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

Respiratory insufficiency of any cause has significant effects on the nervous system. Headache, mental status changes, papilledema, and numerous motor abnormalities including asterixis are commonly seen. Abnormalities in ventilation and gas exchange result in hypoxia, hypercapnia, and respiratory acidosis, and these, in turn, interfere with cerebral metabolism, increase CBF, and may raise intracranial pressure. Chronic respiratory insufficiency can persist for many months with minimal neurologic symptoms, as numerous compensatory mechanisms, particularly renal, may take effect. Treatment includes restoring adequate ventilation and improving gas exchange and may require tracheal intubation and assisted ventilation. Supplemental oxygen therapy should be carefully monitored, as high rates of flow may suppress the hypoxic drive for respiration and lead to significant carbon dioxide retention. The sleep apnea syndromes are a group of disorders in which abnormal respiratory patterns during sleep result in hypercapnia and hypoxemia. Intermittent obstruction of the upper airway and abnormalities of brainstem respiratory centers cause frequent nocturnal awakenings and apneas in these patients. Treatments vary and include weight loss in obese subjects, respiratory stimulants, tracheostomy, and diaphragmatic pacing. Rapid ascent to high altitudes may result in headache, changes in mental status, papilledema, and other neurologic symptoms in certain individuals: a syndrome known as high-altitude sickness. Hypoxia leading to cerebral edema, nocturnal periodic breathing, and hypobaria produces neurologic symptoms in these individuals. Acetazolamide and dexamethasone may be effective in minimizing symptoms of this disorder. Sustained hyperventilation produces acral and circumoral paresthesias and lightheadedness in anxious individuals and can be maintained by relatively normal ventilatory patterns once established. These symptoms are due to hypophosphatemia and respiratory alkalosis, the latter reducing CBF and causing localized tissue hypoxia. Rebreathing into a paper bag at the first awareness of symptoms is the most effective form of treatment.
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PMID:Neurologic manifestations of pulmonary disease. 267 37

The role of drug therapy in the treatment of the sleep apnea/hypopnea syndrome is unclear. In a randomised, double-blind, placebo-controlled study, we investigated the value of 14-day therapy with protriptyline (20 mg daily) or acetazolamide (250 mg 4 times per day) on symptoms and on the frequency of apneas, hypopneas, arousals, and 4% desaturations in 10 patients with obstructive sleep apnea/hypopnea syndrome. Overall, protriptyline did not have a significant effect either on symptoms or on any of the above polysomnographic criteria. Acetazolamide reduced the apnea/hypopnea frequency [placebo 50 +/- 26 (SD); acetazolamide 26 +/- 20/h of sleep, p less than 0.03] and tended to decrease the frequency of 4% desaturations (placebo 29 +/- 20; acetazolamide 19 +/- 16/h of sleep, p = 0.06). Despite these physiological improvements, acetazolamide did not significantly improve symptoms and paraesthesiae were common. Contrary to earlier studies, we conclude that protriptyline may have a limited role in the treatment of the sleep apnea syndrome. The reason why acetazolamide produced a physiological, but not a symptomatic, response requires further investigation.
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PMID:Role of protriptyline and acetazolamide in the sleep apnea/hypopnea syndrome. 306 13

