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)

Digoxin-like immunoreactive factor (DLIF) is an endogenous substance with natriuretic and diuretic activity. Elevated plasma levels of DLIF are found in various clinical states characterized by water and sodium retention. Chronic respiratory failure, particularly of an advanced stage, also is frequently associated with water and sodium retention. In order to determine whether elevated plasma levels of DLIF are present in chronic respiratory failure, we measured plasma DLIF levels in seven patients (four with COPD [two of whom had associated sleep apnea disturbance] and three with kyphoscoliosis) suffering from advanced chronic respiratory failure with severe hypoxemia and hypercapnia. We found that in these patients plasma levels of DLIF were significantly higher than in healthy control subjects. We conclude that patients with advanced chronic respiratory failure respond with increased levels of DLIF. This may represent an attempt at homeostasis of water and sodium metabolism which is frequently deranged in this clinical condition.
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PMID:Endogenous digoxin-like immunoreactive factor is elevated in advanced chronic respiratory failure. 130 96

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

The purpose of this study was to assess the ability of continuous nocturnal oximetry to detect sleep apnea syndrome (SAS) and to recognize nonapneic oxyhemoglobin desaturations. Oxygen saturation oscillations, related to successive apneas in SAS or to apneic episodes in COPD or restrictive patients, were quantified using a new index: delta = 1/n sigma 1 n magnitude of delta(SaO2)/delta(t)(12-s intervals) Twenty-six patients (15 SAS, 8 COPD, and 3 restrictive patients) were included in a prospective study comparing nocturnal oximetry and polysomnography over 34 nights. In apneic patients, we found a strong correlation (r2 = 0.73, p less than 0.01) between time spent in apnea and the delta index. In COPD, the number of apneas was also correlated to the delta index (r2 = 0.92, p less than 0.01). A lower threshold for delta of 1.5 is accurate enough to detect apneas if initial SaO2 is greater than 93 percent. If initial SaO2 is greater than 93 percent, the delta threshold should be 0.8 (sensitivity 95 percent). Such a method could contribute to the accurate selection of patients for polysomnography.
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PMID:Does oximetry contribute to the detection of apneic events? Mathematical processing of the SaO2 signal. 201 70

Six European treatment centers contributed to a controlled trial to study nocturnal hypoxemia in COPD patients having daytime PaO2 of 60-70 mmHg. The trial is composed of two parts: first, patients inclusion, taking men aged under 70 years, excluding sleep apnea syndrome and all other concomitant pathologies leading to nocturnal desaturation. We described this population and determined the frequency and degree of nocturnal desaturation. Correlations between different daytime and sleep parameters have also been established. The second part concerns the study of the two sub-populations of nocturnal desaturators and nondesaturators. This is followed by random allocation of the desaturators to oxygen or no oxygen treatment. We defined significant nocturnal desaturation as cumulated unsaturation period, exceeding 30% of total time, in bed spent under SaO2 lower than 90%. Twenty out of 46 patients were desaturators (43%). Only the first part is dealt with in this article.
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PMID:Nocturnal hypoxemia and long-term oxygen therapy in COPD patients with daytime PaO2 60-70 mmHg. 211 90

While there are many research questions still requiring performance of research sleep studies in patients with COPD, their use is not advocated in routine clinical practice, except in patients who have symptoms of the sleep apnoea/hypopnoea syndrome or possibly in those without daytime hypoxaemia (PaO2 greater than 60 mmHg) who have marked polycythaemia or marked cor pulmonale.
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PMID:Are sleep studies necessary in COPD? 211 15

The possible role of ventilatory control in relation to sleep apnea has not yet been clarified. We investigated the relationship between awake ventilatory drives to hypoxia and hypercapnia and sleep-disordered breathing in 21 subjects with sleep apnea syndrome. The awake hypoxic ventilatory drive, which was evaluated by occlusion pressure responses, was inversely correlated with the magnitude of maximal oxygen desaturation during sleep as well as the ratio of duration with more than 4 and 10% oxygen desaturation to total sleep time. On the other hand, the awake hypercapnic ventilatory drive was not correlated with these parameters of sleep desaturation. Apnea index and duration were not correlated with the degree of hypoxic or hypercapnic ventilatory drive, respectively. Our study concluded that sleep desaturation is better correlated with hypoxic ventilatory drive than with hypercapnic ventilatory drive in patients with sleep apnea syndrome. These results are different from the results obtained in the patients with COPD in our previous study.
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PMID:Abnormal breathing during sleep and chemical control of breathing during wakefulness in patients with sleep apnea syndrome. 249 71

