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

Myotonic dystrophy (MyD) involves a variety of systems. Respiratory disorders are common, namely elevation of diaphragm, alveolar hypoventilation, aspiration pneumonia and sleep apnea. We evaluated respiratory involvement. The subjects were 11 patients with MyD. Also 6 patients with limb girdle muscular dystrophy (LG) were examined to be compared with MyD. Both groups had the similar activities of daily living. All of them never complained of dyspnea. Arterial blood gas studies were performed in supine position and standing position. A new evidence was found that hypoxemia was aggravated and alveolar-arterial oxygen pressure difference was increased in supine position in MyD. Next, pulmonary function tests were done in supine position and sitting position. Functional residual capacity (FRC) were more reduced in supine position in MyD compared with LG. The value to subtract closing capacity from FRC was negative in supine position in MyD, showing closing phenomenon. We propose the mechanism of the aggravation of hypoxemia may be the following. The reduction of FRC caused by respiratory muscle involvement brings out the closing phenomenon. Abnormal uneven distribution of ventilation-perfusion ratio happens and then hypoxemia is worsened in supine position in MyD.
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PMID:[Aggravation of hypoxemia in supine position in myotonic dystrophy]. 129 47

Nocturnal oxygen desaturation (NOD) is commonly seen not only in sleep apnea syndrome (SAS) but also in chronic lung disease (CLD) including chronic obstructive lung disease even without sleep apnea. However, the relationship of NOD to clinical symptoms such as morning headache, sleep deprivation due to breathlessness, and daytime sleepiness is not known. In this study, we examined by polysomnography the relationship between several NOD indexes, parameters of apnea, and subjective symptoms in 25 patients with SAS and 22 patients with CLD. In addition, the relation between daytime arterial blood gas data and NOD indexes, parameters of apnea, was examined. In the SAS group, there were no differences in any parameters of NOD and apnea between patients with subjective symptoms and those without symptoms. However, in the CLD group, symptomatic patients had significantly lower lowest SaO2, higher mean SaO2, and longer total desaturation time. In both groups, daytime PaCO2 had a significant correlation with several NOD parameters such as mean SaO2, lowest SaO2, and total desaturation time. In the SAS group, daytime PaCO2 was also correlated with the parameters of apnea. On the other hand, daytime PaO2 was significantly correlated with mean SaO2 only in the CLD group. From these data, we conclude that in patients with SAS, daytime PaCO2 is a variable that is related to the degree of NOD, and that in patients with CLD, subjective symptoms and daytime PaO2 in addition to daytime PaCO2 are associated with NOD.
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PMID:[Relationship between clinical symptoms and nocturnal oxygen desaturation in sleep apnea syndrome and chronic lung disease]. 140 71

The patient was a 74-year-old woman who had been obese since age 18. Her obesity was refractory to dietary manipulation. She had been suffering from increasing dyspnea for several months and eventually could not even move. She was admitted to a hospital and diagnosed as having heart failure. Although her cardiac function recovered with medical treatment, her symptoms did not improve. The patient was then sent to our hospital. On admission, her height and weight were 149 cm and 81.9 kg, respectively, yielding a body mass index (BMI) of 36.6 kg/m2. Arterial blood gas analysis in room air revealed hypoxemia and an apnea index of 27 per hour. She was given a daily 500-1000 kcal diet. After four months of treatment, her weight decreased to 65 kg with a BMI of 29.3 kg/m2. Weight reduction together with the usage of progesterone-derivatives resulted in marked improvement of sleep apnea. The apnea index decreased to 3/h and arterial blood gas values normalized. This patient seemed to have suffered from both obesity hypoventilation syndrome and sleep apnea syndrome. Improvement of respiratory function was achieved through relief of airway obstruction and weight reduction, with activation of the respiratory center due to progesterone treatment.
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PMID:[Improvement of respiratory function with weight reduction in obese elderly]. 149 51

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.
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PMID:Right and left ventricular functional impairment and sleep apnea. 152 13

In a Rehabilitation Clinic for Diseases of the Respiratory Organs we examined 497 male patients aged 45.9 +/- 11.1 years with a relative weight of 109 +/- 16.7% who were suffering from chronic diseases of the respiratory tract (66.2% chronic bronchitis, 33.8% asthma bronchiale, 49.6% obstruction of the respiratory tract). They were subjected to a detailed physical examination and were given an anamnestic questionnaire for the purpose of diagnosing sleep-related respiratory disturbances (Siegrist et al., 1987). In addition, whole body plethysmography was performed in all patients as well as a pulse-oximetric examination during night sleep. Using factor analysis, it was possible to extract 5 factors from the 23 items of the anamnesis questionnaire. With these 5 factors, 60.5% of the total variance could be explained. These factors describe: 1. Dyspnoea (35.3%); 2. Vigilance (8.5%); 3. Sleep disturbances (6.3%); 4. Headache (5.8%) and 5. Snoring (4.7%). Different factor patterns are seen for different groups of patients. In patients suspected of an obstructive sleep apnoea syndrome, however, it will always be necessary to perform further stage-wise diagnosis to safeguard the diagnosis.
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PMID:[Evaluation of an anamnesis questionnaire for the diagnosis of sleep apnea in patients with chronic diseases of the respiratory organs]. 186 94

