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

A central apnea is a disorder characterized by apneic events during sleep with no associated ventilatory effort. Central sleep apnea syndrome is characterized by repeated apneas during sleep resulting from loss of respiratory effort. Although the etiology of central apnea remains obscure in most cases, current investigations into breathing control system during sleep and association with certain diseases have pointed out possible mechanisms. Ventilation during sleep is highly dependent on the nonbehavioral control system. As a result, any diseases affecting this control system could influence the breathing patterns while the patient is asleep. As our results show, most patients with central sleep apnea and without congestive heart failure had quantifiable abnormalities like diminished carbon dioxide response curves. Neurological diseases affecting the brainstem are able to produce breathing pattern disorders in sleep. Well-known neurological diseases such as arteriosclerosis in the elderly, infarctions, tumors, hemorrhage, accidents with damage of this region, encephalitis, poliomyelitis or other infectious diseases may cause central apnea during sleep, even if in wakefulness no abnormalities of breathing patterns are present. Apneas cause hypoxemia, hypercapnia and increased sympathicotonia. This may result in development of pulmonary artery hypertension or systemic hypertension. Published results demonstrate that medical treatment is ineffective in these patients. Implantation of a diaphragm pacing device is an invasive measure, the efficacy of the diaphragm pacing has not been proven by long-term trials, however. Mechanical ventilation was shown to be the most efficient treatment. A therapeutic procedure using a timed n-BiPAP device is able to normalize blood gases during sleep. The n-BiPAP prevented the development of severe pulmonary artery hypertension during sleep.
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PMID:Central sleep apnea. 904 68

We report on the case of two young patients with type I Arnold-Chiari malformation (ACM), as revealed by a central sleep apnoea (CSA) syndrome without any other neurological defect. Case 1 was a 14-yr-old male patient, who developed severe alveolar hypoventilation and needed long-term mechanical ventilation via a tracheostomy. Case 2 was a 39-yr-old male patient, who developed features suggestive of sleep apnoea and responded to nasal continuous positive airway pressure ventilation despite the central type of apnoeas. These two cases illustrate the different pathophysiological mechanisms involved in CSA, namely a blunted chemical drive (in hypercapnic patients) and an increased chemical drive, which destabilizes the breathing pattern during sleep (in normo/hypocapnic patients). Central sleep apnoea can be the initial manifestation of Arnold-Chiari malformation and can lead to a life-threatening condition.
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PMID:Central sleep apnoea in Arnold-Chiari malformation: evidence of pathophysiological heterogeneity. 987 13

To define fundamental mechanisms for sympathoexcitation could provide a therapeutic opportunity to interrupt the specific site linking sympathetic activation with heart failure. Central sleep apnea is characterized by apnea, hypoxia, sleep fragmentation, and increased sympathetic nerve activity. Since this sympathoexcitation is directly related to the frequency of arousals from sleep and the degree of apnea-related hypoxia, but not to left ventricular ejection fraction, it is therefore not simply a compensatory response to hemodynamic derangement but is excessive and pathologic sympathoexcitation with aftereffects that persist into wakefulness. Thus, central sleep apnea could participate in a vicious pathophysiologic cycle involving the cardiovascular, respiratory, and autonomic nervous system.
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PMID:[Autonomic function and circulatory failure]. 1094 19

