UMLS:C0037315 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

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

Sleep deprivation can induce or worsen nocturnal respiratory disturbances. In patients with sleep apnea hypopnea, sleep abnormalities consist of repetitive episodes of arousals and awakenings that lead to sleep fragmentation. Because the propensity for upper airway collapse is increased in these patients, we wondered if sleep fragmentation could increase upper airway collapsibility and contribute to the pathogenesis of this disease. In eight normal subjects, upper airway collapsibility was assessed during sleep by progressively decreasing the pressure in a nasal mask while recording airflow, mask, and esophageal pressures. The critical pressure was determined by the relationship between breath-by-breath values of maximal inspiratory airflow of each flow-limited inspiratory cycle and the corresponding mask pressure. Critical pressure was measured twice in each subject: after one night of total sleep deprivation and after one night of sleep fragmentation using auditory stimuli. The two measures were done in random order 1 wk apart. A polysomnographic recording was obtained the night after each measurement of critical pressure. Sleep architecture was identical after sleep deprivation and fragmentation. Sleep-related breathing abnormalities were more frequent after sleep fragmentation than after sleep deprivation. Critical pressure was -17.1 +/- 6.8 cm H2O (mean +/- SEM) after sleep deprivation, and -12.3 +/- 6.3 cm H2O after sleep fragmentation (p < 0.05), corresponding to an earlier closing of the upper airway. We conclude that sleep fragmentation leads to a higher upper airway collapsibility than does sleep deprivation.
...
PMID:Effects of sleep deprivation and sleep fragmentation on upper airway collapsibility in normal subjects. 804 33

Central apneas during sleep may arise as a result of reduction in PaCO2 below the apnea threshold. We therefore hypothesized that hyperventilation and arousals from sleep interact to cause hypocapnia and subsequent central apneas in patients with idiopathic central sleep apnea (ICSA). Accordingly, the relationships among preapneic ventilation, arousal from sleep, and the onset and duration of subsequent central apneas were examined during Stage 2 non-REM sleep in eight patients with ICSA (mean +/- SEM, 45.4 +/- 4.7 central apneas and hypopneas/h of sleep). During Stage 2 sleep, all episodes of periodic breathing with central apneas were triggered by hyperventilation. Minute ventilation (VI) was greater (6.3 +/- 0.7 versus 5.4 +/- 0.8 L/min, p < 0.05) and mean transcutaneous PCO2 (PtcCO2) was lower (37.8 +/- 1.3 versus 38.9 +/- 1.6 mm Hg, p < 0.05) during periodic breathing than during stable breathing. VI during the ventilatory phase of the periodic breathing cycle increased progressively with increasing grades of associated arousals from Grade 0 (no arousal) (10.3 +/- 1.4 L/min) to Grade 1 (EEG arousal) (12.6 +/- 1.6 L/min) to Grade 2 (movement arousal) (14.1 +/- 1.6 L/min, p < 0.01). There was a corresponding progressive increase in central apnea length following the ventilatory period from no arousal (14.1 +/- 2.0) to EEG arousal (16.4 +/- 1.8) to movement arousal (18.1 +/- 2.0 s, p < 0.01). We conclude that arousals and hyperventilation interact to trigger hypocapnia and central apneas in ICSA.
...
PMID:Interaction of hyperventilation and arousal in the pathogenesis of idiopathic central sleep apnea. 804 35

Periodic breathing with central apneas during sleep is typically triggered by hypocapnia resulting from hyperventilation. We therefore hypothesized that hypocapnia would be an important determinant of Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with congestive heart failure (CHF). To test this hypothesis, 24 male patients with CHF underwent overnight polysomnography during which transcutaneous PCO2 (PtcCO2) was measured. Lung to ear circulation time (LECT), derived from an ear oximeter as an estimate of circulatory delay, and CSR-CSA cycle length were determined. Patients were divided into a CSR-CSA group (n = 12, mean +/- SEM of 49.2 +/- 6.3 central apneas and hypopneas per h sleep) and a control group without CSR-CSA (n = 12, 4.9 +/- 0.8 central apneas and hypopneas per h sleep). There were no significant differences in left ventricular ejection fraction, awake PaO2, mean nocturnal SaO2, or LECT between the two groups. In contrast, the awake PaCO2 and mean sleep PtcCO2 were significantly lower in the CSR-CSA group than in the control group (33.0 +/- 1.2 versus 37.5 +/- 1.0 mm Hg, p < 0.01, and 33.2 +/- 1.2 versus 42.5 +/- 1.2 mm Hg, p < 0.0001, respectively). Neither group had significant awake or sleep-related hypoxemia. In addition, CSR-CSA cycle length correlated with LECT (r = 0.939, p < 0.001). We conclude that (1) hypocapnia is an important determinant of CSR-CSA in CHF and (2) circulatory delay plays an important role in determining CSR-CSA cycle length.
...
PMID:Role of hyperventilation in the pathogenesis of central sleep apneas in patients with congestive heart failure. 814 43