Central sleep apnea is a disorder characterized by apneic episodes during sleep with no associated ventilatory effort. More commonly than not these apneas are seen in patients who also have obstructive and mixed events. Although patients with this disorder frequently complain of insomnia and depression, frank hypersomnolence is rarely encountered. As these complaints are common ones seen in numerous clinical situations, and since sleep studies are rarely conducted to investigate their etiology, the true incidence of central sleep apnea has not been determined. The etiology of central apnea remains unknown, although the association between these breathing events and a number of other disease processes has increased our understanding of the disorder. Central apneas during sleep commonly occur after hyperventilation with the associated hypocapnic alkalosis. This occurs at high altitude when hyperventilation is induced by hypoxia and at sea level when spontaneous nocturnal hyperventilation occurs. This suggests that PCO2 is the primary stimulus to ventilation during sleep and that loss of this drive, as occurs with hypocapnia, may produce dysrhythmic breathing. Patients with complete absence of ventilatory chemosensitivity such as occurs with Ondine's curse (central alveolar hypoventilation) or the obesity-hypoventilation syndrome may also have central apneas. For reasons that remain unexplained, central sleep apnea is commonly seen in patients with congestive heart failure, nasal obstruction, and certain neurologic disorders. However, in most patients with central sleep apnea no obvious cause or association can be found. The treatment of this disorder is not entirely satisfactory. If it is severe, mechanical ventilation during sleep can be provided by any one of a number of techniques. However, for the patient who simply complains of insomnia and is found to have a moderate number of central apneas, the treatment choices are limited. Acetazolamide has been shown to decrease central apneas during short-term use, but results have been variable with prolonged administration. Other ventilatory stimulants seem to have little efficacy. Interestingly, oxygen administration has been shown to reduce central apneas considerably in a number of studies, although the explanation for its success is unknown. Central sleep apnea therefore remains a relatively rare disorder whose etiology is not fully understood and whose treatment is not completely satisfactory.
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PMID:Central sleep apnea. 393 82

The use of acetazolamide, a carbonic anhydrase inhibitor, in chronic obstructive pulmonary disease (COPD) remains controversial. A substantial improvement in blood gas values has been documented, with correction of metabolic alkalosis in COPD, in hypoxemic sleep apnea at high altitudes and in acute mountain sickness. This randomized, double-blind study examined the short and long term effects of acetazolamide (2 X 250 mg) on 14 patients with hypoxemia, hypercapnia and metabolic alkalosis (paO2 49 +/- 5.2 mm Hg, paCO2 50 +/- 3.6 mm Hg, base excess + 5.7 +/- 2.3). A crossover between acetazolamide and placebo occurred on days 3, 6 and 9. On day 12 the patients were again randomized and one group further treated with acetazolamide for 4 1/2 (1-7) months. During the short term phase, a significant rise in paO2 to 58 +/- 6.6 mm Hg with acetazolamide was noted, followed by a drop to 53 +/- 5.7 mm Hg with placebo. The paO2 of the five patients on long-term acetazolamide therapy remained unchanged (59 +/- 2.5 mm Hg) while the untreated patients showed a significant drop in paO2 to 46 +/- 8.2 mm Hg. No side effects and no severe metabolic acidosis were noted during acute or long term treatment. Acetazolamide appears to improve hypoxemic and hypercapnic COPD patients with metabolic alkalosis on short and long term therapy.
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PMID:[Acetazolamide in hypercapnic chronic obstructive lung disease--a renaissance?]. 682 42

Acetazolamide (ACTZ) reduces sleep apnea in adults exposed to high altitude and augments the ventilatory response to CO2. In order to determine the effect of ACTZ on the ventilatory response to CO2 and the incidence of apnea in preterm infants, 7 infants (BW, 1070 +/- 191 g; postnatal age, 9 +/- 7 days) were randomized to receive ACTZ (5 mg/kg/dose Q6h for 36 hr) and 7 infants (BW, 1092 +/- 292 g; post-natal age, 5 +/- 2 days) received aminophylline (AMINO; 8 mg/kg bolus then 2.5 mg/kg Q12h for 36 hr). Minute ventilation (VE), end-tidal CO2 (PETCO2), ventilatory response to CO2, number of apneic episodes (> or = 15 sec duration), and arterial blood gases were measured before and 24-36 hr after starting therapy. In the AMINO group there was a significant decrease in apnea frequency from 6 +/- 1 to 2 +/- 2 episodes over an 8 hr epoch (P < 0.05), while no significant change was observed in the ACTZ group. The end-tidal CO2 decreased significantly from 44 +/- 7 to 38 +/- 6 mmHg in the AMINO group and from 47 +/- 5 to 36 +/- 5 mmHg in the ACTZ (P < 0.05), which lead to a shift to the left of the CO2-response curve in both groups. The slope of the CO2 response curve did not change significantly in the AMINO group and decreased in the ACTZ group. There was a significant decrease of pH from 7.43 to 7.26 in the ACTZ group, whereas in the AMINO group pH increased from 7.38 to 7.44.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of the effects of acetazolamide and aminophylline on apnea incidence and on ventilatory response to CO2 in preterm infants. 805 22

