Respiration during sleep in pregnancy.

Several changes in maternal physiology may profoundly alter sleep, especially during late pregnancy. Any condition that causes maternal hypoxemia will be worsened during sleep, particularly in the supine position. Although high circulating levels of progesterone increase respiratory drive during sleep, in at least some women this protective mechanism is insufficient to prevent sleep-disordered breathing and hypoxemia. The true incidence of sleep-disordered breathing during pregnancy remains unknown. Although many women report sleep disturbance during pregnancy, those with severe snoring, observed irregular breathing with sleep, or excessive daytime somnolence should be referred for clinical polysomnography. With few data thus far available, nasal CPAP would appear to be the treatment of choice. Given the possible consequences of sleep apnea for fetal outcome, any significant sleep-disordered breathing is probably an indication for treatment.     

Respiratory disturbance during sleep in COPD patients without daytime hypoxemia

Chronic obstructive pulmonary disease (COPD) is associated with significant morbidity and mortality. Its possible association with obstructive sleep apnea is a major cause of concern for clinicians. As the prevalence of both COPD and sleep apnea continues to rise, further investigation of this interaction is needed. In addition, COPD patients are at risk for hypoventilation during sleep due to the underlying respiratory dysfunction. In this study, 13 COPD subjects and 13 non-COPD control subjects were compared for the presence and severity of obstructive sleep apnea and nocturnal hypoventilation. All 26 subjects had presented to a sleep clinic and showed no signs of daytime hypoxemia. After matching for BMI and age, COPD subjects had a similar prevalence of sleep apnea with a lower degree of severity compared to the control subjects. However, less severe events, such as RERA, occurred at similar rates between the two groups. There was no significant difference between groups in the magnitude of oxyhemoglobin desaturation during sleep. Interestingly, severity and presence of nocturnal hypoxemia correlated with that of sleep apnea in the control group, but not in the COPD subjects. In conclusion, COPD without daytime hypoxemia was not a risk factor for sleep apnea or nocturnal hypoventilation in this study.     

Genioglossus activity in children with obstructive sleep apnea during wakefulness and sleep onset

A prominent role for upper airway neuromuscular control mechanisms in the pathophysiology of pediatric obstructive sleep apnea syndrome (OSAS) is suggested by the observation that obstruction does not occur during wakefulness and is infrequently seen during non-REM sleep. Using a custom intraoral surface electrode to record genioglossal activity (genioglossal electromyography [EMGgg]), normalized with a maximal maneuver, we studied 10 children with OSAS and 6 normal control subjects to determine EMGgg activity during (1) wakefulness, (2) the sleep onset period, and (3) stable non-REM sleep. We observed that the EMGgg activity in patients with OSAS compared with control subjects was significantly greater during wakefulness (3.6 +/- 1.8 vs. 1.6 +/- 1.8% maximum, p < 0.05) and had a greater decline during the early and late sleep onset period (p < 0.05). During stable non-REM sleep, EMGgg remained below the wakeful baseline in all normal control subjects but increased above the baseline in four of the patients with OSAS. We speculate that the increased EMGgg activity during wakefulness represents a reflex-driven neuromuscular compensation for an anatomically compromised airway. Furthermore, the larger decline in EMGgg at sleep onset observed in patients with OSAS is consistent with the relative loss of this reflex. Finally, the return of EMGgg activity above baseline in patients with severe OSAS suggests that some chemical or mechanical compensatory mechanisms remain active during stable non-REM sleep in children.     

Respiration and heart rate variability during sleep in untreated Parkinson patients.

Twenty-six patients with untreated mild to moderate Parkinson's disease (PD) lasting 5 years or less, were investigated in the sleep laboratory. Sleep architecture and respiration during sleep did not significantly differ from age-matched controls. PD patients showed defective cardiac autonomic control during sleep, mainly parasympathetic but also sympathetic in nature, although they had normal results in conventional autonomic tests during wakefulness. Therefore, autonomic cardiac involvement seems to be an early sign of PD.     

