Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 63-year-old man with severe non-obstructive sleep apnoea (apnoea index 28; apnoea duration 45-60s; O2 saturation between 72% and 98%), who did not respond to common modes of treatment, was successfully treated with CO2. A tent was perfused with compressed air (6 1/min) and increasing amounts of CO2. A concentration of 3% CO2 (180 ml/min) was sufficient to raise the PaCO2 above apnoea threshold and to suppress apnoeas completely. As a result, O2 saturation remained normal throughout the whole night and the symptoms of sleep apnoea disappeared. We hypothesize that the PCO2 ventilatory drive was intact in our patient and that hypocapnia was the major factor causing the non-obstructive sleep apnoea syndrome. Administration of CO2 with a constant flow system could be a safe and easy alternative for patients with non-obstructive sleep apnoea syndrome who present with hypocapnia and an intact respiratory feedback control system.
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PMID:Beneficial effect of inhaled CO2 in a patient with non-obstructive sleep apnoea. 813 21

The amount of different clinically available lasers is increasing. The ENT surgeon can therefore use the best laser for the planned operation. As the resources of the hospital do not increase with the laser technology, a decision has to be made whether in addition to the universal CO2-laser other types must be acquired and which type is best. This paper presents the characteristics and typical tissue interactions of several lasers for the area of the soft palate. Typical operative examples are shown, e.g. partial resection of the soft palate in patients with bronchopathy and sleep apnoea syndrome, tonsillectomy, tonsillotomy and adenotomy in adults.
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PMID:[Current status of laser surgery in the area of the soft palate and adjoining regions]. 814 48

The diagnosis of sleep apnea syndrome (SAS) requires expensive and complex instrumentation. The purpose of the present study was to determine the value of end-tidal CO2 (EtCO2) in screening for sleep apneas. Thirty-nine patients referred to our sleep laboratory because of suspected SAS and ten normal subjects were studied. The EtCO2 was measured using an infrared spectrometer (POET) designed for simultaneous measurement of CO2 and pulse oximetry. In 29 subjects, expired gas was sampled with a nasobuccal mask (Respiron) with lateral orifices. In the other 20 subjects, sampling was done with nasobuccal prongs (Criticare) comprising a four-channel plastic tube to the mouth and the nostrils. Data from an 8-h night were transferred the following day to a microcomputer (Apple Macintosh) for processing. Apnea was defined as an absence of detection of CO2 for more than 10 s. Conventional polysomnography was performed (Respisomnographe). The number of apneas in 8 h and the apnea index (number of apneas in 1 h) were calculated after visual analysis on the screen of the polysomnograph and also with EtCO2 analysis. For recordings made with a nasobuccal mask, the regression curve between the apnea indices computed with EtCO2 and polysomnography was an order 2 polynomial curve (r = 0.76; p < 0.001), with an inflection point at 39 apneas per hour. For recordings with nasobuccal prongs, the correlation was very significant (r = 0.95; p < 0.0001), and the regression curve was linear. The EtCO2 with nasobuccal prongs appears to be a simple and reliable method for screening for SAS.
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PMID:End-tidal CO2 analysis in sleep apnea syndrome. Conditions for use. 841 66

Diagnosis of a sleep apnoea syndrome in severely snoring patients with diurnal sleepiness is growing in importance in the consulting rooms of general practitioners, internists, ENT specialists and pneumologists. However, time and cost reasons limit the diagnostic procedures conducted by practitioners to outpatient screening. Two different systems are presently available in Germany. The MESAM system (Madaus, Freiburg) records by means of a microphone and various electrodes the oxygen saturation, heart rate, snoring and sleeping position of the patient. The Apnoe-Check System (Medanz, Starnberg) determines the nasal and oral respiratory flow by means of a mask fitted with thermistors. Evaluation is accomplished in the case of MESAM via a conventional personal computer whereas with the Apnoea Check System the apnoeas and their duration can be read off direct from a writer. The cost ratio of these systems is approximately 3:1 (MESAM:Apnoea Check). Wie compared both systems by parallel measurements on 19 female and male patients and controlled the results obtained by measurements with a CO2 infrared absorption spectrometer in our sleep lab. A total of 3201 nocturnal events were recorded via MESAM and 1488 via the Apnoe-Check System. The highest number of apneas was recorded by MESAM in a patient with severe sleep apnea syndrome, namely, 546 apnoeas in one night. The lowest number of apnea events was experienced by a healthy male with 33 apneas in a night. With the Apnoe Check the maximum of nocturnal events was 255, the minimum being 8 events in one patient. In 64.6% of all nocturnal events there was time congruence for both systems.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Efficiency of portable sleep apnea screening instruments]. 849 63

