Nocturnal gastro-oesophageal reflux has been observed in patients with obstructive sleep apnoea (OSA). Negative intrathoracic pressure during apnoeas and arousal have been suggested as the underlying mechanisms.In order to evaluate this hypothesis, the coincidence and sequence in time of arousal, apnoea and reflux events were analysed. Fifteen patients with OSA or heavy snoring were studied by means of standard polysomnograpy with parallel recording of 24-h oesophageal pH.Reflux events during the day were present in all patients, five of whom had symptoms of reflux. In three of these and in five other patients, a total of 69 nocturnal reflux events were found. In 68 events, arousal was found with the reflux event. Only one reflux without arousal was found (sleep stage 2). Seventeen events occurred during wakefulness after sleep onset. The percentage of time with a pH of <4 during wakefulness after sleep onset was significantly higher than the percentage of time with a pH of <4 during total sleep time (p<0.05). In 37 of the 52 reflux events which occurred during sleep, either an apnoea or a hypopnoea was found prior to the event. The investigation of sequence in time did not prove a causal relation between respiratory events and reflux events.The results indicate that gastro-oesophageal reflux and obstructive sleep apnoea are two separate disorders, which both have a high prevalence in obese patients.

Noninvasive positive pressure ventilation (NPPV) can improve ventilation in obese subjects during the postoperative period after abdominal surgery. Compared to nasal continuous positive airway pressure (nCPAP), NPPV was superior in correcting blood gas abnormalities both during the night-time and during the daytime in a subgroup of patients with the obesity hypoventilation syndrome (OHS). However, as it is unknown, if and to what extent NPPV can unload the respiratory muscles in the face of the increased impedance of the respiratory system in obesity, this is what was investigated. Eighteen obese subjects with a body mass index > or = 40 kg x m(-2) were investigated during the daytime, which included five healthy controls (simple obesity (SO)), seven patients with obstructive sleep apnoea (OSA) and six patients with the obesity hypoventilation syndrome (OHS). Assisted PPV was performed with bi-level positive airway pressure (BiPAP), applied via a face mask. Inspiratory positive airway pressure (IPAP) was set to 1.2 or 1.6 kPa and expiratory positive airway pressure (EPAP) was set to 0.5 kPa. Inspiratory muscle activity was measured as diaphragmatic pressure time product (PTPdi). Comparison of spontaneous breathing with BiPAP ventilation showed no significant difference in breathing pattern, although there was a tendency towards an increase in tidal volume (VT) in all three groups and a decrease in respiratory frequency (fR) in patients with OSA and OHS. End-tidal carbon dioxide (PET,CO2) with BiPAP was unchanged in SO and OSA, but was decreased in OHS. In contrast, inspiratory muscle activity was reduced by at least 40% in each group. This was indicated by a decrease in PTPdi with BiPAP 1.2/0.5 kPa from mean+/-SD 39+/-5 to 20+/-9 kPa x s (p<0.05) in SO, from 42+/-7 to 21+/-8 kPa x s (p<0.05) in OSA, and from 64+/-20 to 38+/-17 kPa x s (p<0.05) in OHS. With BiPAP 1.6/0.5 kPa, PTPdi was further reduced to 17+/-6 kPa x s in SO, and to 17+/-6 kPa x s in OSA, but not in OHS (40+/-22 kPa x s). We conclude that noninvasive assisted ventilation unloads the inspiratory muscles in patients with gross obesity.

Sleep related breathing disorders are common. A reliable diagnosis with relatively simple and portable methods is still needed. One approach is to make use of autonomous nervous system changes which accompany disordered breathing during sleep. The peripheral arterial tonometry (PAT) determines the peripheral arterial vascular tone using a plethysmographic method on the finger. The peripheral arterial tone is modulated by sympathetic activity, by peripheral blood pressure, and by the peripheral resistance of the vessels. We investigate a new ambulatory recording device which uses PAT, oximetry and actigraphy in order to detect sleep apnea. For this purpose we performed a comparative study on 21 patients referred to our sleep laboratory due to suspected sleep apnea. Of these 17 valid recordings were compared. The Watch-PAT was used in parallel with cardiorespiratory polysomnography and the validity was determined. The new system is able to detect apneas and hypopneas with a high reliability (r=0.89). It is very sensitive to arousals (r=0.77). Since arousal are not specific to sleep apnea the specificity of the new system could not be finally clarified in this study. We conclude that the new system is very well suited to perform control studies in patients with sleep apnea which are under therapy and require regular follow-up investigations to maintain a high CPAP compliance.

In a systematic study we compared the performance of spectral analysis and detrended fluctuation analysis (DFA) to discriminate sleep stages and sleep apnea. We investigated 14 healthy subjects, 33 patients with moderate, and 31 patients with severe sleep apnea with polysomnography. Discriminance analysis was used on a person and sleep stage basis to determine the best method for the separation of sleep stages and sleep apnea severity. Using spectral parameters 69.7% of the apnea severity assignments and 54.6% of the sleep stage assignments were correct, while using scaling analysis these numbers increased to 74.4% and 85.0%, respectively. Changes in heart rate variability are better quantified by scaling analysis than by spectral analysis. 1. Introduction Sleep as the absence of wakefulness and the missing ability to react on external stimuli is regarded as a unbiased test situation for the autonomic nervous system [1]. Sleep is not just a constant state controlled by metabolic needs for the body being at rest. Instead sleep consists of different well defined sleep stages which follow a well structured temporal order in normal restorative sleep. Heart rate and heart rate variability vary with the sleep stages, and their normal variability is affected in sleep disorders. It has been shown that autonomic activity changes from waking to sleep. Big differences were found between non-REM and REM sleep [2]. Sympathetic tone drops progressively from wakefulness over sleep stage 1 to 4. In contrast REM sleep was characterized by increased sympathetic tone [3]. Parasympathetic tone increases from wakefulness to non-REM sleep. Periods of wakefulness during sleep were found to have an intermediate position between non-REM and REM sleep [4]. Sleep apnea affects heart rate variability during sleep described as cyclical variation of heart rate [5]. The recording of cyclical variation of heart rate together with snoring has been used in order to detect obstructive sleep apnea with ambulatory recording devices [6]. It can be assumed that the cyclical variation of heart rate can be detected by spectral analysis if the appropriate frequency range is investigated. The pattern of bradycardia and tachycardia during apnea has been attributed to an effective parasympathetic control of heart rate during sleep [7] interrupted by sympathetic activation accompanying the intermittent apnea-terminating arousals. Spectral analysis of heart rate variability is well established and provides a quantitative evaluation of sympathetic and parasympathetic activation of the heartbeat [8]. Three major oscillatory components were identified. The physiological interpretation of the very-low-frequency (VLF) component (< 0.04 Hz) is still discussed, the low-frequency (LF) component (0.04-0.15 Hz) reflects baroreflex sympathetic control of blood pressure, and the high-frequency (HF) component (0.15-0.4 Hz) reflects respiratory rhythm and is believed to be related to parasympathetic control of heart rate [9]. Detrended fluctuation analysis (DFA) method ha...

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