Central sleep apnoea, especially Cheyne-Stokes respiration, is found in 45 to 66% of patients with congestive heart failure (CHF) in functional classes NYHA II to IV. Cheyne-Stokes breathing cycles are characterised by central apnoeas, followed by a crescendo--like increase of tidal volume into hyperventilation and a subsequent decline of tidal volume, ending in another central apnoea. Cheyne-Stokes respiration has been shown to be a poor prognostic factor for patients with CHF. Apnoeas and hypopnoeas cause marked oxygen desaturation and rises of carbon dioxide concentrations in the blood. The resumption of breathing is frequently associated with arousals, which might cause daytime symptoms like fatigue and sleepiness as well as persistent activation of the sympathetic nervous system. Elevated concentrations of catecholamines increase cardiac work, adversely affecting cardiac function. Serum catecholamines are known to augment the chemoreceptor susceptibility for carbon dioxide. This might be one reason for the permanent mild hyperventilation found in these patients during wakefulness. Increased chemoreceptor responsiveness destabilises the feedback control of breathing, and hyperventilation below the apnoeic threshold grows more likely. Other contributing factors for the development of Cheyne-Stokes respiration include alterations in the control of breathing during sleep and the increased circulation time between the lung and chemoreceptors in CHF patients. The feedback regulation of breathing might be less dampened since carbon dioxide levels are reduced in these patients. Treatment includes nCPAP, but in many cases this is poorly tolerated in patients with central sleep apnoea. Future approaches to Cheyne-Stokes respiration might focus on improving ventilatory pattern and pharmacological manipulation of carbon dioxide receptor susceptibility.
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PMID:[Heart failure and central respiratory dysregulation. Cheyne-Stokes respiration during sleep in advanced left heart failure]. 1123 52

Central sleep apnea is a common respiratory pattern in healthy neonates. Nevertheless, frequent central sleep apnea associated with drops in oxygen saturation may contribute to infantile morbidity. Recently, low-dose acetazolamide was shown to reduce symptomatic central sleep apnea in adults. We treated 12 infants, median conceptional age 42 weeks (range, 40-44 weeks), with central sleep apnea. In all cases, the central apnea index was >40/h total sleeping time (apnea > or = 3 sec). The cumulative duration of drops in oxygen saturation below 90% was more than 3 min/h total sleeping time. All individuals received acetazolamide 7 mg/kg/day (orally, divided in three doses) for 11 weeks. Polysomnography was begun 10 hours before the first dose and continued for 10 hours after the third dose. Polysomnography was repeated after 6 weeks of treatment and 1 week after acetazolamide therapy was discontinued. Comparison of the respiratory patterns before and after treatment (10-hour recording after the third dose) showed a decrease in the median central apnea index from 74/h (range, 42-152/h) to 13/h (range, 6-49/h). The median of the cumulative duration of drops in oxygen saturation below 90% decreased from 3.6 min/h (range, 3.1-9.2 min/h) to 0.07 min/h (range, 0-0.5 min/h). Basal oxygen saturation increased from 95 (92-97%) to 98% (96-99%). This improvement was maintained in the final polysomnography (12 weeks after therapy was begun and 1 week after completion of the 11-week course). No adverse effects were noted. We conclude that low-dose acetazolamide treatment may be useful for the treatment of central infantile sleep apnea associated with hypoxemia.
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PMID:Acetazolamide treatment for infantile central sleep apnea. 1151 Sep 34

Between 1991-2000 2052 patients (81% men and 19% women) were referred to our Sleep Laboratory because of OSA suspision. In 1194 (58%) subjects (88% men and 12% women) diagnosis of obstructive sleep apnoea (OSA, AHI > 10) was confirmed. In 430 of them (36%) mild OSA (AHI 11-25), in 243 (20%) moderate OSA (AHI 26-40), and in 521 (44%) severe OSA (AHI > 40) was diagnosed. Epworth sleepiness scale score in those groups was 10.4, 10.5 and 13.0 points respectively. 908 (76%) of patients with OSA were submitted to nCPAP treatment. Effective CPAP pressure ranged from 5 to 20 milibars, mean 8.4 mbars. In 21 patients upper airway resistance syndrome (UARS) was diagnosed. Central sleep apnoea, most frequently of Cheyne-Stokes respiration type was diagnosed in 13 patients. The most common diseases accompanying OSA were: systemic hypertension (46%), coronary heart disease (29%), diabetes (12%), and COPD (9%). Majority of OSA patients (61%) were obese (BMI > 30 kg/m2), 32% were over weight (BMI 25-30 kg/m2). Only 7% had normal body weight (BMI 20-25 kg/m2). Long-term (more than one year) compliance to treatment was found in 70% of patients prescribed CPAP.
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PMID:[Ten years experience of the sleep laboratory at the Institute of Tuberculosis and Lung Disease in Warsaw]. 1192 60