We previously demonstrated that central apneas during sleep in patients with idiopathic central sleep apnea (ICSA) are triggered by abrupt hyperventilation. In addition, baseline PCO2 at the time of augmented breaths which triggered central apneas was lower than for augmented breaths which did not trigger apneas. These observations led us to hypothesize that patients with ICSA chronically hyperventilate maintaining their PCO2 close to the threshold for apnea during sleep owing to increased chemical respiratory drive. To test these hypotheses, we recorded transcutaneous PCO2 (PtcCO2) during overnight sleep studies on nine consecutive patients with ICSA and nine sex-, age-, and body-mass-index-matched control subjects. Daytime PaCO2 as well as rebreathing and single breath ventilatory responses to CO2 were also measured. Compared with the control subjects, the patients had significantly lower mean PtcCO2 during sleep (37.8 +/- 1.2 versus 42.7 +/- 10.9 mm Hg, p < 0.01) and lower PaCO2 while awake (35.1 +/- 1.3 versus 38.8 +/- 0.9 mm Hg, p < 0.05). Furthermore, patients with ICSA had significantly higher ventilatory responses to CO2 for both the rebreathing (3.14 +/- 0.34 versus 1.60 +/- 0.32 L/min/mm Hg, p < 0.005) and single breath methods (0.51 +/- 0.10 versus 0.25 +/- 0.04 L/min/mm Hg, p < 0.05). We conclude that: (1) patients with ICSA chronically hyperventilate awake and asleep and (2) chronic hyperventilation is probably related to augmented central and peripheral respiratory drive which predisposes to respiratory control system instability.
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PMID:Hypocapnia and increased ventilatory responsiveness in patients with idiopathic central sleep apnea. 852 Jul 61

Obstructive sleep apnea (OSA) can be associated with depressed hypercapnic ventilatory response (HCVR) (White D.P., N.J. Douglas, C.K. Pickett, C.W. Willich and J.V. Weil, Am. Rev. Respir. Dis 128:984-986, 1983), which might be responsible for aggravating the sleep-related breathing disorder (SRBD). The present study evaluated whether in patients with various types of sleep apnea a significant decrease in the HCVR could be found (COMPARATIVE STUDY). In a second part of the study chronic CPAP therapy (Continuous Positive Airway Pressure) was evaluated in relation to control of breathing (CPAP STUDY). In the comparative study a significant increase of the slope in the normocapnic OSA and overlap group could be seen. A depressed HCVR could only be observed in chronic hypercapnic OSA. In the CPAP-study it was shown that changes in the AHI after CPAP do not parallel the HCVR. We conclude that in eucapnic OSA patients CPAP therapy does not change CO2 drive. We believe that increased chemical CO2 drive can contribute to its pathogenesis.
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PMID:Chronic CO2 drive in patients with obstructive sleep apnea and effect of CPAP. 860

The clinical course and changes in hypercapnic ventilatory drive over time were serially assessed before and after tracheostomy placement in a 14 year old, morbidly obese female patient with Prader-Willi syndrome, severe obstructive sleep apnoea, and obesity-hypoventilation syndrome. A tracheostomy became necessary after supplemental oxygen and continuous positive airway pressure (CPAP) had failed to improve the severity of nocturnal hypoventilation. Continued improvement in the slope to rebreathing hyperoxic hypercapnia occurred from 2-10 weeks after tracheotomy in conjunction with night-time bilevel pressure ventilation, and remained unchanged thereafter. In contrast, increases in mean resting minute ventilation at an end-tidal carbon dioxide tension (PET,CO2) of 8 kPa (60 mmHg) were documented even after 30 weeks. This case study illustrates the time-frame of dynamic ventilatory changes occurring after removal of upper airway resistance and normalization of nocturnal alveolar ventilation.
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PMID:Longitudinal assessment of hypercapnic ventilatory drive after tracheotomy in a patient with the Prader-Willi syndrome. 883 75

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

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


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