Patients with congestive heart failure (CHF) suffer from respiratory muscle weakness which may contribute to dyspnea. Nasal continuous positive airway pressure (NCPAP) can improve left ventricular ejection fraction (LVEF) and reduce dyspnea in patients with CHF and Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) but its effects on respiratory muscle strength are not known. We therefore studied the effects of NCPAP on maximal inspiratory and expiratory pressures (MIP and MEP, respectively), LVEF, dyspnea, and fatigue in patients with chronic CHF and CSR-CSA over 3 mo. Eight patients were randomized to control and nine to nightly NCPAP. There were no significant changes in any of these factors in the control group during the study. In contrast, among the NCPAP group, MIP increased from 79.3 +/- 8.1 to 90.7 +/- 10.4 cm H2O (mean +/- SEM; p < 0.02), LVEF increased from 24.0 +/- 4.0 to 32.6 +/- 6.6% (p < 0.02) and symptoms of dyspnea and fatigue were alleviated. However, MEP did not change. In addition, the number of apneas and hypopneas decreased from 49 +/- 11 to 17 +/- 7 per hour of sleep (p < 0.001) and mean low Sao2 during sleep increased from 87.9 +/- 1.0 to 93.0 +/- 1.0% (p < 0.01). Our data indicate that nightly application of NCPAP in patients with CHF and CSR-CSA improves inspiratory muscle strength and LVEF, and relieves dyspnea and fatigue.
...
PMID:CPAP improves inspiratory muscle strength in patients with heart failure and central sleep apnea. 854 29

The main acute cardiovascular effects of obstructive sleep apnea syndrome (OSAS) are elevation of blood pressure and reflectory bradycardia, which are followed by an abrupt tachycardia on resumption of breathing. This haemodynamic instability is related to hypoxemia and arousal, and may lead to increased risk from cardiac arrhythmias and sudden cardiac death, as well as to the development of chronic arterial hypertension, in these patients. The aim of this study was to apply frequency domain analysis of heart rate variability (HRV) measured from continuous electrocardiogram (ECG) recordings to evaluate how cardiac autonomic function, and especially cardiac sympathovagal tone, changes during sleep apnea episodes. We identified 41 apneas leading to more than 4%-unit arterial oxygen desaturation in 12 patients (11 men, 1 woman (correction for women), age range 27-67 years). Frequency domain analysis of HRV was performed from ECG recordings using 4 min epochs starting 20 min before apnea began and lasting 20 min after the beginning of apnea. The mean (+/-SEM) fall in oxygen saturation during the apnea was 6.8 +/- 0.6%-units. While high frequency band (HF, reflects cardiac vagal activity) remained unchanged, low frequency band (LF, mainly sympathetic activity) showed a constant increase, leading to significant change in the sympathovagal balance (LF/HF ratio). In conclusion, concordantly with previous peripheral sympathetic-nerve recordings, frequency domain analysis of HRV is able to detect sympathetic activation during sleep apnea episodes, leading to marked change in the sympathovagal balance.
...
PMID:Cardiac sympathovagal balance during sleep apnea episodes. 873 9

