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

Cough, sleep fragmentation and oxyhaemoglobin desaturation have all been documented during sleep in patients with cystic fibrosis (CF). It has been proposed that repeated episodes of nocturnal hypoxia act as a stimulus for the development of pulmonary hypertension and right ventricular failure, a complication that is associated with a poor prognosis. In addition, sleep disturbance from these events could lead to poor daytime function and quality of life. This review provides a detailed description of the mechanisms underlying sleep disordered breathing in this population, what is known regarding its effects upon daytime function and current treatment options. Most importantly, we review what is needed from future research in this challenging area of care in patients with CF.
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PMID:Sleep disordered breathing in cystic fibrosis. 1523 53

Chronic alveolar hypoventilation is a classic feature of the "pickwickian syndrome" (i.e. obesity-hypoventilation syndrome) but in fact hypercapnia is observed in a minority of obstructive sleep apnoea syndrome (OSAS) patients. Most recent studies having included large numbers of unselected, consecutive OSAS patients agree on a prevalence of 10-20% of alveolar hypoventilation. The mechanisms of hypercapnia in OSAS are not fully understood but the determining factors of daytime respiratory insufficiency are probably the presence of a marked obesity, leading to the obesity hypoventilation syndrome and, principally, the association of OSAS with chronic obstructive pulmonary disease. This association (the so-called "overlap syndrome") is observed in >10% of OSAS patients. Bronchial obstruction is generally mild to moderate and may be asymptomatic. The severity of the nocturnal events (apnoeas, hypopnoeas) and a (possible) diminished chemosensitivity to hypercapnic and hypoxic stimuli do not appear to be determining factors of hypercapnia. The most important consequence of chronic alveolar hypoventilation is pulmonary hypertension which is only observed in patients with daytime arterial blood gases disturbances, and which can lead to right heart failure. When nasal continuous positive airway pressure fails to correct sleep-related hypoxaemia, supplementary O, must be given or another way of assisted ventilation (BIPAP) must be considered. In the most severe patients (diurnal PaO(2) <55 mmHg) conventional O(2) therapy (>or=16h/24h) is required in addition to nocturnal ventilation.
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PMID:Daytime hypoventilation in obstructive sleep apnoea syndrome. 1531 Apr 91

Sleep has effects on breathing, including changes in respiratory control, airways resistance and muscular contractility. These sleep-related modifications in the respiratory system do not induce adverse effects in healthy subjects, but may cause problems in patients with chronic obstructive pulmonary disease (COPD). Hypo-ventilation causes the most important gas-exchange alteration during sleep in COPD patients, leading to hypercapnia and hypoxemia, especially during rapid-eye-movement (REM) sleep. Blood gases alterations lead to increased arousals, sleep disruption, pulmonary hypertension and higher mortality. The presence of other sleep-related breathing disorders, like sleep apnea syndrome, may induce a more pronounced impairment of gas exchange, both during sleep and wakefulness, and development of symptoms like excessive daytime somnolence. Nocturnal oximetry is recommended to evaluate gas exchange during sleep in COPD patients. Sleep studies are usually indicated when there is a possibility of sleep apnea or obesity-hypoventilation syndrome. The role of non-invasive mechanical ventilation in managing COPD patients with nocturnal hypoventilation is discussed.
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PMID:Sleep disordered breathing in patients with chronic obstructive pulmonary disease. 1533 44

In this article we summarize the available information regarding the epidemiology, the pathophysiology as well as the risk factors and complications of the sleep apnea syndrome (SAS). Central, obstructive and mixed forms of SAS are known, however, the obstructive form is (resulting from the actual high prevalence of obesity) definitely the most frequent. Latest years of experimental and clinical research have pointed towards the clinical importance of this sleep related breathing disorder. High prevalence in the population and especially the cardiovascular complications (e. g. systemic and pulmonary hypertension, atherosclerosis, arrhythmias) have contributed to the recent increase in knowledge about SAS. Nevertheless, there are numerous unsolved problems and unanswered questions in the pathophysiology of SAS. Future studies should, thus, provide us with more information and shed light on regarding the hidden mysteries of SAS.
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PMID:Sleep apnea syndrome and its complications. 1535 82

The aim of this review was to analyse the effects of intermittent hypoxia (IH) on pulmonary haemodynamics, comparing results of animal experiments with results of clinical studies. In animal investigations even short hypoxic exposure, continuously or in short repeated episodes mimicking obstructive sleep apnoea (OSA), leads to pulmonary artery remodelling and to pulmonary hypertension (PH). Results of investigations on effects of nocturnal IH on pulmonary haemodynamics in patients with chronic obstructive pulmonary disease (COPD) are discordant. Earlier studies reported the development of mild PH in subjects desaturating during sleep, while more recent investigations did not confirm those findings. Alveolar IH developing during apnoeic episodes during sleep in OSA patients is a disease-induced model to study its effects on pulmonary haemodynamics. In the majority of studies in OSA patients pulmonary arterial pressure remained within normal values. PH was found in patients with OSA accompanied by COPD and/or extreme obesity. People commuting between lowland and high altitude due to their employment, are also repeatedly exposed to IH. Results of clinical investigations suggest that it did not lead to the development of permanent PH. The mechanisms of discrepancies between effects of intermittent hypoxia in animal models and in humans remain to be studied.
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PMID:Effects of intermittent hypoxia on pulmonary haemodynamics: animal models versus studies in humans. 1564 Mar 39

