Effect of Bedtime Ethanol on Total Inspiratory Resistance and Respiratory Drive in Normal Nonsnoring Men

We have previously reported that bedtime ethanol (2.0 ml/kg of 100 proof vodka) increases upper airway closing pressure in males who habitually snored but were otherwise healthy. We also observed that some of these snorers developed obstructive apneas. To explore this phenomenon in more detail, we measured the inspiratory resistance (R_I) and respiratory drive after bedtime ethanol in 10 nonobese men (ages 23 to 33) with no history of snoring. Subjects went to bed wearing a tightly fitting valved mask over the nose and mouth that allowed measurement of inspiratory and expiratory flow, pressure in the mask, and endtidal CO₂. We measured R_I by calculating the pressure difference between the mouth and a balloon positioned in the midesophagus. Respiratory drive was quantified by the inspiratory occlusion pressure (P_0.1), the ventilatory response to hyperoxic hypercapnia (ΔV_E/ΔP_ETCO₂), and the ventilatory response to isocapnic hypoxia (ΔV_E/ΔS,O₂). Measurements were made during waking and during stage 2 NREM sleep on two nights: (1) when the subjects drank 1.5 ml/kg of 100 proof vodka in orange juice over a 30-min period 15–45 min before lights out and (2) when the orange juice contained less than 0.1 ml of vodka floating on the top. Eight of the nine men in whom we had technically adequate measurements showed a rise in R_I during NREM sleep above the waking level on both control and ethanol nights and the sleeping R_I was greater on the ethanol than on the control night. There was a tendency for P_0.1 to be higher during sleep and greater on the ethanol night, suggesting that the neural output to the respiratory muscles was not depressed and may have been stimulated by the inspiratory “loading” secondary to the increased R_I. The hypercapnic response was significantly depressed during sleep. Whereas the response tended to be less on the ethanol than on the control night, the difference was not significant. The hypoxic response showed little change from waking to sleeping and no significant change with ethanol. We speculate that inspiratory loading due to increased upper airway resistance tends to stimulate respiratory drive and thereby partially offsets the depressant effect of ethanol on the central respiratory chemoreceptors.     

Non‐invasive positive pressure ventilation during sleep at 3800 m: Relationship to acute mountain sickness and sleeping oxyhaemoglobin saturation

Background and objective: Ascent to high altitude results in hypobaric hypoxia and some individuals will develop acute mountain sickness (AMS), which has been shown to be associated with low oxyhaemoglobin saturation during sleep. Previous research has shown that positive end‐expiratory pressure by use of expiratory valves in a face mask while awake results in a reduction in AMS symptoms and higher oxyhaemoglobin saturation. We aimed to determine whether positive pressure ventilation would prevent AMS by increasing oxygenation during sleep. Methods: We compared sleeping oxyhaemoglobin saturation and the incidence and severity of AMS in seven subjects sleeping for two consecutive nights at 3800 m above sea level using either non‐invasive positive pressure ventilation that delivered positive inspiratory and expiratory airway pressure via a face mask, or sleeping without assisted ventilation. The presence and severity of AMS were assessed by administration of the Lake Louise questionnaire. Results: We found significant increases in the mean and minimum sleeping oxyhaemoglobin saturation and decreases in AMS symptoms in subjects who used positive pressure ventilation during sleep. Mean and minimum sleeping SaO₂ was lower in subjects who developed AMS after the night spent without positive pressure ventilation. Conclusions: The use of positive pressure ventilation during sleep at 3800 m significantly increased the sleeping oxygen saturation; we suggest that the marked reduction in symptoms of AMS is due to this higher sleeping SaO₂. We agree with the findings from previous studies that the development of AMS is associated with a lower sleeping oxygen saturation.     