Genioglossus activity during sleep in normal control subjects and children with obstructive sleep apnea

Children with obstructive sleep apnea syndrome (OSAS) have more collapsible airways compared with normal subjects, yet sustain stable breathing during wakefulness and part of sleep. This indicates successful neuromuscular compensation. Using a custom intraoral surface electrode to record pharyngeal dilator muscle activity (the genioglossus [EMGgg] normalized to the wakeful baseline), we performed overnight polysomnograms in three groups of children: (1) patients with OSAS without continuous positive airway pressure (CPAP) (n = 13); (2) patients with OSAS with CPAP (n = 5); and (3) control subjects without CPAP (n = 13). Our objective was to evaluate the EMGgg as a function of sleep state and during disordered breathing, compared with stable sleep and wakefulness. In control subjects, the EMGgg decreased from wakefulness to Stage 2 (mean +/- SD, 65 +/- 6%), and further during REM (51 +/- 9%) (p < 0.05). In patients with OSAS, the EMGgg for apneic breaths during REM (37 +/- 9%) was lower than during stable breathing (83 +/- 17%) (p < 0.05) and wakefulness (p < 0.05). CPAP lowered the EMGgg in patients with OSAS during all sleep states. These data indicate that (1) EMGgg compensatory mechanisms remain active during sleep in patients with severe OSAS; (2) EMGgg reductions are temporally associated with sleep apnea events; and (3) REM sleep is associated with the lowest and most variable EMGgg.     

Respiration and abnormal sleep in patients with congestive heart failure

We investigated the interaction between respiration and sleep in ten male outpatients with severe, stable, maximally treated congestive heart failure (CHF). Cheyne-Stokes respiration (CSR), defined as periodic breathing with apnea or hypopnea, was found in all patients with a mean duration of 120 +/- 87 minutes [50.2 +/- 34.4 percent total sleep time (TST)]. The CSR was found predominantly during stage 1 (20.6 +/- 6.7 percent TST) and stage 2 (25.8 +/- 6 percent TST) NREM sleep and occurred rarely during slow wave sleep (SWS) (1.6 +/- 1 percent TST) and REM sleep (1.6 +/- 0.5 percent TST). All apneas and hypopneas were central. Despite normal awake arterial oxygenation (SaO2) (96.1 +/- 1.6 percent), significant, severe hypoxemia was found during sleep in seven patients with SaO2 less than 90 percent for 9 to 59 percent TST (mean +/- SD, 23 +/- 23 percent TST), and this was significantly related to the duration of CSR (r = 0.66, p less than 0.05). The mean minimum SaO2 for sleep stage was lowest during stage 1 (82.1 percent +/- 2.6 percent) and stage 2 (78.9 percent +/- 2.8 percent) NREM sleep, intermediate during REM sleep (84.5 percent +/- 1.8 percent) and highest during SWS (87.6 percent +/- 2.7 percent). Sleep was disrupted to a variable extent in all patients with a short mean TST (287 +/- 106 minutes), a high proportion of stage 1 sleep (26 +/- 19 percent TST), virtual absence of SWS (5 +/- 7 percent TST) which was found in only four patients, and a high number of sleep stage changes (30 +/- 27/hour) and arousals (28 +/- 25/hour). Arousals occurred predominantly during stage 1 (17 +/- 20/hour) and stage 2 (10 +/- 7/hour) NREM sleep and the majority immediately followed the hyperpneic phase of CSR. The amount of CSR (percent TST) was inversely related to the length of TST (r = -0.73, p less than 0.05), and directly related to the number of sleep stage changes (r = 0.79, p less than 0.01) and the number of arousals (r = 0.66, p less than 0.05). We conclude that in severe, stable CHF, CSR occurs predominantly during light sleep, that despite normal awake arterial oxygen saturation, significant hypoxemia may develop during sleep due to CSR, and that sleep is unstable and disrupted due to frequent arousals caused by the hyperpneic phase of CSR. These sequelae of CSR may be important determinants of the clinical status and outcome of patients with severe CHF.     