Central sleep apnoea is a form of periodic breathing which resembles Cheyne-Stokes respiration but occurs only during sleep. One mechanism in the pathogenesis is a delay in chemical feedback from the lungs to the medullary respiratory centre. We explored the relationship between circulatory feedback delay in a patient with central sleep apnoea and Cheyne-Stokes respiration before and after mitral valve repair. Preoperatively the patient had severe central sleep apnoea and an increased circulation time. Following mitral valvuloplasty the circulation time was decreased with resolution of central sleep apnoea. This case demonstrates the role of feedback delay in central sleep apnoea and suggests that similar haemodynamic mechanisms may lead to central sleep apnoea and Cheyne-Stokes respiration.
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PMID:Elimination of central sleep apnoea by mitral valvuloplasty: the role of feedback delay in periodic breathing. 1476 Jan 62

Central sleep apnoea is often recognized in patients with heart failure. Although the medical treatment to improve cardiac function is effective for sleep apnoea, direct evidence that improved cardiac function ameliorates sleep apnoea has not been reported due to the fact that a particular drug may affect a multitude of organs. We present a chronic heart failure patient with central sleep apnoea whose nocturnal desaturation was improved by percutaneous coronary intervention that resulted in improved cardiac function. This is the first case where percutaneous coronary intervention improved sleep apnoea, suggesting that the improved cardiac function led to amelioration of sleep apnoea.
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PMID:Percutaneous coronary intervention for central sleep apnoea with ischaemic cardiomyopathy. 1503 Jan 36

A 61-yr-old male presented with apparent idiopathic central sleep apnoea but after 4 yrs developed features of autonomic, cerebellar and extrapyramidal dysfunction consistent with a diagnosis of multiple system atrophy (MSA). Though central sleep apnoea can occur in multiple sleep apnoea, it is less frequent than obstructive sleep apnoea and occurs in the later stages of the disease. The pathogenesis of MSA involves gliosis and neuronal cell loss in specific areas of the central nervous system. Central sleep apnoea in MSA may be due to the depletion of cholinergic neurons in the arcuate nucleus of the medulla by apoptosis. This is the first description of multiple system atrophy presenting as central sleep apnoea. The current authors believe that multiple system atrophy should be considered in the differential diagnosis of late onset central sleep apnoea and progressive hypoventilation.
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PMID:Multiple system atrophy presenting as central sleep apnoea. 1533 5

Sleep apnea encompasses 2 forms of sleep disordered breathing, namely obstructive and central sleep apnea. Both these conditions are prevalent in patients with congestive heart failure (CHF) despite quite different etiology and pathogenesis. The last 15 years have seen the development of a large database of mechanistic data implicating both these conditions in the progression of cardiac dysfunction in patients with heart failure. Epidemiological data have also revealed that obstructive sleep apnea may be an independent risk factor for the development of cardiac diseases. Central sleep apnea, conversely, is more likely to emerge as a consequence of severe cardiac dysfunction, but through an elaborate vicious cycle could potentially lead to augmentation of sympathetic activity and contribute to further cardiac decline. In recent years a number of randomized controlled trials suggests secondary endpoints such as symptoms, sympatho-excitation and left ventricular function can be improved with the effective therapies available for both central and obstructive sleep apnea in patients in which these conditions co-exist. Mortality data is emerging also, and the first of a large scale mortality trial assessing the effect of attenuating central sleep apnea with continuous positive airway pressure in patients with moderate to severe CHF, is well underway. This review summarizes the important mechanistic, epidemiological and interventional studies in relation to sleep apnea and congestive heart failure with some commentary on the future direction of this rapidly growing field.
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PMID:Sleep apnea and congestive heart failure. 1533 41


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