Snoring and sleep architecture

The purpose of this study was to examine whether snoring adversely affects sleep architecture and sleep efficiency, and thus may account for the frequent complaints of daytime tiredness and fatigue expressed by heavy snorers. We recruited eight self-confessed heavy snorers and six self-confessed nonsnorers. All subjects had full nocturnal polysomnography, including continuous monitoring of snoring, which was quantified by counting the number of snores per hour of sleep (snoring index), the number of snores per minute of snoring time (snoring frequency), maximal and mean nocturnal sound intensity (dBmax and dBmean, respectively). We found that even the self-confessed nonsnorers snored lightly, with significantly smaller frequency and index than the heavy snorers. Sleep architecture was similar in both groups. Distribution of snoring among the sleep stages differed for light and heavy snorers: light snorers snored uniformly throughout all sleep stages, whereas heavy snorers tended to snore more during slow-wave and REM sleep. Snoring frequency and snoring index were similar during all sleep stages in light snorers, but they were higher during slow-wave sleep in heavy snorers. Wakefulness time after sleep onset and sleep efficiency correlated significantly with the snoring index. We conclude that although snoring does not affect sleep architecture in general, it influences sleep efficiency and wakefulness time after sleep onset; this may have an adverse effect on daytime function of heavy snorers.     

Prevalence of obstructive sleep apnea syndrome and associated symptoms in 3--11-year-old Turkish children

Our objective was to investigate the prevalence of sleep-disordered breathing (SDB) and obstructive sleep apnea syndrome (OSAS) in 3-11-year-old Turkish children. A cross-sectional study was conducted in Zonguldak, northwestern Turkey. Symptomatic children were identified by using a self-administered questionnaire and were classified into three groups: nonsnorers, occasional snorers, and habitual snorers. All habitual snoring children were invited to undergo polysomnography (PSG). Nine hundred fifty-four children (79.5%) were nonsnorers, 205 (17.2%) were occasional snorers, and 39 (3.3%) were habitual snorers. There was no significant relationship between gender and habitual snoring (male, 3.4%; female, 3.1%; P > 0.05; odds ratio (OR), 1.13; 95% confidence interval (CI), 0.59-2.14). There was a statistically significant relationship between habitual snoring and allergic rhinitis (OR, 4.23; 95% CI, 2.14-8.35). Four children who snored every night, and who had apnea spells and/or troubled sleep, underwent adenoidectomy and/or tonsillectomy before polysomnographic evaluation because of clinical detoriation. Twenty-eight of 39 children with habitual snoring participated in PSG evaluation. PSG revealed that 11 children (0.9% of the total population) had OSAS. When 4 operated children were added to these 28 children, we found the minimum prevalence of OSAS to be 1.3% in our study group. There was a significant correlation between OSAS and troubled sleeping (P <0.001; OR, 4.37; 95% CI, 1.33-14.3). We found the prevalence of habitual snoring to be 3.3% in Turkish children by using self-administered questionnaires. Allergic rhinitis was significantly correlated with habitual snoring. Minimum estimated prevalence of OSAS was found to be 1.3%.     

Reduced neurocognition in children who snore

Obstructive sleep apnea syndrome (OSAS) has been associated with reduced neurocognitive performance in children, but the underlying etiology is unclear. The aim of this study was to evaluate the relationship between hypoxemia, respiratory arousals, and neurocognitive performance in snoring children referred for adenotonsillectomy. Thirteen snoring children who were referred for evaluation regarding the need for adenotonsillectomy to a children's hospital otolaryngology/respiratory department underwent detailed neurocognitive and polysomnographic (PSG) evaluation. PSGs were evaluated for respiratory abnormalities and compared with 13 nonsnoring control children of similar age who were studied in the same manner. The snoring children had an obstructive respiratory disturbance index within normal range (mean obstructive apnea/hypopnea index, 0.6/hr). Despite this, several domains of neurocognitive function were reduced in the snoring group. These included mean verbal IQ scores (snorers 92.6 vs. nonsnorers 110.2, P < 0.001), mean global IQ scores (snorers 96.7 vs. nonsnorers 110.2, P < 0.005), mean selective attention scores (snorers 46.4 vs. nonsnorers 11.8, P < 0.001), mean sustained attention scores (snorers 8.0 vs. nonsnorers 2.2, P = 0.001), and mean memory index (snorers 95.2 vs. nonsnorers 112.1, P = 0.001). There was a direct relationship between number of mild oxygen desaturations of > or = 3%, obstructive hypopneas with > or = 3% oxygen desaturations, and respiratory arousals and severity of neurocognitive deficits, with the greatest effect being on memory scores. The disruption of sleep in snoring children produced by relatively mild changes in oxygen saturation or by increases in respiratory arousals may have a greater effect on neurocognitive function than hitherto appreciated. A possible explanation for these neurocognitive deficits may be the combination of the chronicity of sleep disruption secondary to snoring which is occurring at a time of rapid neurological development in the first decade of life. Future studies need to confirm the reversal of these relatively mild neurocognitive decrements post adenotonsillectomy.     

