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

Central sleep apnea is not a single disease but represents the final pathway in a large group of heterogeneous disorders. Control of normal breathing during sleep relies upon finely coordinated anatomical and physiological mechanisms and their destabilization leads to central apnea. The causes of central sleep apnea can be classified into 4 groups: neurologic disorders, periodic breathing, upper airway abnormalities, and idiopathic syndromes. Clinical features result from the interaction between the underlying disorder and control of respiration. Two different prototypes emerge: patients who are hypercapnic (central hypoventilation and/or impaired respiratory mechanics) and those who are eucapnic or hypocapnic (periodic breathing and idiopathic hyperventilation). The causes and severity of apnea can be determined by clinical assessment, pulmonary function testing, and overnight polysomnography. Further management involves specific treatment of the underlying condition and reducing the sequelae of recurrent apneas during sleep, namely cardiorespiratory dysfunction and sleep disruption. This review outlines an approach to the management of central sleep apnea based upon an understanding of its pathophysiology.
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PMID:Mechanisms and management of central sleep apnea. 173 82

Five patients with congestive heart failure (CHF) and 1 with left ventricular dysfunction but without CHF were found to have sleep apnea. Central sleep apnea (CSA) related to Cheyne-Stokes respiration was seen in 4 cases while obstructive sleep apnea (OSA) was seen in 2. All patients had symptoms of sleep apnea. Nasal continuous positive airway pressure (NCPAP) was effective in reversing CSA and OSA in all patients with improvement in sleep structure and alleviation of symptoms of sleep apnea. In addition, all experienced a reduction in cardiac dyspnea. This was associated with a 5% or greater increase in left ventricular ejection fraction while on NCPAP, compared to baseline value off NCPAP in 5 patients and resolution of chronic pleural effusion and pulmonary edema in the sixth. We conclude that Cheyne-Stokes respiration during sleep may give rise to a CSA syndrome that is reversible by NCPAP. In addition, NCPAP therapy may lead to a reduction in cardiac dyspnea and improvement in left ventricular function in patients with left ventricular dysfunction and sleep apnea.
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PMID:Sleep apnea in patients with left ventricular dysfunction: beneficial effects of nasal CPAP. 219 97

Sleep apnoea syndromes are a frequent disease, with an incidence of more than 1% in the adult population, a strong male predominance, and a maximal frequency between 40 and 60 years. Their clinical manifestations are dominated by snoring and daytime sleepiness, at times associated with morning headaches, intellectual deficiency, sexual impotence. Obesity, hypertension and polycythemia are not uncommon. These patients are at risk for accidents due to sleepiness, sudden death due to sleep apnoea-related cardiac arrhythmias, ischemic attacks related to hypertension and polycythemia and right heart failure secondary to pulmonary hypertension and alveolar hypoventilation. The most frequent form of sleep apnoea syndromes include obstructive and mixed apnoeas. Their mechanism involves both anatomic factors (upper airway narrowing) and functional factors (defective activation of upper airways dilatory muscles) which lead to upper airway occlusion upon inspiration during sleep. Two therapeutic strategies are possible: a surgical one, uvulopalatopharyngoplasty, the efficacy of which is inconstant and unpredictable and nasal continuous positive airway pressure, which is constantly efficacious but constraining. Central sleep apnoea syndromes are rare, less clearly defined and more difficult to treat.
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PMID:[Sleep apnea syndromes in adults]. 332 Dec 51

Three of six siblings presented with sleep apnea between 18 and 26 months of age. Twin females and a male had normal growth and development without antecedent neurologic or apparent metabolic disorder. The females presented at 25 and 27 months respectively with irregular respiration and episodes of apnea. Twin A succumbed to an apneic episode while sleeping. Central sleep apnea was diagnosed in twin B at the Stanford Sleep Clinic. She died following an apneic episode three months after evaluation. The male presented at 18 months with fatal sleep apnea. A fourth child was evaluated for sleep apnea at 7 weeks of age with several hospitalizations before her death at 31 months. She and remaining family members were extensively studied for inherited neurologic disorders including subacute necrotizing encephalomyopathy (SANE, Leigh disease). This family with lethal sleep apnea presents an association with SANE with minimal neurologic signs and symptoms and neuropathologic involvement. Lesions were confined to the respiratory centers of the lower brain stem, making sleep apnea explicable. This child and family members tested positive or borderline for inhibitor substance thiamine triphosphate (TTP). All testing for TTP inhibitor substance was performed in Professor Jack R. Cooper's laboratory, Department of Pharmacology, Yale University School of Medicine, New Haven, Conn. These cases present an interesting and instructive lesson emphasizing the need for extensive evaluation of children with unsuspected sleep apnea with early demise.
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PMID:Familial lethal sleep apnea. 371 Apr 78

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 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