Acetazolamide, a carbonic anhydrase inhibitor, is used in patients with chronic obstructive pulmonary diseases and central sleep apnoea syndrome and in the prevention and treatment of the symptoms of acute mountain sickness. In these patients, the drug increases minute ventilation (V'E), resulting in an improvement in arterial oxygen saturation. However, the mechanism by which it stimulates ventilation is still under debate. Since hypoxaemia is a frequently observed phenomenon in these patients, the effect of 4 mg x kg(-1) acetazolamide (i.v.) on the ventilatory response to hypercapnia during hypoxaemia (arterial oxygen tension (Pa,O2)=6.8+/-0.8 kPa, mean+/-SD) was investigated in seven anaesthetized cats. The dynamic end-tidal forcing (DEF) technique was used, enabling the relative contributions of the peripheral and central chemoreflex loops to the ventilatory response to a step change in end-tidal carbon dioxide tension, (PET,CO2) to be separated. Acetazolamide reduced the CO2 sensitivities of the peripheral (Sp) and central (Sc) chemoreflex loops from 0.22+/-0.08 to 0.11+/-0.03 L x min(-1) x kPa(-1) (mean+/-SD) (p<0.01) and from 0.74+/-0.32 to 0.40+/-0.10 L x min(-1) x kPa(-1) (p<0.01), respectively. The apnoeic threshold B (x-intercept of the ventilatory CO2 response curve) decreased from 2.88+/-0.97 to 0.95+/-0.92 kPa (p<0.01). The net result was a stimulation of ventilation at PET,CO2 <5 kPa. The effect of acetazolamide is possibly due to a direct effect on the peripheral chemoreceptors as well as to an effect on the cerebral blood flow regulation. Possible clinical implications of these results are discussed.
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PMID:Effect of low-dose acetazolamide on the ventilatory CO2 response during hypoxia in the anaesthetized cat. 987 70

The number of patients suffering from sleep apnea syndrome(SAS) have been increased. In recent years, many therapeutic approaches such as nasal CPAP, dental appliance, upper airway surgery, pharmacological agents, have been used for the treatment of SAS. The various drugs(acetazolamide, some tricyclic antidepressant, progesterone, theophylline, aminophylline and so on) have been used for pharmacotherapy of SAS. Acetazolamide have been established as the best medication. But all approaches without acetazolamide, could not shown their satisfactory effects on SAS. In this article, drug therapy for SAS is described.
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PMID:[Drug therapy for sleep apnea syndrome]. 1094 32

Theory predicts respiratory instabilities at elevated system loop gain (G), determined by such factors as ventilatory CO(2) sensitivity, set-point PCO(2), and metabolic rate. In anesthetized rabbits, the effects on G of carbonic anhydrase (CA) inhibitors and of different sodium/proton exchanger type 3 (NHE3) inhibitors were studied. Acetazolamide significantly reduced G by 42.0 +/- 9.3% and methazolamide by 35.0 +/- 9.5% (each n = 7, P<0.01). Irrespective of the substance, NHE3 inhibition reduced G by 33.0 +/- 7.8% (n = 10, P<0.01) at 35.5 +/- 1.6 mmHg PaCO(2) (mean +/-SE), but not at lower arterial CO(2) levels (n=5). Since high baseline PCO(2) coincides with elevated brainstem NHE3 mRNA expression, this may also account for a higher risk of sleep apnea (or even occurrence of sudden infant death). Therefore, NHE3 inhibitors may gain similar therapeutic importance in the treatment of irregular breathing as CA inhibitors. Generally, effective treatment should aim at a low system loop gain, by reducing respiratory chemosensitivity, improving blood gases and preventing low metabolic rates.
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PMID:Pharmacological impact on loop gain properties to prevent irregular breathing. 1844 86