Flow-volume curves in obstructive sleep apnea and snoring

The diagnostic value of flow-volume curves for sleep apnea was studied in 32 patients with obstructive sleep apnea, 40 simple snorers, and 30 healthy nonsnorers. A sawtooth appearance of the flow-volume curve was seen in 22 of the sleep apnea patients (69%), 14 of the simple snorers (35%), and 10 of the nonsnorers (33%). The ratio of midexpiratory flow (FEF 50) to midinspiratory flow (FIF 50) was greater than 1 in 6 of the sleep apnea patients (19%), 3 of the simple snorers (8%), and 2 of the nonsnorers (7%). Thus, only the sawtooth sign was more frequently found in sleep apnea patients than in controls (p<0.01). Sleep apnea patients with a sawtooth appearance of the flow-volume curve had a higher apnea index (38.7 ± 22 vs. 21.5 ± 12.1; p<0.01) and lower nocturnal minimum oxygen saturation (68.1% ± 16.8 vs. 81.3% ± 9.97; p<0.01) than those without. In symptomatic snorers, sensitivity of the sawtooth sign for sleep apnea was 72% and specificity 61%, for a FEF50/FIF50 ratio above 1 sensitivity was 17% and specificity 83%. In asymptomatic patients, sensitivity of either sign was extremely poor (33%) and specificity was 67% for the sawtooth sign and 85% for FEF50/FIF50 > 1. We conclude that abnormal flow-volume curves are of limited value for predicting sleep apnea.     

The effect of snoring on mean arterial blood pressure during non-REM sleep.

The purpose of this study was to examine the relationship between snoring and mean arterial blood pressure during sleep. This was accomplished by performing continuous, all-night, simultaneous measurements of snoring, oxygen saturation, sleep stages, and arterial blood pressure in a group of eight snorers and five nonsnoring control subjects. The results were analyzed to determine whether changes in mean arterial blood pressure during non-rapid-eye-movement (non-REM) sleep are different in snorers from those in nonsnorers and whether they are related to nocturnal hypoxemia. Both groups were similar with respect to their anthropometric parameters and sleep architecture. Oxygen saturations during different stages of non-REM sleep were similiar within each group. However, the analysis of variance revealed that among snorers mean arterial blood pressure increased slightly during slow-wave sleep, whereas the nonsnorers reduced their blood pressure by 17.4 +/- 3.7% compared with wakefulness values. We also performed multiple linear regression analysis for the entire group of 13 subjects using the change in mean arterial blood pressure relative to wakefulness as the dependent variable and snoring frequency and mean arterial oxygen saturation as the independent variables; the results demonstrated that only snoring frequency, and not oxygen saturation, correlated significantly with the change in mean arterial blood pressure. We conclude that snoring may influence variation of blood pressure during sleep, preventing the normally observed reduction of arterial blood pressure associated with slow-wave sleep.     

Flow-volume curves in obstructive sleep apnea and snoring

The diagnostic value of flow-volume curves for sleep apnea was studied in 32 patients with obstructive sleep apnea, 40 simple snorers, and 30 healthy nonsnorers. A sawtooth appearance of the flow-volume curve was seen in 22 of the sleep apnea patients (69%), 14 of the simple snorers (35%), and 10 of the nonsnorers (33%). The ratio of midexpiratory flow (FEF 50) to midinspiratory flow (FIF 50) was greater than 1 in 6 of the sleep apnea patients (19%), 3 of the simple snorers (8%), and 2 of the nonsnorers (7%). Thus, only the sawtooth sign was more frequently found in sleep apnea patients than in controls (p less than 0.01). Sleep apnea patients with a sawtooth appearance of the flow-volume curve had a higher apnea index (38.7 +/- 22 vs. 21.5 +/- 12.1; p less than 0.01) and lower nocturnal minimum oxygen saturation (68.1% +/- 16.8 vs. 81.3% +/- 9.97; p less than 0.01) than those without. In symptomatic snorers, sensitivity of the sawtooth sign for sleep apnea was 72% and specificity 61%, for a FEF50/FIF50 ratio above 1 sensitivity was 17% and specificity 83%. In asymptomatic patients, sensitivity of either sign was extremely poor (33%) and specificity was 67% for the sawtooth sign and 85% for FEF50/FIF50 greater than 1. We conclude that abnormal flow-volume curves are of limited value for predicting sleep apnea.     