We hypothesized that the increased arousal threshold to upper airway occlusion exhibited by patients with obstructive sleep apnea (OSA) is in part secondary to the disease process itself. To test this hypothesis, we studied the effects of withdrawal of three nights of nasal continuous positive airway pressure (CPAP) treatment on arousal in six male patients with severe OSA who were using nasal CPAP on a long-term basis. During the control week, patients slept with nasal CPAP at home and on the first of 2 nights in the sleep laboratory (night C1, CPAP; night C2, no CPAP). During the apnea week, patients slept without nasal CPAP for 2 nights at home and 2 nights in the sleep laboratory (AP1, AP2). The control and apnea weeks were consecutive and in random order. The mean (+/-SEM) apnea+hypopnea index was 76.9 +/- 7.1 on AP1 vs 3.1 +/- 1.0 events per hour on C1 (p<0.05). Thus, the laboratory night (and presumably the 2 nights at home) preceding AP2 had dramatic increases in apnea compared with the nights preceding C2. The apnea duration during nonrapid eye movement sleep on nights following apnea was greater (AP2: 28.7 +/- 1.5 vs C2: 25.5 +/- 1. 7 s; p<0/05) and the arousal threshold as reflected by the maximum esophageal pressure deflection preceding arousal was higher (DPmax) (AP2: 55.1 +/- 5.7 vs C2: 45.3 +/- 6.4 cm H2O; p<0.005). We conclude that prior sleep apnea increases the arousal threshold to upper airway occlusion on subsequent nights and prolongs the apneic events.
...
PMID:Sleep apnea impairs the arousal response to airway occlusion. 876 85

Snoring worsens with high alcohol consumption. It is unclear whether moderate alcohol intake worsens sleep and breathing in subjects with obstructive sleep apnoea syndrome (OSAS), and whether alcohol increases the pressure requirement for nasal continuous positive airway pressure (CPAP). Fourteen adult males with untreated OSAS but without heart or lung disease were studied (age 53+/-9 yrs, body mass index (BMI) 33+/-5 kg x m(-2) (mean+/-SD). The subjects underwent overnight polysomnography on four occasions: control, alcohol, CPAP, and alcohol + CPAP. On the alcohol nights, the subjects drank 1.5 mL x kg(-1) body weight (BW) vodka (40% alcohol by volume) (blood alcohol with and without CPAP 0.45+/-0.1 and 0.47+/-0.2 mg x mL(-1) (mean+/-SD)). On the CPAP nights, the pressure required to prevent apnoea, snoring, and silent inspiratory airflow limitation was determined using an autotitrating nasal CPAP system (ResCare AutoSet). Alcohol and control nights were performed in random order. Without CPAP, alcohol produced a small non-significant decrease in the percentage of rapid eye movement (REM) sleep (control 11+/-2 vs alcohol 8+/-1% (mean+/-SEM)), but with CPAP there was no such effect (control 15+/-2 vs 17+/-2%; CPA x alcohol interaction p=0.015). With CPAP, slow-wave sleep in the first 2 h increased slightly with alcohol (control 39+/-6 vs alcohol 51+/-4%; p=0.004). Arousal index without CPAP increased slightly with alcohol (control 43+/-5 vs alcohol 49+/-6 events x h(-1); p=0.02). There was little or no effect of alcohol on other sleep stages, arousal index, apnoea index, apnoea/hypopnoea index, mean or longest event duration, mean or worst arterial oxygen saturation, with or without CPAP, either for the full night or for the first 2 h. There was no change in the pressure requirement for CPAP (full night: control 11.9+/-0.9 vs alcohol 12.5+/-0.9 cm H2O; first 2 h: 10.9+/-0.6 vs 11.1+/-0.8 cm H2O). Moderate alcohol intake (in the form of vodka) has little effect on breathing or saturation during sleep in subjects with mild-to-severe obstructive sleep apnoea, and no effect on the pressure required for continuous positive airway pressure in order to prevent apnoea, snoring, and flow limitation. These results cannot be extrapolated to other doses or forms of alcohol, or to subjects with concurrent heart or lung disease.
...
PMID:Influence of moderate alcohol consumption on obstructive sleep apnoea with and without AutoSet nasal CPAP therapy. 894 88