Acute oxygen in patients with sleep apnea and COPD

Nocturnal oxygen administered to patients with disordered breathing ameliorates hypoxemia. As a result, an important chemical stimulus to arousal is diminished. This could cause prolongation of disordered breathing events, worsen respiratory acidosis, and induce potentially harmful cardiac arrhythmias. The presence of chronic obstructive pulmonary disease (COPD) could further aggravate the situation since such patients may have depressed hypercarbic responses. To test this hypothesis, 20 obese men with sleep apnea and COPD were studied polysomnographically on two nights receiving air on one or oxygen at 4 L/min on the other. Supplemental oxygen increased mean DOB event duration from 25.7 to 31.4 seconds (p less than 0.001), increased end apneic PCO2 from 52.8 to 62.3 mm Hg (p less than 0.025), and decreased mean end apneic pH from 7.34 to 7.28 (p less than 0.001). At the same time, it improved mean sleeping and end-apneic oxygen saturation. The number of ventricular extra-systoles (PVCs) per minute of sleep showed small increases in three subjects while breathing oxygen. Complex ventricular arrhythmias were unaffected by oxygen in five subjects. Oxygen eliminated atrioventricular block in two subjects. We conclude that nocturnal supplemental oxygen does not increase ventricular arrhythmias in the majority of patients with COPD and coexisting disordered breathing events. While the clinical significance of an oxygen associated increase in ventricular extrasystoles in three subjects is unclear, nocturnal monitoring by telemetry or ambulatory recorder should be sufficient to detect such patients.     

慢性阻塞性肺疾病睡眠低氧现状与诊治进展

本文首先介绍了睡眠时动脉血氧和二氧化碳分压的生理性改变,分析比较了慢性阻塞性肺疾病(COPD)患者睡眠时动脉血氧的特征和睡眠时低氧现状,并进一步探讨了COPD睡眠低氧的可能机制、危害、预测因素、检查和相关治疗手段,对提高临床医生对COPD夜间低氧的认识有积极意义。     

Cardiorespiratory adaptation during sleep in infants and children

The cardiorespiratory control system undergoes functional maturation after birth. Until this process is completed, the cardiorespiratory system is unstable, placing infants at risk for cardiorespiratory disturbances, especially during sleep. The profound influence of states of alertness on respiratory and cardiac control has been the focus of intense scrutiny during the last decade. The effects of rapid-eye movement (REM) sleep on various mechanisms involved in cardiorespiratory control are of particular significance during the postnatal period since newborns spend much of their time in this sleep state. In fullterm newborns, REM sleep occupies more than 50% of total sleep time, and this percentage is even greater in preterm newborns. From term to six months of age, the proportion of REM sleep decreases.² Since respiratory and cardiac disturbances are known to occur selectively during REM sleep, the predominance of REM sleep may be a risk factor for abnormal sleep-related events during early infancy.³ Awareness of these developmental changes in sleep patterns is important for clinicians dealing with problems such as apparent life-threatening events (ALTE), sudden infant death syndrome (SIDS), and/or cardiorespiratory responses to respiratory disorders. Our current understanding of respiratory and cardiac control rests mainly on studies conducted during the first months of life. There is a paucity of data on late infancy and early childhood. The present paper will review available data on how sleep affects 1) ventilatory mechanics, in particular of the upper airways and the chest wall; ventilation and apnea; gas exchange; chemoreceptor function; and arousal responses; 2) changes in heart rate and heart rate variability, and the occurrence and mechanisms of bradycardia. © 1995 Wiley-Liss, Inc.     

Myocardial stress. Exercise versus sleep in patients with COPD

Epidemiologic investigation has revealed that patients with pulmonary disease are at increased risk of dying during the early morning hours. To provide a pathophysiologic explanation for these excessive nocturnal mortality statistics, we tested the hypothesis that episodes of arterial O2 desaturation during sleep can produce as severe a stress on the maintenance of myocardial O2 balance as maximal exercise in patients with chronic obstructive pulmonary disease (COPD). Thirty-one subjects with COPD underwent both overnight sleep and treadmill exercise study to their dyspnea-limited maximum. During both activities, systemic blood pressure was directly recorded and myocardial oxygen consumption (MVO2) estimated from the pulse rate (HR) - systolic blood pressure (SBP) product. Arterial O2 content (CaO2) was calculated from hemoglobin concentration and arterial O2 saturation (SaO2) measured by ear oximetry. Using these data and the Fick principle, myocardial blood flow (MBF) was continuously estimated during both exercise and sleep. During sleep, mean SaO2 was 88 +/- 7 percent while the average of the lowest SaO2 recorded for each subject was 71 +/- 14 percent. Episodes of nocturnal oxyhemoglobin desaturation produced consistent elevations in SBP frequently accompanied by an increase in HR. Because this hemodynamic response resulted in increased MVO2 at precisely the times when arterial O2 contents were low, high demands for MBF were generated. The average of the highest individual values for MBF during sleep was 244 +/- 144 (ml/100 g LV/min). This value was not significantly different from the value of MBF = 281 +/- 91 (ml/100 g LV/min) determined for maximal exercise. This finding suggests that the demand for coronary blood flow during episodes of nocturnal hypoxemia can be transiently as great as during maximal exercise in patients with COPD.     