Considering the high prevalence of the obstructive sleep apnea syndrome (OSA), it is expected that many patients with the disorder are traveling to altitude. However, this may expose them to the risk of pronounced hypoxemia, exacerbation of nocturnal breathing disturbances by frequent central apneas, impaired daytime performance, and high blood pressure. Recently, randomized studies specifically investigated the effects of altitude (1630-2590 m) in OSA patients and the optimal treatment in this setting. The results indicate that patients should continue to use continuous positive airway pressure therapy (CPAP) when sleeping at altitude. Since CPAP alone does not control central sleep apnea emerging at altitude, combined treatment with acetazolamide and CPAP should be considered, in particular, in patients with severe OSA and co-morbidities. Supplemental oxygen combined with CPAP might be advantageous in patients with OSA and concomitant cardiopulmonary disease by preventing hypoxemia and central sleep apnea. In patients unable to use CPAP or if electrical power is not available, an optimally fitted mandibular advancement device might be an alternative treatment option that can be combined with acetazolamide during altitude sojourns. Acetazolamide alone is also beneficial and better than no treatment at all, since it improves oxygen saturation, breathing disturbances, and the excessive blood pressure elevation in OSA patients traveling to altitude.
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PMID:How to treat patients with obstructive sleep apnea syndrome during an altitude sojourn. 2220 52

The International Classification of Sleep Disorders, Second Edition (ICSD-2) distinguishes 5 subtypes of central sleep apnea syndromes (CSAS) in adults. Review of the literature suggests that there are two basic mechanisms that trigger central respiratory events: (1) post-hyperventilation central apnea, which may be triggered by a variety of clinical conditions, and (2) central apnea secondary to hypoventilation, which has been described with opioid use. The preponderance of evidence on the treatment of CSAS supports the use of continuous positive airway pressure (CPAP). Much of the evidence comes from investigations on CSAS related to congestive heart failure (CHF), but other subtypes of CSAS appear to respond to CPAP as well. Limited evidence is available to support alternative therapies in CSAS subtypes. The recommendations for treatment of CSAS are summarized as follows: CPAP therapy targeted to normalize the apnea-hypopnea index (AHI) is indicated for the initial treatment of CSAS related to CHF. (STANDARD)Nocturnal oxygen therapy is indicated for the treatment of CSAS related to CHF. (STANDARD)Adaptive Servo-Ventilation (ASV) targeted to normalize the apnea-hypopnea index (AHI) is indicated for the treatment of CSAS related to CHF. (STANDARD)BPAP therapy in a spontaneous timed (ST) mode targeted to normalize the apnea-hypopnea index (AHI) may be considered for the treatment of CSAS related to CHF only if there is no response to adequate trials of CPAP, ASV, and oxygen therapies. (OPTION)The following therapies have limited supporting evidence but may be considered for the treatment of CSAS related to CHF after optimization of standard medical therapy, if PAP therapy is not tolerated, and if accompanied by close clinical follow-up: acetazolamide and theophylline. (OPTION)Positive airway pressure therapy may be considered for the treatment of primary CSAS. (OPTION)Acetazolamide has limited supporting evidence but may be considered for the treatment of primary CSAS. (OPTION)The use of zolpidem and triazolam may be considered for the treatment of primary CSAS only if the patient does not have underlying risk factors for respiratory depression. (OPTION)The following possible treatment options for CSAS related to end-stage renal disease may be considered: CPAP, supplemental oxygen, bicarbonate buffer use during dialysis, and nocturnal dialysis. (OPTION) .
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PMID:The treatment of central sleep apnea syndromes in adults: practice parameters with an evidence-based literature review and meta-analyses. 2294 96


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