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)

To determine whether oxygen desaturation occurs during sleep in high tetraplegics, 10 neurologically stable male patients (aged 17 to 55 years) with complete motor lesions (C4 to C6) had continuous pulse oximetry recordings and sleep observations on two nights. The patients were studied during admissions for nonrespiratory problems (eg, pressure sores, urinary infection, respite). Lung function tests and daytime arterial blood gases were also measured. Mean forced vital capacity was 46% of predicted, but mean awake PaO2 and PaCO2 were normal (95.0 mmHg and 42.8 mmHg, respectively). Three subjects showed severe nocturnal oxygen desaturation spending greater than 10% of the time overnight with arterial oxyhaemoglobin saturation (SaO2) levels of less than 90%. For the group as a whole, the percentage of time spent under 90% SaO2 correlated with body mass index. Mean overnight SaO2 correlated inversely with body mass index and directly with maximal expiratory pressure, a measure of respiratory muscle strength. Low overnight SaO2 was also associated with higher levels of injury. The pattern of nocturnal oxygen desaturation observed was episodic and was suggestive of obstructive sleep apnoea during rapid eye movement (REM) sleep. Levels of nocturnal oxygen desaturation similar to those observed in the three most severely affected patients have been shown, in other disorders, to be associated with cognitive impairment, cardiovascular disease and increased mortality. Our results suggest up to a third of high tetraplegics may be at risk of potentially serious nocturnal hypoxic episodes.
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PMID:Hypoxia episodes during sleep in high tetraplegia. 162 16

Nasal obstruction influences respiration during sleep, and nasal packing may be the cause of obstructive sleep apnoea. In order to investigate this phenomenon, perioperative nocturnal oxygen saturation was monitored for 3 nights with continuous, non-invasive pulse oximetry in 12 patients who had total nasal packs after septoplasty. Significant extension of nocturnal accumulated time of oxygen saturation less than 90% was demonstrated both during the first and second postoperative nights. The clinical significance of these results is as yet unknown, but the use of partial nasal packing in association with septoplasty is advocated and further investigations on nocturnal oxygen saturation are called for.
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PMID:Nasal packing and nocturnal oxygen desaturation. 163 54

The nadir of SaO2 during an obstructive apnea is dependent upon the apnea's duration and the rate of fall of saturation (dSaO2/dt). We postulated that a low Q, such as in patients with congestive heart failure with sleep apnea, or a reduction in Q, as seen in some humans during obstructive sleep apnea, might steepen dSaO2/dt. The mechanism postulated was lowering of SvO2 with increased pulmonary capillary blood oxygen uptake and faster depletion of alveolar oxygen. This study examines dSaO2/dt following the onset of apnea in eight spontaneously breathing adult baboons. Nonrepetitive obstructive apneas (30, 45, and 60 seconds) were created by clamping an indwelling cuffed endotracheal tube at the end of expiration. Following baseline measurements, the animals were given a bolus of a rapid-acting beta-adrenergic blocker followed by continuous infusion to reduce cardiac output and to limit the cardiovascular response to obstructive asphyxia. Fiberoptic catheters were used for continuous monitoring of SaO2, SvO2, and cardiac output. Esophageal pressure and relative thoracic gas volume (Respitrace) were monitored to insure equivalence of lung volume at the onset of apnea. Beta-adrenergic blockade reduced resting Q by a mean of 25 percent. The blocked vs unblocked dSaO2/dt was 0.73 vs 0.72 percent/s, 0.76 vs 0.73 percent/s, and 0.70 vs 0.71 percent/s for 30-second, 45-second, and 60-second apneas, respectively. Thus, mean dSaO2/dt for all durations of apneas was unaffected by beta-adrenergic blockade. We concluded that dSaO2/dt is not influenced by limited Q preceding or induced by obstructive asphyxia.
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PMID:Effect of cardiac output reduction on rate of desaturation in obstructive apnea. 167 Dec 12

This was a comparison of the effects of isradipine and metoprolol on sleep apnea syndrome in 12 hypertensive men who were habitual snorers. Each patient received double-blind isradipine 1.25-2.5 mg twice daily or metoprolol 50-100 mg twice daily after a 4-week placebo period. Static charge-sensitive bed examination was performed during the placebo period and 5-7 weeks after starting treatment. The number of obstructive breathing patterns was increased by metoprolol in five patients, remained the same with isradipine in four, and was decreased by metoprolol in one patient and by isradipine in two. Obstructive patterns increased in the metoprolol group from 24 +/- 26% to 32 +/- 31% and decreased in the isradipine group from 21 +/- 23% to 19 +/- 25% (p less than 0.05, Mann-Whitney U test). Neither drug had a significant effect on blood pressure values. There was no significant difference in oxygen desaturation or in the amount of quiet sleep in either treatment group. On the basis of these results, it would appear that isradipine is more suitable than metoprolol for the treatment of hypertension in patients who are habitual snorers.
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PMID:Sleep disturbances in hypertension: a double-blind study between isradipine and metoprolol. 172 Apr 86

