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

To determine the incidence and frequency of sleep apnea in persons with hypothyroidism, 11 consecutive patients with newly diagnosed disease were studied before and during thyroid hormone replacement therapy. Nine patients had episodes of apnea, with the number of episodes per hour of sleep ranging from 17 to 176 (mean, 71.8). Six of the nine patients were obese and had 99.5 episodes per hour compared with 16.3 episodes per hour in the 3 nonobese patients (p less than 0.02). After 3 to 12 months of thyroxine replacement therapy, mean apnea frequency decreased from 71.8 +/- 18.0 (SE) to 12.7 +/- 6.1 episodes per hour, without reduction in body weight. There were fewer changes in sleep stage per hour during treatment (22.1 +/- 4.9) than pretreatment (57.6 +/- 14.5). Carbon dioxide response tests done under non-loaded and flow-resistive loaded conditions before and during thyroxine replacement therapy showed increases in the loaded respiratory effort and ventilation during thyroxine treatment. Sleep apnea episodes are common in persons with untreated hypothyroidism, even with normal lung function. Thyroxine replacement therapy decreases apnea frequency, even without change in body weight.
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PMID:Obstructive sleep apnea in hypothyroidism. 647 35

The effects of oral medroxyprogesterone acetate (MPA) (20 mg three times daily) were assessed on sleep-disordered breathing and on arterial blood gas levels in awake patients with chronic obstructive pulmonary disease (COPD). Seventeen men and two women (mean baseline PaO2, 65 mm Hg; PaCO2, 41 mm Hg; and FEV1/FVC ratio, 48 percent) participated in a double-blind, placebo-controlled, randomized study. After an initial night of polysomnography and daytime arterial blood gas analysis, the patients were randomized to receive either MPA or an identical placebo for one month; the studies were then repeated. The alternate compound was given for an additional month, and the studies were performed a third time. MPA in awake patients was associated with an increased mean PaO2 value, reduced PaCO2, and increased pH. Although there was no significant change in the number of episodes of sleep apnea, hypopnea, desaturation, or the minimal saturation, MPA marginally decreased the number of minutes of total sleep time when oxygen saturation was less than 90 percent (p = .06). In conclusion, MPA improves oxygenation and CO2 elimination and increases the pH in awake patients with COPD, but during sleep, does not significantly affect disordered breathing and only marginally improves desaturation.
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PMID:Medroxyprogesterone acetate and COPD. Effect on breathing and oxygenation in sleeping and awake patients. 661 74

We studied the responses of ventilation and occlusion pressure (P100) to hypercapnia, with and without the application of an inspiratory flow-resistive load (12 cm H2O/L/sec), in eight control subjects and in eight subjects with obstructive sleep apnea who did not retain carbon dioxide while awake. The hypercapnic response was assessed by a modification of the Read rebreathing technique. For a given endtidal carbon dioxide, ventilation in control subjects was the same with or without load, and P100 was increased with loading. In contrast, the subjects with sleep apnea decreased their ventilation during loading and did not increase their P100 in response to loading. Relationships between ventilation and P100 were similar in the two groups both with and without load. We conclude that patients with occlusive sleep apnea do not exhibit the normal increase in neural drive to compensate for inspiratory flow-resistive loading.
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PMID:Control of breathing in obstructive sleep apnea. 669 97

A patient with sleep apnoea syndrome is presented. The value of a rapid CO2 analyser and an oesophageal pressure recorder in the diagnosis is described.
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PMID:Nocturnal sleep apnoea: method of diagnosis. 678 59

