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

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

The static charge sensitive bed (SCSB) is a simple and noninvasive device used for the detection of sleep apnoea. In addition to episodes of apnoea or hypopnoea, heavy snorers commonly present with episodes of high frequency spiking on the SCSB. These spiking episodes have been claimed to represent partial upper airway obstruction during sleep, but the mechanism of their appearance is not known. We studied the SCSB spiking phenomenon in awake subjects during experimental respiratory challenge. One female and five male volunteers were studied whilst breathing freely, during hypoxia, hypercapnia and inspiratory and expiratory loading. Oxygen saturation, end-tidal carbon dioxide tension, minute ventilation, oesophageal pressure, electrocardiographic activity (ECG), blood pressure and the SCSB signals were monitored. During free breathing, the SCSB high frequency signal consisted of low amplitude complexes with close time relationship to the cardiac cycle. During respiratory challenge, spiking occurred. These spikes showed no time relationship to the cardiac cycle, but were time-linked to the onset of inspiration or expiration. Spike amplitude correlated with breathing frequency (r2 = 0.59; p < 0.005) and variation in oesophageal pressure (r2 = 0.57; p < 0.005). We conclude that during quiet, unobstructed breathing the static charge sensitive bed high frequency signal represents cardiac activity (ballistocardiogram), whereas during high-drive breathing high frequency spikes are produced. These spikes are respiratory in origin and are likely to represent fast components of respiratory movements. Our results support the use of static charge sensitive bed spiking as a noninvasive measure of breathing stimulation.
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PMID:Respiratory challenge induces high frequency spiking on the static charge sensitive bed (SCSB). 888 95

Acute intermittent repetitive hypoxia simulating sleep apnoea syndrome is responsible for acute rises in blood pressure (BP). In the rat, the BP rises are enhanced by added hypercapnia. To investigate the role of the autonomic nervous system (ANS) in acute hypertension during repetitive hypoxia alone, FiO2 (inspiratory fractional concentration of oxygen) 2 to 5%, or combined with hypercapnia FiCO2 (inspiratory fractional concentration of carbon dioxide) 2 to 5%, we used autonomic blockade by atropine (1 mg kg-1) + propranolol (1 mg kg-1)-phentolamine (1 mg kg-1). Seven Wistar male rats were chronically instrumented with two aortic and venous catheters. Repetitive administration of N2 and N2 + CO2 for 10s followed by 20s compressed air was repeated for 4-5 min before (control) and after autonomic blockade. After autonomic blockade there was no significant difference in mean blood pressure (MBP) during severe hypoxia (SHO) (14.9 +/- 0.5 mmHg) compared to control (10.5 +/- 0.9 mmHg), while MBP was significantly decreased in severe hypoxia + hypercapnia (SHOHC) (14.1 +/- 0.4 mmHg) compared to control (26.8 +/- 0.3 mmHg) (p < 0.001). We conclude that the acute BP rise observed during hypoxic breathing is not due to the activation of ANS, but when hypercapnia is added to the hypoxic stimulus about half of pressor response is caused by ANS.
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PMID:Role of the autonomic nervous system in the acute blood pressure elevation during repetitive hypoxic and hypercapnic breathing in rats. 897 56

Most information about the structures within the brain stem that modulate respiration and sleep are gathered from animal experiments. Therefore we examined 10 patients several weeks after an infarction of the brain stem by means of polysomnography and tested the chemosensitive drives of respiration. None of these patients complained about symptoms of sleep disordered breathing. In each case polysomnographic measurements and ventilatory response curves revealed pathologic findings. The respiratory response to CO2 was diminished or completely abolished in each patient. In some cases hypoventilation or disturbances of the respiratory rhythmicity could be seen. In several cases missing REM sleep, sleep fragmentation or the reduction of slow wave sleep were observed. The study indicates that on the base of results from animal research the comparison of morphological and pathophysiological data is helpful to gain a better understanding on the coupling of the respiratory system with sleep at the brain stem level as well as on the pathomechanism of sleep related breathing disorder.
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PMID:[Sleep and breathing disorders in patients with brain stem lesions]. 901 59

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 hypothesized that reductions in arterial PCO2 (PaCO2) below the apnea threshold play a key role in the pathogenesis of idiopathic central sleep apnea syndrome (ICSAS). If so, we reasoned that raising PaCO2 would abolish apneas in these patients. Accordingly, patients with ICSAS were studied overnight on four occasions during which the fraction of end-tidal CO2 and transcutaneous PCO2 were measured: during room air breathing (N1), alternating room air and CO2 breathing (N2), CO2 breathing all night (N3), and addition of dead space via a face mask all night (N4). Central apneas were invariably preceded by reductions in fraction of end-tidal CO2. Both administration of a CO2-enriched gas mixture and addition of dead space induced 1- to 3-Torr increases in transcutaneous PCO2, which virtually eliminated apneas and hypopneas; they decreased from 43.7 +/- 7.3 apneas and hypopneas/h on N1 to 5.8 +/- 0.9 apneas and hypopneas/h during N3 (P < 0.005), from 43.8 +/- 6.9 apneas and hypopneas/h during room air breathing to 5.9 +/- 2.5 apneas and hypopneas/h of sleep during CO2 inhalation during N2 (P < 0.01), and to 11.6% of the room air level while the patients were breathing through added dead space during N4 (P < 0.005). Because raising PaCO2 through two different means virtually eliminated central sleep apneas, we conclude that central apneas during sleep in ICSA are due to reductions in PaCO2 below the apnea threshold.
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PMID:Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea. 907 83

