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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.

Heart block during sleep has been described in up to 10% of patients with obstructive sleep apnoea. The aim of this study was to determine the relationship between sleep stage, oxygen desaturation and apnoea-associated bradyarrhythmias as well as the effect of nasal continuous positive airway pressure (nCPAP)/nasal bi-level positive airway pressure (nBiPAP) therapy on these arrhythmias in patients without electrophysiological abnormalities. Sixteen patients (14 males and two females, mean age 49.6+/-10.4 yrs) with sleep apnoea and nocturnal heart block underwent polysomnography after exclusion of electrophysiological abnormalities of the sinus node function and atrioventricular (AV) conduction system by invasive electrophysiological evaluation. During sleep, 651 episodes of heart block were recorded, 572 (87.9%) occurred during rapid eye movement (REM) sleep and 79 (12.1%) during nonrapid eye movement (NREM) sleep stages 1 and 2. During REM sleep, the frequency of heart block was significantly higher than during NREM sleep: 0.69+/-0.99 versus 0.02+/-0.04 episodes of heart block x min(-1) of the respective sleep stage (p<0.001). During apnoeas or hypopnoeas, 609 bradyarrhythmias (93.5%) occurred with a desaturation of at least 4%. With nCPAP/ nBiPAP therapy, apnoea/hypopnoea index (AHI) decreased from 75.5+/-39.6 x h(-1) to 3.0+/-6.6 x h(-1) (p<0.01) and the number of arrhythmias from 651 to 72 (p<0.01). We conclude that: 1) 87.9% of apnoea-associated bradyarrhythmias occur during rapid eye movement sleep; 2) the vast majority of heart block episodes occur during a desaturation of at least 4% without a previously described threshold value of 72%; and 3) nasal continuous positive airway pressure or nasal bi-level positive airway pressure is the therapy of choice in patients with apnoea-associated bradyarrhythmias.

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.

Objective: To study the influence of obstructive sleep apnea (OSA) on 24-h BP., Setting: Sleep laboratory of the Medical Department, Neukölln Hospital, Berlin, Germany., Methods: In 93 subjects, noninvasive 24-h BP monitoring was performed with BP recordings made at 15-min intervals. Apnea severity was evaluated by means of a portable device that allows calculation of an oxygen desaturation index (ODI). A normal 24-h BP profile (dipping) was defined by a night/day BP ratio of 0.9., Results: ODI was related to systolic and diastolic daytime (p<0.001) and nighttime BP (p<0.001) as well as systolic and diastolic BP night/day ratios (p<0.001). Multiple regression analysis showed that age and ODI were independently related to daytime BP. When subjects were grouped according to apnea severity, daytime BP increased as ODI increased: 127/80+/-10/11 mm Hg in habitual snorers (ODI 0 to 5), 135/87+/-15/9 mm Hg in mild OSA (ODI 6 to 30), and 140/90+/-13/10 mm Hg in severe OSA (ODI >30) (p values <0.05 for comparisons of OSA groups with habitual snorers). Compared to subjects with mild OSA or habitual snorers, BP night/day ratios were greater in patients with severe OSA (p values <0.05). Accordingly, hypertension and nondipping increased as ODI increased., Conclusion: OSA is associated with hypertension independent of the confounding factors of age and obesity. Nondipping is related to apnea severity. These alterations might contribute to the increased mortality in patients with severe OSA.

We completed polysomnography and complementary measurement of the oesophageal pressure and airflow in 6 subjects (2 volunteers, 4 patients with sleep-related breathing disorder). The evaluation of the physiological parameters of the breathing over the whole night showed a strong correlation between the pressure-time product and the work of breathing. Our results revealed distinct differences between the parameters of the breathing mechanics in volunteers versus in patients. The continuous long-term analysis of respiration during sleep may contribute to reveal further pathological mechanisms of the respiratory system.

We studied 24-h blood pressure (BP) in 17 hypertensive patients with polysomnographic verified moderate to severe obstructive sleep apnea (OSA) before, after 1-3 days and after 4-6 months of treatment with nasal continuous positive airway pressure (nCPAP). BP was recorded using an ambulatory blood pressure monitoring (ABPM) device with oscillometric measurement method (SpaceLabs 90207) over a period of 24 h with intervals of 15 min in daytime and nighttime. Hypertension was defined as mean BP in the daytime period > 135/85 mm Hg; OSA was diagnosed when a full night polysomnography indicated an apnea hypopnea index (AHI) > 10/h. Hypertensive systolic/diastolic daytime BP values decreased significantly from 144.8/94.4 mm Hg at baseline to 138.9/89.4 mm Hg after short-term, and to 136.4/86.9 mm Hg after long-term nCPAP-therapy. Nighttime BP values, too, were reduced significantly from 137.6/87.1 mm Hg at baseline to 129.9/82.3 mm Hg after short-term, and to 128.6/ 79.8 mm Hg after long-term therapy. In addition to these data the heart rate fell significantly from 82.5 b/min to 74.8 b/min after 4-6 months in daytime, and from 70.9 b/min to 63.6 b/min in nighttime. The beneficial effect on diurnal and nocturnal hypertension in patients with nCPAP-therapy of OSA suggests a causal relationship between systemic hypertension and obstructive sleep apnea.

The pathogenesis of obesity hypoventilation is incompletely understood. We investigated 505 patients with sleep apnoea in respect of determinants that correlate with chronic hypercapnia. 14 patients (2.8 per cent) exhibited daytime hypercapnia (PCO2 greater than or equal to 45 mmHg). Compared with the entire group of patients, these patients showed heavier overweight (p less than 0.001) and their nightly respiratory dysregulation defined by the apnoea index was more severe (p less than 0.001). If these patients were compared with 14 normocapnic controls matched for apnoea index, weight and age, there was no difference in respect of lung function data. We conclude that overweight and the severity of sleep apnoea are determinants that predispose to chronic alveolar hypoventilation.