Effect of three alcohol doses on breathing during sleep in 30-49 year old nonobese snorers and nonsnorers

To test the effect of alcohol ingestion and snoring on sleep-disordered breathing (SDB), the sleep and respiration of 31 nonobese healthy males ages 30-49 (15 snorers, 16 nonsnorers) were studied overnight after alcohol ingestion. Subjects received placebo, 0.32, 0.65, and 0.81 g alcohol/kg body weight prior to their evening bedtime, with each dose given on one of four nonconsecutive nights in a repeated-measures counterbalanced design. On each night, respiration was assessed by recording respiratory effort from intercostal surface electromyography (EMG), ventilation from oral and nasal thermistors, and arterial oxygen saturation (SaO2) from an ear oximeter (BIOX III). Snorers had significantly: (a) more total SDB, (b) more obstructive sleep apnea (OSA), and (c) lower minimum SaO2 than nonsnorers after the placebo and each alcohol dose. Snorers had more hypoxic events than nonsnorers after each alcohol dose but not after placebo. Increasing alcohol dose caused a statistically significant (p = 0.0004) decrease in minimum SaO2 in snorers only, but this decrease was small and probably not clinically important. Alcohol did not cause significant increases in SDB and hypoxic events, and did not have different effects on SDB and hypoxic events for snorers versus nonsnorers. Because this experiment included only nonobese 30-49-year-old males, these results do not imply that alcohol has no significant effects on obese subjects or those older than 50.     

Effect of Three Alcohol Doses on Breathing during Sleep in 30–49 Year Old Nonobese Snorers and Nonsnorers

To test the effect of alcohol ingestion and snoring on deep-disordered breathing (SDB), the sleep and respiration of 31 nonobese healthy males ages 30-49 (15 snorers, 16 nonsnorers) were studied overnight after alcohol ingestion. Subjects received placebo, 0.32, 0.65, and 0.81 g alcohol/kg body weight prior to their evening bedtime, with each dose given on one of four nonconsecutive nights in a repeated-measures counterbalanced design. On each night, respiration was assessed by recording respiratory effort from inter-costal surface electromyography (EMG), ventilation from oral and MMI thermistors, and arterial oxygen saturation (SaO₂) from an ear oximeter (BIOX III). Snorers had significantly: (a) more total SDB, ( b ) more obstructive deep apnea (OSA), and (c) lower minimum SaO₂ than nonsnorers after the placebo and each alcohol dose. Snorers had more hypoxic events than nonsnorers after each alcohol dose but not after placebo. Increasing alcohol dose caused a statistically significant ( p = 0.0004) decrease in minimum SaO₂ in snorers only, but this decrease was small and probably not clinically important. Alcohol did not cause significant increases in SDB and hypoxic events, and did not have different effects on SDB and hypoxic events for snorers versus nonsnorers. Because this experiment included only nonobese 30–49-year-old males, these results do not imply that alcohol has no significant effects on obese subjects or those older than 50.     

Upper airway mechanics and post-hypoxic ventilatory decline during NREM sleep

Termination of hypoxia results in a transient ventilatory decline referred to as post-hypoxic ventilatory decline (PHVD). We wished to determine whether PHVD is due to changes in ventilatory motor output or upper airway mechanics. We studied 19 healthy normal subjects (15 men, 4 women) during stable non-REM (NREM) sleep. Subjects were exposed to multiple episodes of brief (3 min) hypoxia that terminated with one breath of 100% FI_O2. Minute ventilation (V _I), tidal volume (V _T), timing, and upper airway resistance (R _ua) were measured during the control, hypoxia, and for the first six breaths immediately after cessation of hypoxia. In addition, we measured diaphragmatic electromyograms (EMGdia) via surface electrodes in four subjects. V _I and V _T decreased during the recovery period to a nadir of 81and 83% of room air control, respectively. However, there was no significant change in respiratory frequency or upper airway resistance during the post-hypoxic recovery period. Decreased V _I was associated with a comparable decrease in EMGdia. We conclude that: (1) PHVD occurs in normal humans during NREM sleep, (2) there is no evidence of post-hypoxic frequency decline in humans during NREM sleep, and (3) PHVD is centrally mediated and not driven by upper airway mechanics.     