Obstructive sleep apnea syndrome (OSA) is a condition affecting up to 5% of the population, in which episodes of upper airway obstruction lead to temporary cessation of airflow, disturbed sleep architecture and daily somnolence. The health consequences of OSA also include psychological and cognitive deficits, an increased risk of systemic and pulmonary hypertension, coronary disease, bradyarrhythmias and motor vehicle accidents. Symptoms and complications of OSA lead to a significant decrease of health-related quality of life (HRQOL) of affected patients. We review the current literature on HRQOL effects of OSA and its treatment. There is good evidence of beneficial effect of the continuous positive airway pressure (CPAP) therapy on the quality of life of patients with OSA. Improvements in HRQOL are most appreciable in patients with moderate to severe OSA, although they also seem to be present in selected patients with mild OSA. The effects of dental devices and surgical procedures on HRQOL of patients with OSA have not been studied in randomized, placebo-controlled trials. Health-related quality of life has become one of the major outcome measures in patients with sleep apnea. Assessment of HRQOL has become a crucial part of any clinical study involving patients with OSA.
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PMID:[Quality of life in patients with obstructive sleep apnea]. 1575 24

QT interval dispersion (QT(d)) reflects inhomogeneity of repolarisation. Delayed cardiac repolarisation leading to the prolongation of the QT interval is a well-characterised precursor of arrhythmias. Obstructive sleep apnoea syndrome (OSAS) can cause cardiovascular complications, such as arrhythmias, myocardial infarction, and systemic and pulmonary hypertension. The aim of this study was to assess QT(d) in OSAS patients without hypertension. A total of 49 subjects without hypertension, diabetes mellitus, any cardiac or pulmonary diseases, or any hormonal, hepatic, renal or electrolyte disorders were referred for evaluation of OSAS. An overnight polysomnography and a standard 12-lead ECG were performed in each subject. According to the apnoea-hypopnoea index (AHI), subjects were divided into control subjects (AHI <5, n = 20) and moderate-severe OSAS patients (AHI > or =15, n = 29). QT(d) (defined as the difference between the maximum and minimum QT interval) and QT-corrected interval dispersion (QT(cd)) were calculated using Bazzet's formula. In conclusion, the QT(cd) was significantly higher in OSAS patients (56.1+/-9.3 ms) than in controls (36.3+/-4.5 ms). A strong positive correlation was shown between QT(cd) and AHI. In addition, a significantly positive correlation was shown between QT(cd) and the desaturation index (DI). The AHI and DI were significantly related to QT(cd) as an independent variable using stepwise regression analysis. The QT-corrected interval dispersion is increased in obstructive sleep apnoea syndrome patients without hypertension, and it may reflect obstructive sleep apnoea syndrome severity.
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PMID:QT interval dispersion in obstructive sleep apnoea syndrome patients without hypertension. 1580 42

The activation of adrenergic and renin-angiotensin-aldosterone (RAA) systems observed in patients with obstructive sleep apnoea syndrome (OSA) strongly affects functional status of the cardiovascular system. In this paper we discuss the link between obstructive sleep apnoea syndrome and common cardiovascular diseases such as systemic and pulmonary hypertension, ischaemic heart disease, stroke, arrhythmia and ventricular hypertrophy. We also present the importance of early pharmacologic treatment in preventing cardiac hypertrophy and ventricular dysfunction in patients with obstructive sleep apnoea syndrome.
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PMID:[Cardiovascular abnormalities in patients with obstructive sleep apnoea syndrome]. 1599 58

The modern era in cardiopulmonary medicine began in the 1940s, when Cournand and Richards pioneered right-heart catheterization. Until that time, no direct measurement of central vascular pressure had been performed in humans. Right-heart catheterization ignited an explosion of insights into function and dysfunction of the pulmonary circulation, cardiac performance, ventilation-perfusion relationships, lung-heart interactions, valvular function, and congenital heart disease. It marked the beginnings of angiocardiography with its diagnostic implications for diseases of the left heart and peripheral circulation. Pulmonary hypertension was discovered to be the consequence of a large variety of diseases that either raised pressure downstream of the pulmonary capillaries, induced vasoconstriction, increased blood flow to the lung, or obstructed the pulmonary vessels, either by embolism or in situ fibrosis. Hypoxic vasoconstriction was found to be a major cause of acute and chronic pulmonary hypertension, and surprising vasoreactivity of the pulmonary vascular bed was discovered to be present in many cases of severe pulmonary hypertension, initially in mitral stenosis. Diseases as disparate as scleroderma, cystic fibrosis, kyphoscoliosis, sleep apnea, and sickle cell disease were found to have shared consequences in the pulmonary circulation. Some of the achievements of Cournand and Richards and their scientific descendents are discussed in this article, including success in the diagnosis and treatment of idiopathic pulmonary arterial hypertension, chronic thromboembolic pulmonary hypertension, and management of hypoxic pulmonary hypertension.
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PMID:Pulmonary hypertension. 1599 64

Chronic cor pulmonale involves the enlargement of the right ventricle as a result of pulmonary hypertension due to pulmonary disorders involving the lung parenchyma, bellows function, or ventilatory drive. The right ventricular hypertrophy that occurs in chronic cor pulmonale is a direct result of chronic hypoxic pulmonary vasoconstriction and subsequent pulmonary artery hypertension, leading to increased right ventricular work and stress. We discuss methods by which hypoxic vasoconstriction and reduction in the pulmonary vascular bed lead to the development of pulmonary artery hypertension. This article reviews the interaction of the pulmonary vasculature and right ventricle in the non-diseased state as well as during disease exacerbations. Ventricular dependence and its contribution to the pathophysiology of right ventricular failure are also reviewed. In addition, we provide an overview of specific disease states that can result in the development of chronic cor pulmonale including chronic obstructive pulmonary disease (COPD), interstitial lung disease, sleep apnea, alveolar hypoventilation disorders, and primary pulmonary hypertension. We also review the current diagnostic studies used to evaluate and study cor pulmonale.
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PMID:Cor pulmonale: an overview. 1608 45


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