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

Many nocturnal cardiac arrhythmias and conduction defects have been reported in the adult sleep apnoea syndrome. The most original is the great variability of the heart rate which is cyclical and related to the apnoeic episodes, and easily differentiated from simple respiratory sinus arrhythmia. It is characterised by an initial bradycardia followed by rebound tachycardia. The bradycardia is vagally dependent (inhibited by atropine) probably secondary to carotid chemoreceptor stimulation by the hypoxaemia. The tachycardia is mainly attributed to the cessation of vagal hypertonicity although catecholamine stimulation has been suggested. The origin of these changes is purely functional, regressing with treatment of apnoea (waking, tracheotomy), the maintenance of arterial oxygen concentrations with oxygen therapy and parasympathetic blockade (atropine). The intensity of the phenomenon is related to the degree of arterial desaturation, which is itself related to basal arterial saturation (SaO2) and the duration of the apnoeas. Prolonged systole due to paroxysmal sino-atrial or atrioventricular block may be observed at night in these patients. The influence of vagal overactivity is confirmed (suppression of vagotomy) with no organic pathology (diurnal absence, tracheotomy, normal electrophysiological testing) in favour of a relationship with apnoea. Though less common than conduction abnormalities, atrial arrhythmias (extrasystoles, flutter, fibrillation) are also possible complications of sleep apnoea. The absence of an organic substrate is indicated by their regression post-tracheotomy and the efficacy of atropine (again in favour of a vagally-induced mechanism). Finally, nocturnal ventricular hyper-excitabilty is sometimes observed, the probable mechanism being the association of severe hypoxaemias (SaO2 < 60%) and the increased sympathetic tone at the end of the apnoea.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Arrhythmia and syndrome of obstructive sleep apnea in adults]. 802 77

We have performed sleep nasendoscopy on 54 adult snorers in whom obstructive sleep apnoea had been excluded by an overnight sleep study. The purpose of the study was to identify the site or sites of noise production in each case. This was successfully achieved in 50 of the 54 and 70% showed palatal flutter snoring only. In a further 20%, palatal flutter snoring was combined with evidence of noise generation at another site. The second site was supraglottic in 10%, tonsillar in 8% and tongue base in 2%. The tongue base was also the sole site of noise generation in 8% and the epiglottis was the sole site in 2%. This study suggests that sleep nasendoscopy can identify different mechanisms of snoring in individual patients. This information is likely to be of use in formulating a logical surgical treatment plan.
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PMID:Observation of the mechanism of snoring using sleep nasendoscopy. 854 73

Ten subjects known to suffer from heavy snoring but not obstructive sleep apnoea were studied using the technique of sleep nasendoscopy. The mechanism of snoring was noted for each and sound recordings of the snoring noise were made. Six subjects were observed to snore using their soft palate only, three snored using only their tongue base and one snored using a combination of palate and tongue base. The sound recordings were subjected to computer analysis of waveform and frequency. Palatal flutter snoring and tongue base snoring appear to have distinct waveform and frequency patterns which allows them to be differentiated from each other.
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PMID:The differentiation of snoring mechanisms using sound analysis. 873 94

It is now widely accepted that snoring causes significant social dysfunction. In the absence of obstructive sleep apnoea syndrome, palatal surgery offers a very good chance of eliminating or reducing snoring. The traditional operation of uvulopalatopharyngoplasty remains the 'gold standard', but may be complicated by velopharyngeal incompetence, severe post-operative pain and even nasopharyngeal stenosis. A newer technique to reduce snoring caused by palatal flutter by using a neodymnium:yttrium aluminum garnet laser to stiffen the soft palate has been introduced recently by another unit. We show that this procedure can be carried out using a CO2 laser, and present the initial results of the first 29 patients operated on at The Royal National Throat, Nose and Ear Hospital.
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PMID:CO2 laser palatoplasty: early results. 886 9

This study assessed the effect on the upper airway during sleep nasendoscopy of mimicking the action of a mandibular advancement splint. Twenty-seven subjects with a diagnosis of sleep-disordered breathing were referred for mandibular advancement splint therapy following sleep nasendoscopy. Sleep nasendoscopy was repeated for all subjects with, and without, the appliance in situ. Follow-up sleep studies with a mandibular advancement splint in situ were undertaken for 19 individuals with significant obstructive sleep apnoea. With the mandibular advancement splint, subjective snoring levels and airway patency improved as predicted in all but one individual. Residual palatal flutter was predicted for five subjects and occurred in eight individuals. Follow-up sleep studies showed highly statistically significant reductions in median apnoea-hypopnoea index (from 28.1 to 6.1, p < 0.001). Mimicking the action of a mandibular advancement splint during sleep nasendoscopy helps considerably in the patient selection process for this form of treatment.
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PMID:Sleep nasendoscopy as a predictor of treatment success in snorers using mandibular advancement splints. 1582 62

Sleep apnea (SA) is more prevalent in patients with atrial fibrillation (AF), but the impact of cardioversion on disordered breathing is unknown. Thus, we investigated the influence of restoring sinus rhythm in patients with AF and atrial flutter (AFlut) on SA. The 16 patients (mean age 63.1 +/- 11.2) with AF (n = 6) or AFlut (n = 10) and SA (apnea-hypopnea index >10) received cardioversion or ablation of cavotricuspid isthmus. We compared the severity of SA by sleep polygraphy under AF/Aflut with the first night after restoring sinus rhythm and after 4 weeks. Apnea-hypopnea index before and immediately after restoring sinus rhythm was similar (31.7 +/- 13.2 vs 30.1 +/- 15.7, p = NS) despite a significantly reduced heart rate (86.7 +/- 26.5 vs 67.8 +/- 11.9 beats/min, p <0.02). After 4 weeks, apnea-hypopnea index remained unchanged (38.1 +/- 18.1, p = NS) although heart rate was further reduced (61.8 +/- 8.8 beats/min, p <0.003). In our study, SA could not be improved by cardioversion of AF/AFlut. Therefore, although it is well known that SA leads to AF, eliminating AF does not cure or improve SA. In conclusion, our study shows that AF should be regarded more as an innocent bystander than a causative or aggravating condition in SA.
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PMID:Effect of restoring sinus rhythm on sleep apnea in patients with atrial fibrillation or flutter. 1877 93

We will review some diseases that interfere most with management of heart failure : anemia, chronic renal failure, chronic pulmonary diseases, diabetes, atrial fibrillation/flutter, sleep apnea, angina, systemic arterial hypertension, rheumatic disease, depression and anticancer chemotherapy. We will retain principally their therapeutic implications. Anemia can be partially corrected by administration of intravenous iron or erythropoietin. Chronic renal failure requires adaptation of the treatment, in particular for drugs of the renin-angiotensin-aldosterone system. Chronic pulmonary diseases complicate diagnosis of heart failure and may lead to sub prescription of beta-blockers. Diabetes does not alter the usual recommendations for the treatment of heart failure but some hypoglycemic medications should be prescribed with caution. In the presence of atrial fibrillation or flutter, the main purpose of the treatment is to improve the quality of live and to diminish the thromboembolic risk ; it may be obtained by rhythm or rate control. Therapeutic approach of sleep apnea is based on optimal treatment of heart failure and weight loss. In the presence of angina, systemic arterial hypertension, rheumatic disease or depression, certain drugs usually prescribed are contraindicated or must be prescribed with caution. Finally, chemotherapy can be cardiotoxic and require careful monitoring of cardiac function.
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PMID:[Management of comorbidities in heart failure]. 2395 55