Increased upper airway collapsibility in children with obstructive sleep apnea during wakefulness

Upper airway collapsibility (UAC) is increased in children with sleep-disordered breathing (SDB), but during wakefulness, active neural processes preserve upper airway patency, such that measurement of upper airway dynamics using acoustic pharyngometry may contribute to diagnostic accuracy in snoring children. Upper airway cross-sectional area obtained from acoustic pharyngometry measurements was assessed in 247 children referred for evaluation of suspected SDB and control subjects, before and after application of cetacaine 1% spray to the pharyngeal introitus under visual inspection. UAC was determined from the precentage change in cross-sectional area after topical anesthesia. UAC measurements were reproducible 1 week apart in both control subjects and patients with SDB (p < 0.005). A UAC less than or equal to -30% exhibited high sensitivity and specificity in identification of all children with obstructive apnea-hypopnea index greater than 5/hour total sleep time in a prospective initial sample of 54 children and in a subsequent post hoc sample of 94 snoring children. Thus, upper airway dynamic testing during wakefulness in response to a topical airway anesthetic may provide a useful clinical adjunct to the evaluation of snoring children, with more accurate identification of those children with SDB.     

Are sleep studies necessary in COPD?

While there are many research questions still requiring performance of research sleep studies in patients with COPD, their use is not advocated in routine clinical practice, except in patients who have symptoms of the sleep apnoea/hypopnoea syndrome or possibly in those without daytime hypoxaemia (PaO₂>60 mmHg) who have marked polycythaemia or marked cor pulmonale.     

Aldosterone excretion rates in children and adults during sleep

The present study undertook to examine aldosterone excretion during sleep as an integrated measurement of aldosterone production. A 24-hour urine collection was divided into awake and sleep fractions. Urinary aldosterone and electrolyte excretion were measured in 26 healthy children (mean age, 8.9 +/- 1.9 [SD] years) and 28 adults (mean age, 29.9 +/- 9.5 years). Aldosterone excretion in children was 5.6 +/- 3.9 (SD) micrograms/g creatinine during the awake period, which was significantly different from the 3.9 +/- 4.1 micrograms/g creatinine value recorded during sleep (p less than 0.002). In adults, awake aldosterone excretion was significantly greater than that during sleep; 4.9 +/- 2.7 versus 3.2 +/- 1.6 micrograms/g creatinine (p less than 0.001). Sleep aldosterone excretion values were highly correlated with the corresponding 24-hour aldosterone excretion values (r = 0.85, p less than 0.001) in children and in adults (r = 0.64, p less than 0.001). Sleep aldosterone excretion was correlated with 24-hour potassium excretion (p less than 0.02) only in children. Sleep aldosterone excretion correlated with neither sleep nor 24-hour sodium excretion in children or adults. Sleep electrolyte excretion rates were highly correlated with 24-hour excretion rates in both children and adults. Dexamethasone, 1 mg, administered the night before to suppress the normally high morning levels of endogenous adrenocorticotropic hormone, had no discernible effect on sleep aldosterone excretion. These results indicate that measurement of aldosterone excretion in an easily collected sleep urine sample provides a reliable index of aldosterone production in children and adults.     

家庭氧疗对存在睡眠呼吸紊乱的稳定期COPD患者的临床研究

目的 探讨早期介入家庭氧疗对存在睡眠呼吸紊乱的稳定期COPD患者的疗效.方法 将存在睡眠呼吸紊乱（AHI 5～30次/h）的患者138例随机分为实验组和对照组,实验组入组病例69例,对照组入组病例69例.给予实验组中的COPD患者长期家庭氧疗治疗（吸氧流量1～2 L/min,吸氧时间＞15 h/d）＋常规治疗,而对照组中的COPD患者仅常规治疗2年.应用圣乔治呼吸问卷（SGRQ）对两组患者治疗前后进行评分.结果 实验组经长期家庭氧疗治疗2年后SGRQ总评分较前下降,差异具有统计学意义（t＝38.42,P＜0.05）,其中呼吸症状评分、疾病影响评分亦较前下降,差异具有统计学意义（t值分别为26.38、33.73,P值均＜0.05）.对照组治疗2年后SGRQ总评分、呼吸症状评分、活动受限评分、疾病影响评分差异无统计学意义（t值分别为5.22、4.61、2.23、2.781,P值均＞0.05）.结论 长期家庭氧疗是延缓COPD患者病情进展、生活质量得以提高的一种简便、安全、有效的治疗手段.     

