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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

Sleep-induced narrowing of the upper airways underlies the widespread and supposedly trivial complaint of snoring, which may not only constitute a risk factor for the cardiocirculatory system, but in predisposed individuals may lead to the OSAS. The latter is a life-threatening condition characterized by repeated episodes of cessation of respiration at night with an associated drop in SaO2. Patients frequently present with hypersomnia, systemic and pulmonary hypertension, and even heart failure. HSD is the term we use to describe the evolutive stages from snoring to OSAS. ICAH, or Ondine's curse, is the clinical syndrome of sleep-related respiratory insufficiency in the absence of airway stenosis. We do not consider central sleep apnea to be an independent disorder. For the treatment of HSD, weight reduction should be attempted first. Also, if there are malformations in the upper airway, they should be surgically corrected. The use of various medications has been rather discouraging, and CPAP and other devices that are intended to overcome the obstruction are poorly tolerated by patients. The most effective surgical treatment for OSAS, even in progressed stages of the disease, is tracheostomy.
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PMID:Sleep-related respiratory disorders. 333 61

Both obstructive sleep apnea and chronic lung disease can be associated with intermittent or chronic hypoxemia leading to pulmonary hypertension and cor pulmonale. When these problems coexist, it is possible that the cardiopulmonary effects are additive. We hypothesized that hemodynamic disturbances in patients with apnea and lung disease would be more severe than in those with apnea alone, and that hemodynamic improvement should follow apnea cure, but perhaps at a slower rate than in those with apnea alone. To test these hypotheses, we prospectively followed 24 patients with sleep apnea syndrome. They were divided into 3 nonrandomized groups. Nineteen patients had both apnea and lung disease. Nine of these agreed to curative tracheostomy (Group 1). The other 10 subjects (Group 2) refused tracheostomy but accepted noncurative therapies, including nocturnal oxygen (n = 9), uvulopalatopharyngoplasty (n = 2), and protriptyline (n = 4). Five subjects with apnea but without clinically obvious lung disease received tracheostomies (Group 3). Subjects were followed at yearly intervals (mean follow-up, 27.2 months) with radionuclide motion studies and, in 15 of 24 who consented, right heart catheterization. The 3 groups did not vary with respect to age, percent ideal weight, or severity of apnea symptoms. The severity of right-sided hemodynamic dysfunction in the group with apnea but no obvious lung disease was less than that in the 2 groups with lung disease. A substantial decrease in pulmonary artery pressure (p = 0.056) and significant improvement in right ventricular ejection fraction occurred in the tracheostomized group with both apnea and lung disease. Pulmonary vascular resistance decreased in both groups receiving tracheostomy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term cardiopulmonary sequelae in patients with sleep apnea and chronic lung disease. 382 78

Sleep apnea syndrome is estimated to affect as many as 2 to 3 percent of the adult male population. Excessive snoring and daytime sleepiness are but a few of the many clues to diagnosis. The hypoxemia occurring as a result of apnea may lead to pulmonary hypertension. Depressed respiratory center neural output or upper airway occlusion during sleep may cause the apnea. There are a number of treatment options available.
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PMID:Sleep apnea syndrome. 389 92

The pulmonary artery pressure values of 65 patients with sleep apnea syndrome were measured at rest and during ergometer exercise up to 100 W. Pulmonary hypertension at rest was found in 13, and during exercise in 31 more patients. Only 8 patients with pathological pressure findings suffered from pulmonary hypertension in combination with a pulmonary or cardiac disease. In the other 36 patients, no indication of a primary cause of pulmonary hypertension apart from sleep apnea syndrome could be found. Out of the 65 patients, 11 with a finding of more than 20 apnea episodes per hour's sleep underwent polysomnographic recordings in the sleep laboratory. The hemodynamic parameters were continuously measured. All 11 patients had a finding of severe sleep apnea with more than 300 apnea episodes during the night of recording. In 6 patients, the appearance of apnea episodes was accompanied by only moderate changes in pulmonary artery pressure. In 5 patients, there were critical increases in pulmonary artery pressure, which went along with increases in cardiac output and in pulmonary capillary wedge pressure. Increases in pulmonary vascular resistance were established in 3 out of these 5 patients, and a slight decrease in 2. The mechanism of hypoxic vasoconstriction of the pulmonary arteries may account for the pressure increases in 3 of our patients, but fails to explain the findings in the other 2 patients. Nocturnal changes in pulmonary artery pressure in patients with sleep apnea may therefore have different causes. Pulmonary hypertension constitutes a severe complication in patients with sleep apnea.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sleep apnea and pulmonary hypertension. 395 Nov 69

