Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

In the literature, depending upon the group of subjects investigated and the diagnostic criteria applied, the prevalence of the sleep apnea syndrome (SAS) is reported to be between 1 and 10%. In the present study, 220 nonselected male patients (age range: 45.1 +/- 11.4 years, Brocca index 109.0 +/- 18.0%, 147 cases of chronic bronchitis, 65 of bronchial asthma, 8 with other diseases of the airways, 44.1% obstructive ventilation disturbances, 41.8% smokers) were investigated. As a screening method, nocturnal monitoring of oxygen saturation with the aid of a digital pulse oximeter (Draeger) was carried out. On average, 65.4 +/- 136.5 cases of desaturation to less than 90% SaO2/8 hours sleep were observed. In 48 patients with a Brocca index of more than 120%, desaturations at 156.1 +/- 244.5 were significantly more frequent than in 172 patients with a low relative weight (40.2 +/- 67.0, p less than 0.0001). Forty-eight patients (21.8%) revealed more than 80 episodes of SaO2 drops per night. Twenty-two patients were submitted to polysomnographic investigation. In 13 patients--6% of the overall group--who had more than 100 episodes of apnea/hypopnea (AHI 47.2 +/- 30.1), a sleep apnea syndrome was demonstrated.
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PMID:[Study of the prevalence of sleep apnea syndrome in patients with chronic diseases of the respiratory organs using pulse oximetry and polysomnography]. 260 51

In addition to the well-known medically oriented examination procedures and forms of treatment of sleep apnea, we are also interested in the psychological aspects of this pathological condition. Against the background of our experience of patients treated with nCPAP--here we have observed, among other things, an increase in general activity--we investigated the question as to whether typical personality traits are to be observed among persons suffering from sleep apnoea. As a psychodiagnostic procedure, the Freiburg personality inventory (FPI-R) was employed in the following persons: a) Persons with diagnosed sleep apnea, b) persons with unconfirmed suspected sleep apnea, c) persons with diagnosed chronic bronchitis. An initial consideration of the results reveals an unremarkable personality profile of the person with SAS who, however, in comparisons with other groups does reveal certain peculiarities. Although the results presented here do not permit any reliable specific psychodiagnostic statement to be made with the aid of the procedure employed, in several points they do provide clues as to features that should be subjected to a differential investigation.
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PMID:[Personality markers in patients with sleep apnea syndrome]. 260 57

The most common causes of hypoxic cor pulmonale are chronic bronchitis and emphysema. Although the clinical situation in some patients is characterized early by hypoxemia, oedema is rare in patients with an arterial pO2 above 60 mm Hg. The presence of oedema can be regarded as an unfavorable prognostic indicator. For many years, peripheral oedema had been considered an expression of congestive cardiac failure; it may be assumed, however, that neither right nor left ventricular failure is prerequisite to the development of oedema. Oedema formation can be attributed to excessive retention of salt and water or a redistribution of body water into the extracellular compartment. Hypercapnia and acidosis affect direct stimulation of renal hydrogen ion secretion. The resulting electrochemical imbalance is compensated by reabsorption of sodium. Hypercapnia and, in acute phases possibly, hypoxia lead to a fall in renal blood flow mediated by alpha-adrenergic stimulation through activation of the renin-angiotensin-aldosterone system. An increase in plasma ADH may also contribute to development of oedema. The development of cor pulmonale or respiratory insufficiency can be enhanced by nocturnal hypoventilation and hypoxia during sleep as well as by sleep apnoea. Nocturnal hypoxia, smoking and reduced oxygen tension in the relevant kidney cells responsible for erythropoietin release promote the occurrence of secondary polycythaemia. For treatment of acute exacerbations in cor pulmonale associated with infections bronchitis antibiotics such as amoxycillin and cotrimoxacol are drugs of first choice. While the use of digoxin is of doubtful value, the cautious administration of diuretics may bring symptomatic relief. In addition to physiotherapy, beta-2-selective bronchodilators and nebulized bronchodilator therapy can be useful; theophyllines dilate airways and increase cardiac output but they can cause arrhythmias and a deterioration of arterial blood gases in hypoxic patients. If the patient has been treated chronically with corticosteroids, the dosage will have to be incremented; if asthma is suspected, corticosteroid treatment is essential. Controlled oxygen therapy is the most important single therapy aimed at relief of severe arterial hypoxaemia. Oxygen should be titrated initially (for the first one or two days) to achieve an arterial tension of at least 48 mm Hg. Thereafter, the oxygen flow should be increased to yield an arterial tension in excess of 60 mm Hg during continued treatment for two to three weeks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypoxic cor pulmonale: a review. 294 54