We hypothesize that stimulation of upper-airway mechanoreceptors during obstructive apnea augments upper airway muscle activity. If so, upper-airway anesthesia (UAA) should reduce mechanoreceptor output and therefore upper-airway muscle activity. To test this hypothesis, we studied the effect of UAA on the relationship between the phasic activity of the moving-time average (MTA) of the genioglossus electromyogram (EMG-GG) and the esophageal pressure deflection (DP) during obstructive apneas in non-rapid-eye-movement (NREM) sleep in a group of six men with severe sleep apnea. Before UAA, the phasic EMG-GG was linearly related to the deflections in esophageal pressure (DP) during the last three occluded breaths (both progressively increased). After UAA, the mean ratio of EMG-GG to DP decreased to 23% of the control value, from 0.17 +/- 0.04 to 0.04 +/- 0.01 (mean +/- SEM) arbitrary units/cm H2O (p < 0.05). The mean slope of the EMG-GG-versus-DP regression lines also decreased to 23% of the control value, from 0.22 +/- 0.03 to 0.05 +/- 0.01 arbitrary units/ cm H2O (p < 0.01). These findings suggest that stimulation of upper-airway mechanoreceptors during obstructive apnea in NREM sleep augments phasic genioglossus activity.
...
PMID:Upper airway anesthesia reduces phasic genioglossus activity during sleep apnea. 923 Jul 36

We have previously shown that AutoSet satisfactorily improves sleep-disordered breathing and sleep architecture in subjects with obstructive sleep apnoea (OSA) syndrome. The aim of this study was to determine, in subjects treated with long-term conventional fixed pressure continuous positive airway pressure (CPAP) at the AutoSet recommended pressure, whether: the long-term compliance is satisfactory; the improvement persists once initial rebound is over; the titration pressure is stable with time; and the titration pressure is comparable with manual titration pressure using a similar end-point. Twenty males with OSA, previously studied with full polysomnography on their diagnostic night, at manual and AutoSet titration, and at the AutoSet recommended fixed pressure, were re-studied after a mean of 3 and 8 months of treatment at the recommended fixed pressure. Re-study included home respiratory monitoring (Nellcor EdenTrace), and repeated manual and AutoSet titration with polysomnography. Compliance was assessed with hour-meter readings. Mean (+/-SEM) usage was 5.7 +/- 0.1 h.night-1 at 3 and 8 months. The arousal index remained normalized. Diagnostic respiratory disturbance index (RDI) was 60.3 +/- 5.7 events.h-1. On AutoSet at fixed CPAP, RDI was initially 2.6 +/- 0.7 events.h-1, then rose slightly (p < 0.001) to 4.3 +/- 0.6 events.h-1 at 3 months, and was 3.6 +/- 0.5 events.h-1 at 8 months. AutoSet titration pressure was: 9.9 +/- 0.4 cmH2O initially, 10.6 +/- 0.4 cmH2O at 3 months, and 9.7 +/- 0.5 cmH2O at 8 months (NS). Manual titration pressure at 8 months was 10.4 +/- 0.4 cmH2O. The standard deviation of the discrepancy with AutoSet was 0.84 cmH2O. In conclusion, the AutoSet recommended pressure varies little with time, and closely predicts the final manual titration pressure; the improvement in respiratory disturbance index was largely maintained, and compliance was good, although probably enhanced by close supervision.
...
PMID:AutoSet nasal CPAP titration: constancy of pressure, compliance and effectiveness at 8 month follow-up. 931 5

Most patients with sleep apnoea/hypopnoea syndrome (SAHS) are middle-aged men. As there are conflicting data on the effects of age and gender on upper airway calibre, we tested the hypothesis that increasing age and the male sex predispose to upper airway narrowing in normal subjects. We measured upper airway calibre using acoustic reflection in 60 men and 54 women (median 35, range 16-74 yrs) both seated and supine. All upper airway dimensions, except oropharyngeal junction (OPJ), decreased with increasing age in both men and women (r > -0.24, p < or = 0.05) while supine (r2 > 0.06). Men had greater changes in airway area at OPJ on lying down (mean (SEM) 0.5 (0.1), 0.2 (0.1) cm2; p < 0.02). Men had greater body mass indices (mean (SD) 26 (4), 24 (4) kg.m-2; p = 0.04), and larger neck circumferences (mean (SD) 38 (3), 33 (2) cm; p < 0.0001) than women. For any body mass index, neck circumference was larger in men than women (p < 0.001). This study shows that upper airway size decreases with increasing age in both men and women, and that men have greater upper airway collapsibility on lying down at oropharyngeal junction than women.
...
PMID:The effect of age, sex, obesity and posture on upper airway size. 931 8

<< Previous 1 2 3 4 5 6 Next >>