The effects of nitrazepam and flunitrazepam on oxygen desaturation during sleep in patients with stable hypoxemic nonhypercapnic COPD

Serious respiratory depression has been described in COPD patients receiving hypnotics during acute exacerbations. There are few studies quantifying the effects of hypnotics on oxygenation during sleep in patients with stable hypoxemic COPD. In this study, the effects of single therapeutic doses of nitrazepam and flunitrazepam on SaO2, apneas during sleep and other sleep variables were measured in 14 COPD patients. All patients used theophylline. Sleep-induced decrease in mean SaO2 was 1.3 percent after placebo, 1.4 percent after nitrazepam and 1.9 percent after flunitrazepam (no significant differences). Sleep apneas were not more common or longer after nitrazepam or flunitrazepam, but sleep quality seemed to improve. It is concluded that oxygenation during sleep in these nonobese patients with stable hypoxemic nonhypercapnic COPD, all on maintenance theophylline therapy, was affected very little by single therapeutic doses of nitrazepam or flunitrazepam.     

Increased sleep latency and reduced sleep duration in children with asthma

Study objective

Sleep disturbance is reported to be more prevalent in children and adolescents with asthma than those without. However, this has not been described adequately using objective measures. The aim of this study was to objectively characterise sleep disturbance in asthmatic and non-asthmatic children and adolescents.

Methods

A retrospective analysis of polysomnography recordings from children aged 5–17 years old, with (n?=?113) and without asthma (n?=?104), referred for a sleep study over the period 2005–2010 at the Paediatric Sleep Unit, John Hunter Children’s Hospital in Newcastle, NSW Australia, was carried out.

Results

Polysomnographic recordings were analysed to compare sleep quality and quantity between asthmatic and non-asthmatic children. Sleep latency was significantly longer in asthmatic children compared to controls. However, this result was significant for females only (46.2 (5.6) vs 33.2 (2.7) min, p?<?0.05). Male asthmatics had significantly shorter sleep duration (425.9 (5.4) vs 441.8 (5.4) min, p?<?0.05) than male controls.

Conclusions

Sleep disturbance exists in children with asthma and manifests differently in males and females. Further investigation into the clinical implication of increased sleep latency and reduced sleep duration upon daytime functioning and lifestyle behaviours in children and adolescents with asthma is warranted.     

Changes in upper airway size during tidal breathing in children with obstructive sleep apnea syndrome

We performed respiratory-gated magnetic resonance imaging to evaluate airway dynamics during tidal breathing in 10 children with obstructive sleep apnea syndrome (OSAS; age, 4.3 +/- 2.3 years) and 10 matched control subjects (age, 5.0 +/- 2.0 years). We hypothesized that respiratory cycle fluctuations in upper airway cross-sectional area would be larger in children with OSAS. METHODS: Studies were performed under sedation. Respiratory gating was performed automatically at 10, 30, 50, 70, and 90% of inspiratory and expiratory volume. Airway cross-sectional area was measured at four ascending oropharyngeal levels at each increment of the respiratory cycle. RESULTS: We noted the following in subjects with OSAS compared with control subjects: (1) a smaller upper airway cross-sectional area, particularly during inspiration; (2) airway narrowing occurred during inspiration without evidence of complete airway collapse; (3) airway dilatation occurred during expiration, particularly early in the phase; and (4) magnitude of cross-sectional areas fluctuations during tidal breathing noted in OSAS at levels 1 through 4 were 317, 422, 785, and 922%, compared with 19, 15 17, and 24% in control subjects (p < 0.001, p < 0.005, p < 0.001, and p < 0.001, respectively). CONCLUSIONS: Fluctuations in airway area during tidal breathing are significantly greater in subjects with OSAS compared with control subjects. Resistive pressure loading is a probable explanation, although increased airway compliance may be a contributing factor.