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

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

A 47 year old man with a long history of chronic loud snoring and daytime sleepiness presented with hypercapnic respiratory failure and right ventricular failure. The diagnosis of obstructive sleep apnoea (OSA) leading to the 'obesity-hypoventilation syndrome', was supported by the findings of an overnight cardio-respiratory monitoring during sleep. His symptoms and arterial blood gases improved following treatment with nocturnal nasal continuous positive airway pressure (CPAP).
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PMID:Cor pulmonale due to obstructive sleep apnoea. 818 51

Patients with obstructive sleep apnea demonstrate both acute and chronic hemodynamic changes attributable to their disease. Acutely, these patients experience repetitive nocturnal hemodynamic oscillations. Sudden increases in heart rate and arterial pressure occur in association with decreases in left ventricular stroke volume immediately following apnea termination. These hemodynamic changes are likely attributable primarily to the effects of oxygen desaturation and arousal, an abrupt change in state. These acute changes occur against a background of altered cardiovascular control. Patients with sleep apnea, even when sleeping without obstructions, fail to display the normal nocturnal decline in arterial pressure of 10-15% from the waking value. The absence of a nocturnal decline may have chronic consequences, such as development of left ventricular hypertrophy. Another chronic hemodynamic consequence of sleep apnea may be sustained diurnal hypertension. Epidemiologic studies suggest individuals with sleep disordered breathing are at greater risk of daytime hypertension, even after controlling for other risk factors. Although sleep apnea may contribute to pulmonary, as well as systemic hypertension, sleep apnea alone does not appear to be a cause of decompensated right heart failure. Although knowledge of the hemodynamic consequences of sleep apnea has grown in recent years, much remains to be learned.
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PMID:Hemodynamic consequences of obstructive sleep apnea. 884 30

Obstructive sleep apnoea (OSA) produces immediate effects on pulmonary haemodynamics during sleep in all subjects. In addition, in some subjects, OSA is accompanied by chronic abnormalities of the pulmonary circulation. During sleep, pressure in the main pulmonary artery oscillates within each apnoea, in synchrony with intrathoracic pressure changes; in addition, it may increase progressively as a consequence of prolonged severe hypoxaemia. Pulmonary capillary wedge pressure may increase during inspiratory efforts, possibly reflecting a mechanical limitation of left ventricular function. Cardiac output decreases at apnoea resolution as an effect of a decreased right ventricular stroke volume, despite increased cardiac frequency. During wakefulness, postcapillary pulmonary hypertension occurs on exercise in many OSA patients, whilst pulmonary hypertension at rest is precapillary and occurs in patients with an altered daytime respiratory function. Development of right ventricular hypertrophy and a decrease in right ventricular ejection fraction appear to be related to the severity of respiratory alterations during sleep, whilst an overt right heart failure requires an altered daytime respiratory function. Long-term treatment of the obstructive sleep apnoea syndrome is more effective in increasing right ventricular ejection fraction than in decreasing pulmonary artery pressure during wakefulness.
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PMID:Acute and chronic influences of obstructive sleep apnoea on the pulmonary circulation. 927 Feb 54

There is conclusive evidence that obstructive sleep apnoea syndrome (OSAS) influences right heart haemodynamics and can also induce pulmonary hypertension. It is not known, however, whether right ventricular dysfunction can occur in patients with OSAS in the absence of lung disease. We studied 107 patients (94 males, 13 females, mean age 55 +/- 11 yrs) with polysomnographically verified OSAS in whom clinically significant lung disease was excluded. Right ventricular ejection fraction (RVEF) was determined by radionuclide ventriculography. In addition, pulmonary function tests, arterial blood gas analysis and right heart catheterization were performed. RVEF was impaired in 19 patients (18%). Eighteen (95%) had signs or symptoms consistent with mild right ventricular failure. Patients with or without impaired RVEF did not differ with respect to body mass index, age or lung function. Stepwise multiple logistic regression analysis revealed that RVEF was significantly associated with the apnoea/hypopnoea index (r = -0.68; p = 0.0009) and the extent of nocturnal oxyhaemoglobin saturation (r = 0.42; p = 0.035), but not with age, body mass index, blood gas analysis, gender, lung function, pulmonary artery pressure and left ventricular ejection fraction. We conclude that in patients with otherwise unexplained right ventricular failure, obstructive sleep apnoea syndrome may underlie the right ventricular dysfunction.
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PMID:Right ventricular dysfunction in patients with obstructive sleep apnoea syndrome. 931 6

The prevalence of sleep apnea syndrome (SAS) is approximately 7.5% in Japanese adults aged 18-68 years old. SAS is characterized by repeated episodes of apnea, especially obstructive apnea, during sleep. Severe SAS has life-threatening complications such as pulmonary hypertension, arrhythmias, right heart failure or brain damage, which could be caused by hypoxemia and/or hypercapnia. Upper airway relaxation is responsible for the obstruction during apnea, and an increase in the activities of the upper airway muscles dilates and stiffens the upper airway wall. Maintaining the activities of the upper airway muscles may contribute to keeping the airway patent. Submental electrical stimulation of the upper airway muscles would be a novel treatment method for obstructive apnea.
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PMID:New strategies of screening and treatment for sleep apnea syndrome. 1032 56

Ventricular hypertrophy is associated with an increased risk of cardiovascular death and cardiac events. In response to a haemodynamic load, ventricular hypertrophy may either be eccentric (dilation in response to volume overload) or concentric (increase in wall thickness in response to pressure overload). Ventricular hypertrophy increases with age, weight, blood pressure, and the presence of cardiovascular disease. It is greater in men than in women when adjusting for other variables. Echocardiography is the best method for accurate quantification of left ventricular mass and for detecting right ventricular hypertrophy. In obstructive sleep apnoea there are reports of both eccentric and concentric hypertrophy of the left ventricle. However, many of these reports have failed to control for patient weight or age. More recent reports indicate that much of the hypertrophy of the left ventricle reported in obstructive sleep apnoea can be related to patients' age, blood pressure, or size. However, right ventricular hypertrophy appears to be distinctly associated with the presence and severity of obstructive sleep apnoea. Right ventricular hypertrophy secondary to obstructive sleep apnoea may be the substrate for the eventual development of cor pulmonale and right heart failure. Its pathophysiological significance and potential use as a marker of severe OSA requires further investigation. Further investigation into left ventricular hypertrophy and sleep apnoea must control for the potentially confounding variables listed above and will require population-based and/or carefully matched case control studies.
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PMID:Ventricular hypertrophy in sleep apnoea. 1060 97

A 6-year-old boy with Hurler's syndrome presented with right heart failure and pulmonary hypertension secondary to severe obstructive sleep apnoea. Both his sleep apnoea and cor pulmonale were effectively controlled with continuous positive airway pressure therapy.
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PMID:Hurler's syndrome with cor pulmonale secondary to obstructive sleep apnoea treated by continuous positive airway pressure. 1296 15

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


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