This study was designed to determine the impact of central sleep apnea with or without Cheyne-Stokes respiration (CSR) on morbidity and mortality. Central sleep apnea was found in 77 male general medical ward in-patients. Cheyne-Stokes respiration was found in 49 of the 77 men; in 15 men, CSR was severe, ie, > or = 25 percent of the night spent in CSR, in 34 men CSR was mild (1 to 25 percent CSR). Twenty-eight men had central sleep apnea but no CSR. An additional 31 patients had no sleep apnea and no CSR. The patients with severe CSR had more central apneas, more, but shorter desaturations, more awakenings and more wake time during the night, but spent more time in bed than those with no CSR or no apnea. Radiographic evidence was consistent with an association of CSR and heart failure. In addition, patients with severe CSR were at almost twice the risk of dying compared with those with no apnea and had a shorter survival time. Nevertheless, we could not confirm that CSR was an independent predictor of elevated mortality risk, implying that some other factors specific to severe CSR predispose these patients to shorter survival time.
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PMID:Comparison of patients with central sleep apnea. With and without Cheyne-Stokes respiration. 808 59

A high prevalence of sleep disorders and sleep apnea syndrome in hemodialysis (HD) patients has been known for 10 years. Acetate, the buffer once most commonly used, favors intradialytic hypoxemia through hypoventilation and ventilation-perfusion changes. The aim of the present study was to assess the influence of buffer, acetate or bicarbonate, on sleep and ventilation during the night subsequent to an afternoon (2-7 p.m.) dialysis session. Ten patients, 8 males and 2 females, aged 35-71 years, dry weight 55-72 kg, on dialysis 15 h a week for 6-67 months, were randomly assigned first to acetate or bicarbonate, then to the other mode of treatment. After a series of six sessions using the same buffer, polysomnographic recordings from 9.00 p.m. to 6.00 a.m. were obtained. Sex, age, weight, data of first dialysis, blood pressure and sleep disorder-related symptoms were not correlated with the sleep apnea syndrome. Prolonged or important oxygen desaturations were never observed. Central apnea occurred more frequently during the night following acetate dialysis: x = 33 (0-180) versus 3 (0-15), p < 0.05. Obstructive apneas were not different. A defective modulation of ventilatory control after acetate HD might be held responsible for central apnea, which would constitute one more case for a widespread use of bicarbonate HD.
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PMID:Sleep apnea incidence in maintenance hemodialysis patients: influence of dialysate buffer. 856 43

Sleep apnea has been recorded in many infants, but little data exist concerning the amount and range of apnea in infants. We studied 49 infants referred to the sleep disorders unit. Single polysomnographic studies were performed on each infant. We examined the amount of apnea, presence and amount of upper airway obstruction and the sleeping pattern in each infant. Central apnea was common to all infants and varied in amount. Upper airway obstruction, recorded as mixed apnea, was found in 36 infants. Twenty of these infants had only occasional mixed apnea ( < 2 apneas/hour), whereas 16 infants displayed a higher amount of obstruction. All infants were separated into two groups according to amount of apnea and obstruction. Sixteen infants with obstruction plus 3 infants with a high amount of central apnea represented group I. The remaining 30 infants represented group II. Marked differences in the sleeping pattern were found when the groups of infants were separated. Infants from group I had significantly less rapid eye movement (REM) sleep than infants from group II. We conclude that sleep-disordered breathing in infants is associated with disruptions in sleep.
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PMID:Sleep-disordered breathing and its effects on sleep in infants. 865 Apr 61

Obstructive and central sleep apnea are common in patients with congestive heart failure (CHF). These sleep-related breathing disorders are characterized by two pathophysiologic features that could have important implications for disease progression in CHF: sympathetic nervous system activation, and adverse changes in cardiac loading conditions. In patients with obstructive sleep apnea, blood pressure is frequently elevated as a result of excessive sympathetic nervous system activity elicited by the combination of apnea, hypoxia, and arousals from sleep. The generation of exaggerated negative intrathoracic pressure during obstructive apneas further increases left ventricular afterload, reduces cardiac output, and may promote the progression of pump failure. Increased afterload and hypoxia can also predispose such patients to myocardial ischemia and arrhythmias. In patients with CHF, abolition of coexisting obstructive sleep apnea by nasal continuous positive airway pressure improves left ventricular function. Central sleep apnea (i.e., Cheyne-Stokes respiration) is also characterized by apnea, hypoxia, and increased sympathetic nervous system activity and, when present in CHF, is associated with increased risk of death. Recent medium-term trials involving small numbers of patients have demonstrated that nocturnally applied continuous positive airway pressure in patients with CHF and central sleep apnea alleviates central sleep apnea, improves left ventricular function, reduces sympathetic nervous system activity and improves symptoms of CHF. These studies emphasize the importance of considering obstructive and central sleep apnea in the differential diagnosis of conditions that could contribute to the development or progression of CHF. They also suggest that continuous positive airway pressure is a promising nonpharmacologic adjunctive therapy for patients with CHF and coexisting sleep-related breathing disturbances that warrants further investigation.
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PMID:Pathophysiologic and therapeutic implications of sleep apnea in congestive heart failure. 889 61


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