstructive sleep apnoea syndrome. 191 66


1 2 3 4 5 6 7 8 9 10 Next >>