In a double-blind placebo controlled randomised study, the effects of almitrine bismesylate on the sleep induced Hb desaturations, associated or not with disorders of breathing, were tested. Patients (37-75 yrs, 8M and 2F) were affected by chronic bronchitis (out of any exacerbation) and obesity (weight excess at least 20%). They were known to have at least one nocturnal episode of hypoxemia (SaO2 fall higher or equal to 10%) with respect to the wakefulness level. Patients received either placebo or almitrine (1.5 mg/Kg/day) for 18 days and nocturnal polysomnography was performed both before and the last day of treatment. Almitrine induced an increase in PaO2 during wakefulness (p less than .05), an increase in mean SaO2 during sleep (p less than .01) and a decrease in the quantity of desaturation (Qd) during sleep, defined as the product of the mean desaturation by the duration of the episodes of desaturation (p less than .025). No clear effect could be observed either on the mean duration of the sleep disordered breathing (SDB) events or on their frequency whereas the desaturations due to them had a decrease.
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PMID:Effects of almitrine bismesylate on nocturnal hypoxemia in patients with chronic bronchitis and obesity. 309 64

Hypoxaemia during the rapid eye movement phase of sleep is common in older healthy normal subjects over 55 years of age; the sleep apnoea syndromes--such as obstructive sleep apnoea, where oro-nasal airflow ceases for more than 10 seconds on many separate occasions throughout the night, due to failure of contraction of the genio-glossus muscle; "blue and bloated" patients with chronic bronchitis and emphysema, where profound nocturnal hypoxaemia is common in REM sleep, and is associated with further elevation of pulmonary arterial pressure; the overlap syndrome--where "blue and bloated" chronic bronchitis is associated with an obstructive sleep apnoea syndrome; and bronchial asthma, where hypoxaemia is associated with irregular breathing and possibly nocturnal bronchoconstriction. Although absolute recognition depends upon all night sleep studies, monitoring of ear oxygen saturation, breathing patterns, and EEG, the clinical features when awake can lead to suspicion of sleep hypoxaemia--as, for example, obesity and obstructive sleep apnoea with loud snoring and restlessness in sleep, hypoxaemia during wakefulness in the overlap syndrome, and nocturnal awakening with wheeze in bronchial asthma. Treatment depends on the cause, and may vary from weight loss and nasal continuous positive airway pressure in obstructive sleep apnoea, to nocturnal oxygen in "blue bloaters", a combination of these two in the overlap syndrome, and long acting bronchodilators such as slow release theophyllines in nocturnal asthma. Recognition and appropriate treatment of nocturnal hypoxaemia is an important new development in respiratory medicine.
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PMID:Breathing during sleep. 390 86

In five patients with hypoxic chronic bronchitis and emphysema we measured ear O2 saturation (SaO2), chest movement, oronasal airflow, arterial and mixed venous gas tensions, and cardiac output during nine hypoxemic episodes (HE; SaO2 falls greater than 10%) in rapid-eye-movement (REM) sleep and during preceding periods of stable oxygenation in non-REM sleep. All nine HE occurred with recurrent short episodes of reduced chest movement, none with sleep apnea. The arterial PO2 (PaO2) fell by 6.0 +/- 1.9 (SD) Torr during the HE (P less than 0.01), but mean arterial PCO2 (PaCO2) rose by only 1.4 +/- 2.4 Torr (P greater than 0.4). The arteriovenous O2 content difference fell by 0.64 +/- 0.43 ml/100 ml of blood during the HE (P less than 0.05), but there was no significant change in cardiac output. Changes observed in PaO2 and PaCO2 during HE were similar to those in four normal subjects during 90 s of voluntary hypoventilation, when PaO2 fell by 12.3 +/- 5.6 Torr (P less than 0.05), but mean PaCO2 rose by only 2.8 +/- 2.1 Torr (P greater than 0.4). We suggest that the transient hypoxemia which occurs during REM sleep in patients with chronic bronchitis and emphysema could be explained by hypoventilation during REM sleep but that the importance of changes in distribution of ventilation-perfusion ratios cannot be assessed by presently available techniques.
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PMID:Mechanism of transient nocturnal hypoxemia in hypoxic chronic bronchitis and emphysema. 407 77