A patient with congenital micrognathia, hypersomnia and severe pulmonary hypertension which resulted in sudden death during sleep is described. Hypersomnolence is a well-recognized manifestation of the pickwickian syndrome. A less recognized but similar disorder may affect patients with congenital or acquired micrognathia. The pathogenesis of this syndrome and obstructive sleep apnoea are reviewed. Tracheostomy timeously performed may be life-saving and the value of early resort to this apparently drastic procedure in a high-risk patient is emphasized.
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PMID:Micrognathia, obstructive sleep apnoea and cor pulmonale--a case for tracheostomy. 396 2

Hypoxia is the major cause of pulmonary hypertension and right ventricular hypertrophy in chronic obstructive pulmonary disease, cystic fibrosis, kyphoscoliosis, chronic mountain sickness, and the obesity-hypoventilation and sleep apnea syndromes. Pulmonary hypertension develops in these patients because the long-standing vasoconstriction produced by hypoxia causes muscular hypertrophy of the pulmonary arteries and arterioles. These pathologic changes may regress if alveolar hypoxia is corrected and hypoxic pulmonary vasoconstriction is continuously inhibited. Intermittent inhibition of hypoxic pulmonary vasoconstriction does not reverse these pathologic changes. Since patient noncompliance with oxygen therapy makes it difficult to achieve continual relief of alveolar hypoxia, a drug that inhibits hypoxic vasoconstriction may be useful. Experimental findings indicate that hypoxic pulmonary vasoconstriction requires calcium influx and can be inhibited by certain slow-channel calcium blockers. Studies also demonstrate that slow-channel calcium antagonists can attenuate the pulmonary hypertension and right ventricular hypertrophy produced in rats by chronic hypoxia. Recently, two studies have shown that nifedipine inhibits hypoxic pulmonary vasoconstriction in patients with chronic obstructive pulmonary disease. If further studies demonstrate that these short-term effects are sustained, certain slow-channel calcium blockers may become a useful adjuvant to low-flow oxygen therapy in the treatment of hypoxic pulmonary hypertension.
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PMID:Calcium channel blockers in hypoxic pulmonary hypertension. 397 91

This study describes the case of a 58 year old man who presented with an episode of acute respiratory failure and right heart decompensation. After recovery from the acute illness, hypoxaemia, hypercapnia and pulmonary arterial hypertension remained, the causes of which were not known. There was no airway obstruction, only a moderate restrictive ventilatory defect, a little weight increase and a unilateral diaphragmatic paralysis. Obstructive sleep apnoea was finally suspected and confirmed by sleep recording. The obstructive sleep apnoea probably explained the respiratory insufficiency and the pulmonary hypertension. Loss of weight was associated with the disappearance of hypercapnia and pulmonary hypertension. As a result of this study, the value of sleep recording is emphasized. When respiratory failure or pulmonary hypertension seem unexplained, think of obstructive sleep apnoea.
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PMID:[Value of sleep polygraph examination in the etiological diagnosis of apparently inexplicable respiratory insufficiency]. 404 63

Neurologists are becoming increasingly aware of the frequency and clinical importance of sleep-related respiratory impairment. Sleep-induced narrowing of the upper airways underlies the widespread and supposedly trivial complaint of snoring, which may not only constitute a risk factor for the cardiocirculatory system, but in predisposed individuals, may lead to a sleep apnea syndrome, with its array of serious disturbances, including hypersomnia, systemic and pulmonary hypertension and ultimately heart failure. Idiopathic chronic alveolar hypoventilation, or Ondine's curse, is a fairly stereotyped clinical syndrome: sleep-related respiratory insufficiency in the absence of airways stenosis. Finally, sleep, and REM sleep in particular, significantly aggravates hypoventilation in patients with chronic obstructive pulmonary disease (COPD), kyphoscoliosis or chest musculoskeletal disorders.
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PMID:Sleep-related respiratory disorders. 408 59

Sleep apnea is characterized by recurrent upper airway obstruction, resulting in periodic apneic episodes that are associated with oxygen desaturation and frequent awakenings. This leads to daytime somnolence and, possibly, pulmonary hypertension and cor pulmonale. Tracheostomy has been the standard treatment for severe sleep apnea with life-threatening complications. Several recent studies have reported benefits of protriptyline in obstructive sleep apnea. The drug does not completely resolve the apnea, but does improve nocturnal oxygenation and reduce daytime hypersomnolence. Protriptyline should be considered an alternative to tracheostomy in patients with benign or moderately severe obstructive sleep apnea.
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PMID:Sleep apnea. 662 25


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