A 57-yr-old man with idiopathic central apnea is reported. He presented at our hospital complaining of excessive daytime sleepiness. Polysomnography, including esophageal pressure monitoring, confirmed central sleep apnea with an apnea index of 27/h. He had mild non-insulin-dependent diabetes mellitus (NIDDM) but no signs of diabetic neuropathy or other background diseases. The ventilatory responses to hypoxia and hypercapnia tested while he was awake indicated increased respiratory chemosensitivity. We applied nasal continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BPAP) in an attempt to compare the possible difference in therapeutic efficacy. Although nasal CPAP completely reversed central apnea, nasal BPAP adversely affected both apnea length and frequency in an applied pressure-dependent manner. Arterial blood gas analyses while he was being treated indicted alveolar hypoventilation with CPAP and hyperventilation with BPAP. Additionally, administration of a mixed gas containing 5% CO2 through a face mask had a significant effect on the disappearance of central apnea in this patient. These findings support the theory that the arterial PCO2 level is critical in generating idiopathic central apnea and that nasal CPAP therapy may be effective in eliminating central apnea by raising the PaCO2.
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PMID:Continuous versus bilevel positive airway pressure in a patient with idiopathic central sleep apnea. 910 99

The respiratory control system guarantees acid-base-homeostasis as well as the rhythmic activities of the respiratory motor system in accordance with exercise and behavioural programmes of the human being. Cortical patterns and synchronized respiratory patterns with tracheal flow and pressure variations in the fetus indicate the common network of respiration and sleep-wake mechanisms in an early stage already. During fetal life acid-base-homeostasis is dependent on progesterone controlled mechanisms. CO2 partial pressure of the uterine artery reduces to 32 mmHg. The O2 Partial pressure of the umbilical vein is 25-30 mmHg only. The raise of PCO2 during delivery is accompanied by a shower of sensory input to the reticular formation causing arousal and the opening of the lungs. The continuation of postnatal breathing is the consequence of the integration of the central chemosensitive mechanism and the reticular activating system at an adequate threshold. Perinatal defense reflexes, functional patterns and strategies in early life may outline later pathophysiological mechanisms for sleep apnea, apparently life threatening event (ALTE), sudden infant death, and congenital central hypoventilation syndrome.
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PMID:[Control and development of breathing, pathophysiological aspects]. 924 85

It has been hypothesized but not firmly established that sleep-related hypoxaemia could favour the development of pulmonary hypertension in chronic obstructive pulmonary disease (COPD) patients without marked daytime hypoxaemia. We have investigated the relationships between pulmonary function data, sleep-related desaturation and daytime pulmonary haemodynamics in a group of 94 COPD patients not qualifying for conventional O2 therapy (daytime arterial oxygen tension (Pa,O2) in the range 7.4-9.2 kPa (56-69 mmHg)). Nocturnal desaturation was defined by spending > or = 30% of the recording time with a transcutaneous O2 saturation < 90%. An obstructive sleep apnoea syndrome was excluded by polysomnography. Sixty six patients were desaturators (Group 1) and 28 were nondesaturators (Group 2). There was no significant difference between Groups 1 and 2 with regard to pulmonary volumes and Pa,O2 (8.4+/-0.6 vs 8.4+/-0.4 kPa (63+/-4 vs 63+/-3 mmHg)) but arterial carbon dioxide tension (Pa,CO2) was higher in Group 1 (6.0+/-0.7 vs 53+/-0.5 kPa (45+/-5 vs 40+/-4 mmHg); p<0.0001). Mean pulmonary artery pressure (Ppa) was very similar in the two groups (2.6+/-0.7 vs 2.5+/-0.6 kPa (19+/-5 vs 19+/-4 mmHg)). No individual variable or combination of variables could predict the presence of pulmonary hypertension. It is concluded that in these patients with chronic obstructive pulmonary disease with modest daytime hypoxaemia, functional and gasometric variables (with the noticeable exception of arterial carbon dioxide tension) cannot predict the presence of nocturnal desaturation; and that mean pulmonary artery pressure is not correlated with the degree and duration of nocturnal hypoxaemia. These results do not support the hypothesis that sleep-related hypoxaemia favours the development of pulmonary hypertension.
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PMID:Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia. 927 11

Sleep apnea with neuromuscular disorders has been successfully treated with bi-level positive airway pressure ventilation (BiPAP), which, unlike continuous positive airway pressure ventilation (CPAP), creates pressure difference between expiratory and inspiratory phases. Hence if the respiration of patients stops longer than a pre-set duration, BiPAP can automatically force them to breath through a nasal mask. We report a 60-year-old woman with olivo-ponto-cerebellar atrophy (OPCA), whose mixed-type sleep apnea was difficult to treat with conventional CPAP. We therefore tried BiPAP on this patient at night. Nocturnal CO2 retention was nearly resolved, and unexpectedly daytime PaCO2 was also corrected with marked improvement of daytime somnolence. BiPAP is totally non-invasive, and may be one of the most effective treatments in patients with OPCA suffering from sleep apnea.
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PMID:[Efficacy of nasal bi-level positive airway pressure ventilation in a patient with olivo-ponto-cerebellar atrophy suffering from sleep apnea syndrome]. 936 76


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