Effect of hypercapnia on total pulmonary resistance during wakefulness and during NREM sleep.

We investigated the effect of different levels of hypercapnia on total pulmonary resistance (RL) in 13 subjects ranging from nonsnorers with low RL to snorers with high RL and dynamic narrowing of the upper airway during inspiration. Added CO2 was adjusted to achieve a steady-state increase in PETCO2 of +2, +4, or +6 mm Hg. RL was measured at peak inspiratory flow (RLpf), at maximal resistance within breath (RLmax), and at 10 equally spaced points within inspiration in several trials. During wakefulness, hypercapnia was associated with decreased RLmax. During steady state +6 mm Hg hypercapnia, RLmax decreased by 30% (p less than 0.01). During NREM sleep, low levels of hypercapnia did not affect RL. However, +6 mm Hg hypercapnia was associated with decreased RLmax in six of eight subjects (p = 0.07), especially in subjects with high RLmax during room air breathing. The effects of hypercapnia on RLpf paralleled its effect on RLmax. We concluded that (1) the decrease in RL during awake hypercapnia suggests an increase in upper airway dimensions and stiffness, (2) the absence of increased RL during low level NREM hypercapnia (despite the increase in inspiratory flows and collapsing pressures) also suggests an increase in upper airway dimensions and stiffness, and (3) upper airway dilating muscles appear to be recruited in a coordinated fashion with inspiratory muscles in normal humans during NREM sleep. The implications of these findings in patients with obstructive sleep apnea are not clear at this point.     

Sleep-related changes in the human 'neuromuscular' ventilatory response to hypoxia

The ventilatory responses to hypercapnia and hypoxia are reduced during sleep compared to wakefulness. However, sleep-related increases in upper airways' resistance could reduce these ventilatory responses independently of any change in the neural output to the respiratory pump muscles. It is therefore possible that respiratory chemosensitivity, per se, is unchanged by sleep. To investigate this, four healthy male subjects were mechanically ventilated to abolish spontaneous respiratory muscle activity. The response to transient isocapnic hypoxia was quantified from the magnitude of the electromyographic activity induced in the diaphragm and from the associated reduction in peak inspiratory pressure; these indicies of respiratory motor output will not be affected by any sleep-related changes in upper airways' resistance. In all individuals, the responses to hypoxia were markedly attenuated during sleep compared to wakefulness. These observations, assessing the 'neuromuscular' ventilatory response, are consistent with a sleep-related reduction in respiratory chemosensitivity that is independent of any changes that may be due to increases in upper airways' resistance.     

Inspiratory neural drive response to hypoxia adequately estimates peripheral chemosensitivity in OSAHS patients.

The aim of the present study was to examine the relationships between the responses to progressive isocapnic hypoxia and hypoxic withdrawal test in patients with obstructive sleep apnoea-hypopnoea syndrome (OSAHS) and to analyse the determinants of carotid body sensitivity in OSAHS. Nineteen consecutive OSAHS patients and 13 healthy subjects were selected. Ventilatory (delta V'I/Sa,O2/BSA) and inspiratory neural drive (delta P0.1/Sa,O2) responses to progressive isocapnic hypoxia were determined. Peripheral chemosensitivity was evaluated by the hypoxic withdrawal test, which measures the decrease in ventilation caused by two breaths of 100% oxygen (%delta V'I). Withdrawal response and ventilatory and inspiratory neural drive responses to hypoxia were lower in OSAHS patients than in control subjects. In patients with OSAHS, %delta V'I correlated significantly with delta V'I/Sa,O2/BSA and with delta P0.1/Sa,O2. On stepwise multiple linear regression analysis, a strong correlation between %delta V'I and delta P0.1/Sa,O2 was found. Moreover, %delta V'I, delta V'I/Sa,O2/BSA and delta P0.1/Sa,O2 were significantly correlated with minimum arterial oxygen saturation and with arousal index. Obstructive sleep apnoea-hypopnoea syndrome patients have a strong relationship between peripheral chemosensitivity and respiratory response to hypoxia, suggesting that hypoxic stimulation of central chemoreceptors is minimally relevant in obstructive sleep apnoea-hypopnoea syndrome. Moreover, sensitivity of the carotid body in patients with obstructive sleep apnoea-hypopnoea syndrome is related to sleep disruption and to nocturnal hypoxia.     