This study was designed to test a hypothesis that patients with sleep apnea have higher blood pressure in the morning, following a night spent in apnea and hypoxemia, than in the evening. To accomplish this, we prospectively studied a set of 611 patients referred to our clinic because of suspicion of sleep apnea. All patients had full nocturnal polysomnography, including measurement of snoring. Blood pressure was measured in the evening, prior to onset of sleep, and in the morning, immediately on awakening. We found that patients without apnea and hypoxemia had lower blood pressure in the morning compared with the evening value, while patients with severe sleep apnea and hypoxemia had higher blood pressure in the morning; these evening-to-morning blood pressure differences, although statistically significant, were small, typically 1 to 4 mm Hg. Morning blood pressures were higher in patients with sleep apnea and hypoxemia than in nonapneic normoxic patients. However, this difference disappeared after the groups were matched for age and body mass index. We conclude that (1) patients with sleep apnea and nocturnal hypoxemia lose the expected morning dip in arterial blood pressure, and (2) age and body mass index are more important correlates of blood pressure than apnea and nocturnal oxygen desaturation. We speculate that the loss of evening-to-morning drop in blood pressure, if present over a long period of time, may lead to sustained elevations in arterial blood pressure frequently observed in patients with sleep apnea.
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PMID:Evening-to-morning blood pressure variations in snoring patients with and without obstructive sleep apnea. 173 59

Nasal obstruction influences respiration during sleep and nasal packs may cause obstructive sleep apnoea. In order to investigate this, the perioperative oxygen saturation was monitored for 3 nights with continuous pulse oximetry in 12 patients, who had bilateral nasal packs after septoplasty. A significant increase in the number of nocturnal episodes of hypoxia and a significant prolongation of the mean duration of the individual hypoxic periods were demonstrated during the first and the second post-operative nights. The clinical significance of these results is as yet unknown, but the use of partial nasal packing in septoplasty is advocated. Further investigations of nocturnal oxygen desaturation and design of nasal packs, securing the post-operative nasal airway, are needed.
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PMID:Episodic nocturnal hypoxia and nasal packs. 174 88

Presented in an illustrative case report and a review of the anesthetic management of obstructive sleep apnea patients. Preoperative evaluation should include a thorough airway evaluation and a comprehensive cardiovascular and pulmonary evaluation. With polysomnography, identification of the severity of sleep apnea can be idenified. Although sleep centers vary in their definitions, severe obstructive sleep apnea is diagnosed if the patient demonstrates an apnea index greater than 70 and an oxygen (O2) desaturation less than 80% with cardiovascular sequelae. Severe sleep apnea patients are at extreme risk for general anesthesia. These risks should be discussed preoperatively with the patient. Unsupervised preoperative sedation should be avoided because of the extreme sensitivity of these patients to sedatives and airway obstruction. Intraoperative management of the obstructive sleep apnea patient varies depending on the severity of the sleep apnea. Invasive monitoring may be necessary if the patient demonstrates evidence of cardiopulmonary dysfunction. With the assistance of the otolaryngologist, the anesthesiologist can formulate an approach to establishing an airway. Intraoperative opioids and sedatives should be limited. The recovery of the sleep apnea patient is extremely important and is the time when most airway emergencies occur. Extubation of the patient should occur when appropriate surgical personnel and equipment are available in case of an airway emergency. Steroids may be used to decrease the amount of airway swelling. Supplemental O2 should be used in patients who demonstrate desaturation. Opioids and sedatives should be avoided, as should other drugs that have central and sedating effects. Postoperative pain is effectively controlled with acetaminophen and topical anesthetic sprays. Postoperative monitoring for apnea, desaturation, and dysrhythmias is a necessity in sleep apnea patients.
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PMID:Anesthetic management of obstructive sleep apnea patients. 176 Jan 69

This article reviews current recommendations for the home care of geriatric patients with chronic pulmonary disease. Special attention is given to new bronchodilators, indications for home oxygen and ventilator use, as well as the use of nasal CPAP in elderly sleep apnea patients. The necessity of do not resuscitate (DNR) orders is also discussed.
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PMID:Home care for respiratory problems. 176 Jul 94

Sleep disorders, including a high incidence of sleep apnea, have been recognized as a significant problem in chronic renal failure (CRF) patients. In a preliminary study, we examined CRF patients on maintenance hemodialysis for three nights; one control night, and thereafter randomized to infusion of saline (placebo) for one night and 4% branch-chain amino acid (BCAA) solution for one night. Polysomnographic and respiratory data [respiratory rate, oxygen saturation and end-tidal CO2 (ETCO2)] was recorded continuously throughout the nights and data from each hour compared with baseline (awake) values. The patients studied were characterized by reduced sleep quality and decreased amount of rapid eye movement (REM) sleep. The BCAA infusion was associated with a return of REM sleep to normal and a significant decrease in ETCO2 during both REM and non-REM sleep (P less than 0.05). Our findings demonstrate respiratory stimulation during sleep with infusion of BCAA; this stimulatory effect on respiration (in contrast to many respiratory stimulants) is associated with an increased amount of REM sleep.
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PMID:Branched-chain amino acid in chronic renal failure patients: respiratory and sleep effects. 178 51

Ten patients with obstructive sleep apnoea syndrome cured by uvulopalatopharyngoplasty were compared to nine patients considered as surgical failures, using cardiovascular reflex tests--Valsalva manoeuvre, respiratory sinus arrhythmia, isometric handgrip and head-up tilt. Two patients had signs of moderate vagal dysfunction, but no case of definite autonomic nervous dysfunction was diagnosed. The overall results indicated sympathetic overreactivity, positively correlated to oxygen desaturation indices and remaining after successful treatment. Four patients did not exhibit bradycardia during sleep apnoea. Two of them had decreased respiratory sinus arrhythmia when awake, but two had normal values. This implies a difference in vagal responsiveness between the awake and sleeping states, or that other factors besides vagus function influence the bradycardia response to apnoea. The group mean values were all within normal limits. There was no significant difference between the two groups in any test. Autonomic nervous dysfunction therefore does not seem to contribute to surgical failure, nor to occur with increased incidence among patients with primary obstructive sleep apnoea syndrome.
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PMID:Autonomic nervous system function in patients with primary obstructive sleep apnoea syndrome. 182 59


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