A 58-yr-old man with hypothyroidism and sleep apnea syndrome was studied to determine the cause of the nocturnal obstructive apnea and oxygen desaturation. Control studies showed free thyroxine (T4) concentration of 0.7 ng/dl (normal, 0.8 to 2.3 ng/dl), and thyroid-stimulating hormone of 32 microIU/ml (normal, less than 12 microIU/ml). Weight, pulmonary function, arterial blood gases, minute ventilation to carbon dioxide production ratio (VE/VCO2), and the ventilatory response to exercise (delta VE/delta VCO2) were normal. Episodes of obstructive apnea (4 per hour during non-REM (NREM) and 10 per hour during REM) and oxygen desaturation (9 per hour during NREM and 11 per hour during REM) were common during sleep. Oxygen saturation ranged between 72 and 99% and 70 and 97% during NREM and REM sleep, respectively. Medroxyprogesterone acetate (MPA) therapy for 4 wk caused a reduction in awake PaCO2 (38 to 33 mm Hg), and an increase in VE/VCO2 (17%), mouth occlusion pressure (50%), and AVE/VCO2 (23%). During sleep, apneas were completely eliminated and only one episode of oxygen desaturation occurred. L-thyroxine therapy for 2 months after a placebo period caused an awake isocapnic hyperpnea with no change in PaCO2 and VE/VCO2 despite a 23% increase in VE. Mouth occlusion pressure increased 37% but delta VE/delta VCO2 was unchanged. Obstructive apnea and oxygen desaturation during sleep were completely eliminated with L-thyroxine. The patient noted completed relief of symptoms with both MPA and L-thyroxine. We concluded that the sleep apnea syndrome was the presenting manifestation of hypothyroidism in this patient and was solely responsible for his symptoms and disability.
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PMID:Disordered breathing during sleep in hypothyroidism. 679 57

We studied the effects of hyperoxia and hypercapnia on obstructive apneic episodes (OAE) in a 39-year-old male with the sleep apnea and hypersomnolence syndrome (SAHS). While inspiring room air, our patient spent approximately 50% of his non-REM sleep time in OAE. When the inspired gas was changed to 100% oxygen, the frequency of the OAE decreased slightly, but a statistically significant increase in the duration of each episode was noted. Additionally, a CO2 rebreathe under hyperoxic conditions was carried out during non-REM sleep; no OAE were noted during this rebreathe. Therefore, this latter observation suggests that hypercapnia under hyperoxic conditions may reduce the frequency of OAE in patients with the SAHS.
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PMID:Effects of respiratory gases on the frequency and duration of obstructive apneic episodes in a patient with the sleep apnea-hypersomnolence syndrome. 680 21

To define the roles of mechanical loading, respiratory neuromuscular control, and sleep apnea in the pathogenesis of obesity hypoventilation, respiratory muscle drive and output, assessed by diaphragmatic electromyogram (EMGdi) and mouth occlusion pressure (P 0.15), respectively, were determined during CO2 chemostimulation in nonobese volunteers who were subjected to abdominal mass loading, and in three groups of markedly obese patients: eucapnic obese without sleep apnea (O), eucapnic obese with sleep apnea (OSA), and hypercapnic obese with sleep apnea (OH). The P0.15 responses were decreased in OSA and OH, but the EMGdi responses were not significantly different from those in control subjects. In O patients EMGdi responses were significantly greater than those in control subjects as well as those in OSA and OH patients. EMGdi and P0.15 responses increased in all nonobese subjects when they were subjected to mass loading. We conclude that both OSA and OH patients were equally unable to develop the expected increase in respiratory muscle drive and output. The presence of sleep apnea, possibly by causing nocturnal hypoxemia and/or sleep fragmentation, may result in impaired mass load compensation and predispose obese patients to develop hypercapnia.
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PMID:Mass loading, sleep apnea, and the pathogenesis of obesity hypoventilation. 681 71