The effect of chronic nocturnal oxygen administration upon sleep apnea

Administration of nocturnal oxygen for 1 night to patients with obstructive sleep apnea (OSA) causes a moderate reduction in apnea frequency without improving hypersomnolence. Therefore, we administered oxygen chronically to patients with OSA to determine: whether apnea frequency would be further reduced, whether the effect of oxygen upon apnea frequency is correlated with an increased ventilatory response to hypoxia and hypercapnia, and whether hypersomnolence improves with more prolonged oxygen administration. In a single-blinded, nonrandomized trial, we compared the effects of 1 month of oxygen (4 L/min by nasal cannula) with room air (4 L/min by nasal cannula) placebo during sleep in 7 men and 1 woman with obstructive sleep apnea. During non-REM sleep, acute oxygen administration elevated the average low oxy-hemoglobin saturation during apneic events and decreased apnea frequency. These acute effects persisted during chronic oxygen administration but reverted to the preoxygen effects immediately upon discontinuing oxygen. One month of oxygen did not affect the waking ventilatory response to hypoxia or hypercapnia; however, waking PaCO2 increased from 40 +/- 1 mm Hg (mean +/- SE) after placebo to 43 +/- 1 mm Hg after oxygen (p less than 0.01). Neither subjective nor objective hypersomnolence consistently improved after 1 month of oxygen administration. We conclude that: first, oxygen has no effect upon apnea frequency beyond the period of administration, and the reduction of apnea frequency is not correlated with an increased sensitivity to chemical ventilatory stimuli. The reduced apnea frequency may be related to an increased PaCO2 stimulating ventilation during sleep.(ABSTRACT TRUNCATED AT 250 WORDS)     

Randomized controlled trial of fluticasone in preschool children with intermittent wheeze

Previous studies have suggested that during non-rapid eye movement (NREM) sleep, neither large short-duration resistive loads nor sustained normoxic hypercapnia alone leads to increased genioglossus muscle activation. However, in normal individuals during stable NREM sleep, genioglossus activity rises above baseline as PCO2 rises and airway resistance increases. We therefore hypothesized that combinations of chemical (PCO2, PO2) and mechanical stimuli during NREM sleep would lead to increased genioglossal activation. We studied 15 normal subjects (9 males, 6 females) during stable NREM sleep, measuring genioglossus electromyogram, epiglottic/choanal pressure, and airflow under six conditions: (1) baseline, (2) inspiratory resistive loading (-5 to -15 cm H2O/ L/second), (3) increased PCO2 (5-10 mm Hg above baseline), (4) combined resistive loading and increased PCO2, (5 ) hypoxia (SaO2 80-85%), and (6 ) combined hypoxia/inspiratory resistive loading. Only the combined condition of hypercapnia and resistive loading led to significantly increased genioglossal activation, 3.91 +/- 0.77% to 9.64 +/- 1.96% of maximum. These data suggest that the genioglossus muscle is less responsive to either chemical stimuli (hypercapnia, hypoxia) or inspiratory resistive loading alone during NREM sleep at the degrees tested. When hypercapnia is combined with resistive loading, the muscle does respond. However, the possibility that higher levels of PCO2 or greater resistive loading alone could activate the muscle cannot be excluded.     

Effect of Moderate Doses of Ethanol and Phenobarbital on Pituitary and Thyroid Hormones and Testosterone

Effects of ingestion of .8 g/kg of body weight of ethanol or 100 mg of phenobarbital on seven consecutive nights on plasma LH, TSH, prolactin, T₃, T₄, and testosterone levels were studied in five healthy young men. Ethanol increased plasma TSH levels during sleep whereas phenobarbital decreased plasma TSH levels during sleep and awake periods. Neither ethanol nor phenobarbital had significant effects on plasma prolactin, total T3, T4, or testosterone levels.     