It is known that patients suffering from severe cardiomyopathy may develop cyclic changes in breathing (Cheyne-Stokes-breathing) (2, 3). Coughing and dyspnea may be linked to periodic breathing. Specific detailed polysomnographic studies of sleep architecture and oxygen saturation have not been published. Eight patients suffering from dilatative cardiomyopathy (NYHA III-IV) were studied by pulse oximetry and polysomnography. Six of eight patients had severe breathing irregularities. These disturbances became manifest partially as Cheyne-Stokes breathing, partially as central sleep apnea. During these periods, oxygen saturation dropped as far as to 65 per cent of the original level.
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PMID:[Oxygen saturation and sleep structure in patients with dilated cardiomyopathy]. 186 3

One male and two female cases in a family of Machado-Joseph disease were reported. Two cases showed typical symptoms that are characterized by bulging eyes, ophthalmoplegia, dystonia, ataxia, spasticity of extremities and amyotrophy, and were consistent with Type II (Rosenberg et al). But another one lacked diversity of the symptoms, showing mainly progressive cerebellar ataxia for over 10 years. We pointed out the existence of a new type of MJD case exhibiting only progressive cerebellar ataxia over a long period. A female patient had dyspnea and insomnia after 20 years in her clinical course, and central sleep apnea was revealed by respiratory monitor. But, the apnea and irregular respiration appeared in both awake and sleep stages. We described the importance of attention to the apnea as a new complication of Machado-Joseph disease.
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PMID:[A family of Machado-Joseph disease with a patient having frequent apnea in all day]. 191 27

Several well controlled epidemiologic and hemodynamic studies suggest that about 20% of sleep apnea syndrome (SAS) patients will have chronic obstructive pulmonary disease (COPD), and the majority of these patients (with combined diseases) will have pulmonary hypertension. Indeed it has been suggested that only patients with underlying hypoxemia, such as that from COPD, will develop right heart failure in the OSA setting. Experience shows that apnea/COPD patients will have severe hypersomnolence associated with the OSA, cough and dyspnea with the airways disease, and edema and plethora related to chronic hypoxemia. Many patients present with respiratory failure and are diagnosed at the time of initial intubation and mechanical ventilation. Episodic nocturnal hypoxemia may be worsened by a steeper rate of desaturation due to lower alveolar and blood oxygen stores, and longer apneas perhaps contributed to by depressed chemosensitivity. Daytime hypoxemia may also add to the severe hemodynamic disturbances. Since COPD cannot be cured, aggressive treatment of SAS is critical. Past studies have shown that tracheostomy or nasal CPAP in this setting not only leads to resolution of episodic nocturnal desaturation but may lead to rapid improvement in daytime oxygenation in many patients. Pulmonary hypertension and other measures of cardiopulmonary function improve when apnea is cured. Elimination of the SAS may disclose nonapneic REM related desaturation that could require supplemental oxygen therapy in addition to tracheostomy or nasal CPAP. Pulmonary function testing in SAS patients with smoking histories, followed by aggressive treatment of SAS, is recommended.
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PMID:Chronic lung disease in the sleep apnea syndrome. 211 88

Five patients with congestive heart failure (CHF) and 1 with left ventricular dysfunction but without CHF were found to have sleep apnea. Central sleep apnea (CSA) related to Cheyne-Stokes respiration was seen in 4 cases while obstructive sleep apnea (OSA) was seen in 2. All patients had symptoms of sleep apnea. Nasal continuous positive airway pressure (NCPAP) was effective in reversing CSA and OSA in all patients with improvement in sleep structure and alleviation of symptoms of sleep apnea. In addition, all experienced a reduction in cardiac dyspnea. This was associated with a 5% or greater increase in left ventricular ejection fraction while on NCPAP, compared to baseline value off NCPAP in 5 patients and resolution of chronic pleural effusion and pulmonary edema in the sixth. We conclude that Cheyne-Stokes respiration during sleep may give rise to a CSA syndrome that is reversible by NCPAP. In addition, NCPAP therapy may lead to a reduction in cardiac dyspnea and improvement in left ventricular function in patients with left ventricular dysfunction and sleep apnea.
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PMID:Sleep apnea in patients with left ventricular dysfunction: beneficial effects of nasal CPAP. 219 97

We describe in six men, recurrent episodes recurring over months or years, of sudden, brief complete obstruction to respiration followed by dyspnoea with loud inspiratory stridor lasting two to five minutes. Attacks occurred during wakefulness and/or sleep. In one patient an episode was witnessed endoscopically: the initial obstruction was seen to be caused by complete laryngeal closure. The false vocal cords then opened, but the vocal cords remained adducted and caused inspiratory stridor. The similarity of the attacks described by the other patients suggests that they were all caused by laryngeal closure. Furthermore, they could simulate the episodes by voluntarily adducting their vocal cords. The symptoms were usually preceded by a sensation of throat irritation and in four cases symptoms of upper respiratory infection were present. Associated features present in some of the patients included post-nasal discharge, snoring, sleep apnoea and gastro-oesophageal reflux. None was hypocalcaemic. Although stimulation of laryngeal receptors is known to produce reflex laryngeal closure, cough is the usual response during wakefulness. Treatment aimed at reducing upper airway irritation and voluntary inhibition of coughing appeared successful in reducing the incidence and severity of the episodes. Recognition of the condition is important as it may be confused with other causes of acute dyspnoea and it appears to respond to specific management.
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PMID:Brief upper airway (laryngeal) dysfunction. 228 83


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