We have previously demonstrated a relationship between abnormal speech and obstructive sleep apnea in a small subject sample. The present study was designed to replicate the previous one with a much larger population, analyze the perceptual characteristics of the speech quality, and determine the degree to which each of three descriptors of speech abnormality contributed to the perception of speech abnormality. Ten graduate students in speech pathology listened in two 1.5 hour sessions to 252 random speech samples presented on a master tape. There were 81 subjects comprised of 27 sleep apnea patients, 27 matched chronic obstructive pulmonary disease control patients, and 27 matched normal control subjects. Rating the speech along an equally-appearing interval scale from 1 to 7, the judges heard abnormal resonance, articulation or phonation in 74 percent of the sleep apnea subjects, 53 percent of the COPD subjects, and 7 percent of the normal subjects (significant difference by chi 2 test at the .01 level of confidence). Discriminant function equations based on these speech descriptors correctly identified 96.3 percent of the normal subjects and 63.0 percent of the sleep apnea subjects. Analysis of abnormal speech resonance, articulation and phonation may identify obstructive sleep apnea or may provide insight into its pathology.
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PMID:Speech dysfunction of obstructive sleep apnea. A discriminant analysis of its descriptors. 276 17

Clinical observation suggested that speech disorder seemed to be associated with sleep apnea. We recorded a standard speech sample from 39 matched subjects in three groups, 13 sleep apnea individuals, 13 subjects with COPD, and 13 subjects without sleep apnea or COPD. Three speech pathologists in a single blind listening task of the recorded samples judged whether or not speech disorder was present. Eight of the sleep apnea subjects were judged to have disordered speech compared to three of the COPD group and one of the non-sleep apnea, non-COPD (normal) group. These results were statistically significant. This supports a clinical impression that speech disorder is more common in sleep apnea than expected. There may be common anatomic and physiologic disturbances present between the two conditions, and perhaps disordered speech is a sign of sleep apnea.
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PMID:Preliminary observation of speech disorder in obstructive and mixed sleep apnea. 330 47

We studied 152 COPD patients with a daytime PaO2 greater than or equal to 60 mm Hg using formal polysomnography (EEG, airflow, respiratory muscle movement, ear oximeter) to detect the presence of nocturnal, nonapneic, oxyhemoglobin desaturation. Nine subjects were disqualified by the unexpected discovery of sleep apnea, as were another eight because they could not sleep in the laboratory setting. Of the remaining 135 subjects, 37 (27 percent) desaturated below a baseline sleep saturation of 90 percent for five minutes or more, reaching a nadir saturation of at least 85 percent. Anthropomorphic, pulmonary function, and historic factors comparing desaturators and nondesaturators failed to separate the groups. Awake PaO2 at rest in the desaturators was significantly lower than in the nondesaturators. The PaCO2 was higher in the desaturators. Reversibility of the desaturation phenomenon was demonstrated in three patients during subsequent polysomnographic studies following periods of clinical improvement. Continuous oxyhemoglobin monitoring during sleep remains the only reliable tool for detecting nocturnal desaturation.
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PMID:Nocturnal oxyhemoglobin desaturation in COPD patients with arterial oxygen tensions above 60 mm Hg. 365 46

HFH has had an evolving home ventilator program since 1976 with the greatest growth in organization and volume since 1979. Technical advancements have made long-term home ventilator use a feasible, manageable, adjunctive, therapeutic modality in the care of patients with chronic respiratory failure. It appears to have more potential benefit for patients with sleep apnea and kyphoscoliosis than for persons with COPD. Many questions still are not answered regarding its use in patients with progressive nonrehabilitative neuromuscular disease. Critical components that must be included in all home ventilator programs include: (1) development of a "team" to train patients, families, and staff; (2) development of a standardized method of communication between the hospital personnel, family, durable medical equipment company, and home care agencies; (3) development of a screening mechanism to evaluate patient's/family's self-care potential in the use of home ventilators; (4) development and refinement of networks between acute care settings and the community agencies; and (5) development of clear channels of communication between patients and health care providers.
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PMID:Multidisciplinary approach for the patient on a home ventilator. 656 9


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