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

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

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

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

Rare upper airway lesions may be mistaken for asthma. A 16-year-old Hispanic male athlete presented to our allergy clinic with a 4-month history of wheezing and snoring with hoarseness and progressive fatigue on exertion or during sleep. His mother taped periods of harsh stridor and sleep apnea. There was no family history of vocal cord abnormalities. A year before the onset of symptoms, he suffered injury to his oral cavity with a loss of consciousness during a wrestling match. He denied dysphagia or dysphonia. He failed to respond to bronchodilators, cromolyn, or prednisone therapy during 4 weeks. On referral to our clinic, his physical examination and tape recording were characterized by harsh inspiratory stridor. His pulmonary function tests were significant for peak flow depressed out of proportion to FEV1 with reduced FVC, no response to bronchodilator, and flattened inspiratory loop unresponsive to cough or panting. Fluoroscopy and endoscopy of the upper airway was consistent with "marked bilateral limitation of vocal cord abduction." Sleep study demonstrated desaturation with CO2s in the 60s during sleep. He was started on continuous positive airway pressure, 10 cm at night, with no desaturation or sleep disturbance on follow-up.
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PMID:Bilateral abductor paresis masquerading as asthma. 337 24

Post-poliomyelitis respiratory impairment is extremely common and entails considerable risk of morbidity and mortality. Respiratory muscle weakness is the primary etiological factor but post-poliomyelitis individuals (PPIs) also have a high incidence of scoliosis, obesity, sleep disordered breathing, and bulbar muscle dysfunction, all of which can add to the risk. One hundred forty-five PPIs were managed by noninvasive alternatives to intermittent positive pressure ventilation (IPPV) via an indwelling tracheostomy. When properly managed in this manner, acute respiratory failure requiring hospitalization, tracheal intubation, and bronchoscopies were avoided. Timely introduction of mouthpiece IPPV, nasal IPPV, manually and mechanically assisted coughing, and noninvasive blood gas monitoring in the home were the principal techniques used for optimizing quality of life and for avoiding complications.
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PMID:Management of post-polio respiratory sequelae. 761 64

We have analysed the clinical manifestations of nine patients with brief upper airway dysfunction (BUAD) who attended the thoracic department of a major teaching hospital between 1987 and 1991. Episodes of BUAD developed within 1-4 months of presentation in three patients but were undiagnosed for 2.5-12.5 years in six. The mean age at onset was 51 years ranging from 37 to 66 years. The episodes occurred at irregular intervals. They lasted approximately 1-5 min, were frightening and consisted of an initial phase of obstructive apneoa lasting a few seconds to 2 min and a second phase of respiratory distress with inspiratory stridor lasting 1-4 min. Daytime episodes occurred in all and at night in five, waking three of the patients from sleep. In most instances, throat irritability triggered the episodes which were often preceded by cough. Potential causes of throat irritability included respiratory tract infection, allergy, oesophageal reflux and obstructive sleep apnoea. After treatment of throat irritability BUAD has ceased for at least a year in six of the eight with adequate follow-up. In conclusion, BUAD has characteristics clinical features which should enable it to be recognized more frequently, ensuring successful management.
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PMID:Brief upper airway dysfunction. 814 10

It has long been recognised that patients with respiratory and cardiac disease suffer from symptoms during the night when they would normally be seeking respite. These disturbances include nocturnal dyspnea, cough, wheezing and angina. Until the advent of polysomnographic monitoring about 25 yr ago, however, the pathophysiology of these nocturnal disturbances remained elusive. Since that time, investigators have made significant advances in the understanding of the pathogenesis of many of these disturbances which will be briefly reviewed below. As the subject of this article is disturbances of sleep in patients who suffer from respiratory and cardiac disease, the sleep apnea syndromes which are unique to sleep, will not be discussed except as they may contribute to symptoms of respiratory and cardiovascular disease.
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PMID:Sleep disturbances in respiratory and cardiovascular disease. 844 82