Thirteen patients with sleep apnea syndrome, nine with narcolepsy, and age-matched controls were studied to evaluate possible impairment of autonomic nervous control of cardiovascular and pulmonary function. The sleep apnea group had subnormal increases in heart rate and blood flow in the resting arm upon muscle contraction, although they were higher than seen in the narcolepsy group. Some sleep apnea patients had marked bradycardia in response to a dive reflex test. Other cardiovascular results did not differ from controls. Some sleep apnea patients had low ventilatory response to CO2. One had abnormal spirometry, two had enlarged tonsils, and five were snorers. The narcolepsy group had subnormal heart rate, blood pressure, and forearm blood flow responses to muscle contraction, subnormal respiratory sinus arrhythmia, and subnormal heart rate response to the Valsalva maneuver. Ventilatory function was normal. Thus, narcolepsy is associated with attenuation of some cardiovascular reflexes. The impairment is probably of central origin. The causative factor for the sleep apnea syndrome is probably also in the central nervous system rather than in the pulmonary or upper airway region. Great interindividual variations in the sleep apnea group point to a more multifactorial etiology. Thus, the two conditions of increased sleepiness are associated with autonomic dysfunction, but the differences in autonomic abnormalities reinforce that sleep apnea and narcolepsy, also in this respect, represent different clinical entities.
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PMID:Autonomic regulation of cardiopulmonary functions in sleep apnea syndrome and narcolepsy. 681 32

The prevalence of reported sleep disturbances in a general population is high. Many of the complaints are the result of sleep-related breathing disorders, due mainly to the occurrence of obstructive and central apnoeas. Obstructive sleep apnoea is a fully described and well-recognized entity. Central sleep apnoea (CSA) however, has been poorly studied. There is accumulating evidence that central sleep apnoea should be considered as the end of a spectrum. Instability in the breathing pattern is the main underlying mechanism and is due to the interaction of many factors. Breathing during sleep is dependent on metabolic control and the activity of the respiratory muscles. Decreased chemical drive and/or failing respiratory muscle function are associated with CSA and usually also with ongoing hypoventilation during wakefulness, characterized by chronic daytime hypercapnia. Central respiratory drive can also be inhibited by upper airway reflexes. Mostly, however, CSA occurs as the hallmark of unstable breathing during sleep brought about by an overall increase in loop gain (especially in light sleep stages) and the unmasking of a CO2 threshold. Arousal following central apnoeas acts as an amplification of the instability. Micro electroencephographic (EEG) arousals are often observed as a consequence of CSA. They are responsible for sleep fragmentation and hypersomnolence during the day. The daytime hypersomnolence and complaints of awakenings during sleep in patients with CSA can be striking. CSA can occur in specific pathologies, such as chronic heart failure and (post-traumatic) brain lesions, that are associated with irregular breathing. Treatment strategies are remarkably few in number. Use of nasal ventilation and the inhalation of CO2 are mainly of theoretical interest, since patients do not often tolerate these more invasive therapies. Drug treatment, especially with acetazolamide, is easier to perform. Stimulation of upper airway reflexes, by less invasive methods, seems to be promising for the near future.
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PMID:Central sleep apnoea, pathogenesis and treatment: an overview and perspective. 748 5

We studied ventilatory and neurocirculatory responses to combined hypoxia (arterial O2 saturation 80%) and hypercapnia (end-tidal CO2 + 5 Torr) in awake humans. This asphyxic stimulus produced a substantial increase in minute ventilation (6.9 +/- 0.4 to 20.0 +/- 1.5 l/min) that promptly subsided on return to room air breathing. During asphyxia, muscle sympathetic nerve activity (intraneural microelectrodes) increased to 220 +/- 28% of the room air baseline. Approximately two-thirds of this sympathetic activation persisted after return to room air breathing for the duration of our measurements (20 min in 8 subjects, 1 h in 2 subjects). In contrast, neither ventilation nor sympathetic outflow changed during time control experiments. A 20-min exposure to hyperoxic hypercapnia also caused a sustained increase in sympathetic activity, but, unlike the aftereffect of asphyxia, this effect was short lived and coincident with continued hyperpnea. In summary, relatively brief periods of asphyxic stimulation cause substantial increases in sympathetic vasomotor outflow that outlast the chemical stimuli. These findings provide a potential explanation for the chronically elevated sympathetic nervous system activity that accompanies sleep apnea syndrome.
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PMID:Combined hypoxia and hypercapnia evokes long-lasting sympathetic activation in humans. 755 21


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