Entrainment of respiration in humans by periodic lung inflations. Effect of state and CO(2).

Lack of synchrony between a patient and the mechanical ventilator occurs when the respiratory rhythm of the patient fails to entrain to machine inflations. Entrainment implies a resetting of the respiratory rhythm such that a fixed temporal relationship exists between the onset of inspiratory activity and the onset of a mechanical breath. We examined the entrainment response to mechanical ventilation of normal humans over a range of machine rates during wakefulness and during isocapnic and hypercapnic NREM sleep. Wakefulness facilitated 1:1 entrainment of the respiratory rhythm to the mechanical ventilator over a wider range of machine frequencies than during NREM sleep (p < 0.001); isocapnic and hypercapnic conditions did not differ (p = 0.95). To evaluate the Hering-Breuer reflexes in the resetting of the respiratory rhythm during sleep, we examined changes in neural inspiratory time (TI) as the relationship between inspiratory efforts and onset of machine inflations changed. As inspiratory efforts extended into the machine inflation cycle, neural TI shortened. We conclude that entrainment responses of normal humans to mechanical ventilation differ depending on state, but mild increases in respiratory drive caused by CO(2) stimulation do not affect these entrainment responses. Furthermore, the changes in neural TI are consistent with observations in animal studies in which Hering-Breuer reflexes mediated entrainment.     

Older individuals have increased oro-nasal breathing during sleep.

Breathing route during sleep has been studied very little, however, it has potential importance in the pathophysiology of sleep disordered breathing. Using overnight polysomnography, with separate nasal and oral thermocouple probes, data were obtained from 41 subjects (snorers and nonsnorers; 25 male and 16 female; aged 20-66 yrs). Awake, upright, inspiratory nasal resistance (Rn) was measured using posterior rhinomanometry. Each 30-s sleep epoch (not affected by apnoeas/hypopnoeas) was scored for presence of nasal and/or oral breathing. Overnight, seven subjects breathed nasally, one subject oro-nasally and the remainder switched between nasal and oro-nasal breathing. Oral-only breathing rarely occurred. Nasal breathing epochs were 55.79 (69.78) per cent of total sleep epochs (%TSE; median (interquartile range)), a value not significantly different to that for oro-nasal (TSE: 44.21 (68.66)%). Oro-nasal breathing was not related to snoring, sleep stage, posture, body mass index, height, weight, Rn (2.19 (1.77) cm H2O x L(-1) x sec(-1)) or sex, but was positively associated with age. Subjects > or = 40 yrs were approximately six times more likely than younger subjects to spend >50% of sleep epochs utilising oro-nasal breathing. Ageing is associated with an increasing occurrence of oro-nasal breathing during sleep.     

Snoring, pregnancy-induced hypertension, and growth retardation of the fetus

STUDY OBJECTIVE: Our purpose was to study the relationship between snoring and pregnancy-induced hypertension and growth retardation of the fetus. DESIGN: Retrospective, cross-sectional, consecutive case series. SETTING: The Department of Gynecology and Obstetrics, University Hospital, Umea, Sweden. Participants and measurements: On the day of delivery, 502 women with singleton pregnancies completed a questionnaire about snoring, witnessed sleep apneas, and daytime fatigue. Data concerning medical complications were taken from the women's casebooks. RESULTS: During the last week of pregnancy, 23% of the women reported snoring every night. Only 4% reported snoring before becoming pregnant. Hypertension developed in 14% of snoring women, compared with 6% of nonsnorers (p < 0.01). Preeclampsia occurred in 10% of snorers, compared with 4% of nonsnorers (p < 0.05). An Apgar score < or = 7 was more common in infants born to habitual snorers. Growth retardation of the fetus, defined as small for gestational age at birth, had occurred in 7.1% of the infants of snoring mothers and 2.6% of the remaining infants (p < 0.05). Habitual snoring was independently predictive of hypertension (odds ratio [OR], 2.03; p < 0.05) and growth retardation (OR, 3.45; p < 0.01) in a logistic regression analysis controlling for weight, age, and smoking. CONCLUSIONS: Snoring is common in pregnancy and is a sign of pregnancy-induced hypertension. Snoring indicates a risk of growth retardation of the fetus.