A 52-year-old man had been asymptomatic except for nasal speech since his third decade of life. A chest roentgenogram obtained during a health screening one year before admission revealed elevation of the right hemidiaphragm and infiltrates in the right lower lung field. Because the pulmonary shadows had gradually increased, he was admitted to the hospital, for further examination. Based on physiological findings and on the results of electromyography, myotonic dystrophy was diagnosed. The chest roentgenographic abnormalities were regarded as resulting from complications of this disease. Arterial blood gas analysis showed hypercapnic hypoxia and a spirogram showed that the vital capacity and maximum voluntary ventilation were about half of their respective predicted values. The hypercapnic ventilatory response was also abnormally low. An overnight study of oxygen saturation showed episodes of marked desaturation, and polysomnography revealed central sleep apnea. Inhalation of capsaicin showed an abnormally high cough threshold. Patients with undiagnosed myotonic dystrophy rarely present with chest roentgenographic abnormalities.
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PMID:[A patient with myotonic dystrophy who presented with chest roentgenographic abnormalities and alveolar hypoventilation]. 893 45

To assess the relationship between chronic bronchitis and obstructive sleep apnoea, a postal survey was performed. A postal questionnaire was sent to 523 subjects identified as having chronic bronchitis or long-standing cough and sputum production in the Obstructive Lung Disease in Northern Sweden Study I (OLIN I). In 1986-88, all 6610 adults born in 1919-20, 1934-35 and 1949-50 living in representative areas in Northern Sweden were screened for airway diseases according to different methods. A random sample of healthy adults identified in the screening were chosen as references (n = 625). Subjects were asked about a variety of airway symptoms, smoking habits and symptoms related to obstructive sleep apnoea syndrome (OSAS). In the bronchitic group, 20% did not report bronchitic symptoms in the present study, and 26% of the formerly healthy reference group reported at least one bronchitic symptom in the present study. Snoring, apnoea and liability to 'nod off' during activity were much more common in the bronchitic group in both men and women, and most common in men, as expected. Snoring was reported by 29% of the men in the bronchitic group and by 14% in the reference group. In women, the corresponding figures were 14 and 8%, respectively, and for apnoea, the figures were 25 vs. 11% in men and 6 vs. 4% in women. The prevalence of OSAS symptoms was similar in subjects with attacks of breathlessness, long-standing cough, sputum production and recurrent wheezing. Bronchitic symptoms may influence quality of sleep and contribute to daytime tiredness, but this does not fully explain the high prevalence of snoring and apnoea reported by subjects in this cohort. This study indicates a positive correlation between chronic bronchitis and OSAS, but sleep studies are required to confirm this.
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PMID:Symptoms related to snoring and sleep apnoea in subjects with chronic bronchitis: report from the Obstructive Lung Disease in Northern Sweden Study. 906 11

In patients with obstructive sleep apnoea (OSA) nCPAP may irritate the mucous membranes of the upper airways. We investigated in this study whether nCPAP can induce bronchial hyperreactivity (BHR). Forty-one patients (33 men, mean age 52.6 years) were treated with nCPAP due to OSA. All of them were tested for BHR with histamine ("pari-provo-Test") before and six weeks after initiation of the nCPAP therapy. Thirty-five of the patients showed BHR neither before nor after the beginning of CPAP. Six patients developed a BHR of moderate degree (PD20: 50-100 micrograms) during the study; four of these six patients were not symptomatic. The two other patients complained about more colds than usual or about noctumal cough. Both of them received inhaled steroids and a moistening system. Nobody of the enrolled patients was obliged to finish CPAP therapy due to BHR. Four patients had already a BHR before nCPAP therapy began. Most of the patients did not acquire a BHR during the first 6 weeks after nCPAP therapy had started. A BHR bronchial may develop, but in the majority it remains without clinical relevance. In patients with a BHR and OSA, the benefits of nCPAP therapy excel the potential adverse effects.
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PMID:[Bronchial hyperreactivity and nCPAP therapy]. 934 Jun 37


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