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

The possibility of nocturnal oxygen desaturation (NOD) in patients with chronic bronchitis and emphysema (CBE) even with basal hypoxemia greater that 55 mmHg is well recognised. Nocturnal hypoventilation is admitted as the main cause for this NOD. In this study we evaluate how the presence of left ventricular dysfunction (LVD) could aggravate NOD. Thirty-six patients with CBE and basal stabilised PaO2 55-70 mmHg underwent right heart catheterisation and polysomnographic study. NOD was defined as more than 30% of total sleep time with SaO2 less than 90%; LVD was defined as capillary pressure greater than 15 mmHg. Six patients were excluded from analysis because of sleep apnoea syndrome. In the remaining 30 patients (20 men, 10 women; mean age = 65.88.6 years; mean FEV1 = 0.970.31 litres; 43.316.6% predicted; mean basal PaO2 = 61.83.6 mmHg) 8 had LVD and 18 and NOD. Patients with NOD had a greater diurnal level of hypoventilation (basal PaCO2 = 44.63.8 vs. 414.1 mmHg; p = 0.025). Patients with LVD, despite identical diurnal pulmonary function, showed a significantly p < 0.05) greater degree of NOD (mean nocturnal SaO2 = 84.56.4 vs 89.52.5; minimal nocturnal SaO2= 68.517.3 vs. 79.47.8; Time spent with SaO2 < 90% = 78.833.7 vs. 43.138.7). We conclude that the presence of LVD in patients with CBE and PaO2 55-70 mmHg aggravates the intensity and the time spent with NOD, probably because of aggravation of hypoventilation or ventilation/perfusion mismatching.
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PMID:[The effect of left ventricular dysfunction on nocturnal desaturation in patients with chronic emphysematous bronchitis and PaO2 55-70 mmHg]. 934 Oct 31

We investigated the clinical usefulness of continuous nocturnal oxygen saturation monitoring in patients undergoing home oxygen therapy (HOT). The subjects were 11 patients with chronic respiratory disease in the process of healing from acute exacerbation. None were mechanically ventilated. Each subject underwent full overnight oximetry. One patient was excluded from further investigation because of periodic desaturation suggestive of sleep apnea. The remaining 10 subjects included 5 patients with sequelae of pulmonary tuberculosis, 2 with diffuse panbronchiolitis, 1 with chronic pulmonary emphysema, 1 with chronic bronchitis, and 1 with kyphoscoliosis. All underwent full overnight and 30 min daytime oximetry monitoring for 23.7 +/- 7.4 (mean +/- SD) consecutive days. Daytime oximetry was performed when subjects were awake and resting in supine position. Mean nocturnal oxygen saturation (NmSpO2) and mean daytime oxygen saturation (DmSpO2) were calculated from data obtained from 0:00 through 5:00 hrs and from data obtained during a stable 10 min daytime period, respectively. The difference between NmSpO2 and DmSpO2 (delta SpO2), the percentage of total sleep time with SpO2 < or = 90% (DST 90) and nocturnal lowest oxygen saturation (NLSpO2) were calculated once daily for each subject. There were significant (p < 0.05) correlations between NmSpO2 and NLSpO2, between NmSpO2 and DST 90, and between NLSpO2 and DST 90 in all subjects. However, significant (p < 0.05) correlations between NmSpO2 and DmSpO2 were observed in only 6. During acute exacerbation, NmSpO2 was lower than DmSpO2, and delta SpO2 increased. Conversely, with the amelioration of acute symptoms, delta SpO2 decreased and NmSpO2 was higher than DmSpO2. There was a significant (p < 0.05) reverse correlation between NmSpO2 and delta SpO2 in 9 subjects. We concluded that monitoring nocturnal oxygen saturation is clinically useful to assessments of oxygenation status in patients undergoing HOT, and that it may assist the early diagnosis of acute exacerbation of respiratory failure.
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PMID:[Continuous oximetry monitoring in patients undergoing home oxygen therapy for chronic respiratory failure]. 1054 Aug 34


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