Breathing at very low lung volumes might be affected by decreased expiratory airflow and air trapping. Our purpose was to detect expiratory flow limitation (EFL) and, as a consequence, intrinsic positive end-expiratory pressure (PEEPi) in grossly obese subjects (OS). Eight OS with a mean body mass index (BMI) of 44 +/- 5 kg/m2 and six age-matched normal-weight control subjects (CS) were studied in different body positions. Negative expiratory pressure (NEP) was used to determine EFL. In contrast to CS, EFL was found in two of eight OS in the upright position and in seven of eight OS in the supine position. Dynamic PEEPi and mean transdiaphragmatic pressure (mean Pdi) were measured in all six CS and in six of eight OS. In OS, PEEPi increased from 0.14 +/- 0.06 (SD) kPa in the upright position to 0.41 +/- 0.11 kPa in the supine position (P < 0.05) and decreased to 0.20 +/- 0.08 kPa in the right lateral position (P < 0.05, compared with supine), whereas, in CS, PEEPi was significantly smaller (<0.05 kPa) in each position. In OS, mean Pdi in each position was significantly larger compared with CS. Mean Pdi increased from 1.02 +/- 0.32 kPa in the upright position to 1.26 +/- 0.17 kPa in the supine position (not significant) and decreased to 1. 06 +/- 0.26 kPa in the right lateral position (P < 0.05, compared with supine), whereas there were no significant changes in CS. We conclude that in OS 1) tidal breathing can be affected by EFL and PEEPi; 2) EFL and PEEPi are promoted by the supine posture; and 3) the increased diaphragmatic load in the supine position is, in part, related to PEEPi.

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Sinus arrest and atrioventricular (AV) block have been demonstrated in as much as 30% of patients with sleep apnea (SA). The reversal of heart block after tracheostomy has been shown. Nasal continuous positive airway pressure (nCPAP) now is widely used as the treatment of SA, but little data are available on the effect of nCPAP on heart block in patients with SA. During a 17-mo period 239 patients were found to have SA in an ambulatory study. Heart block was identified in 17 (16 male, one female) of these patients. Standard polysomnography and two-channel long-term ECG before and during nCPAP therapy were performed in order to assess the effect of nCPAP on SA and heart block. Mean age of the 17 patients was 50.7 yr (range, 27 to 78 yr), mean respiratory disturbance index (RDI) was 90/h (SD +/- 36.1) before nCPAP and 6/h (SD +/- 6.2) on the second treatment night. The number of episodes of heart block during sleep decreased significantly (p < 0.001) from 1,575 before therapy to 165 during nCPAP. In 12 patients (70.6%) heart block was totally prevented by nCPAP. In another three patients, there was a 71 to 97% reduction in the number of episodes of heart block on the second treatment night, and in two of them a complete reversal occurred thereafter. Two patients exhibited an increase in block frequency during nCPAP, which was reversed after 4 wk of nCPAP in one but persisted in the other.(ABSTRACT TRUNCATED AT 250 WORDS)

R Ri is sk k o of f t tr ra af ff fi ic c a ac cc ci id de en nt ts s i in n p pa at ti ie en nt ts s w wi it th h s sl le ee ep p--d di is so or rd de er re ed d b br re ea at th h--i in ng g: : r re ed du uc ct ti io on n w wi it th h n na as sa al l C CP PA AP P Fifty nine patients completed the study. The accident rate was significantly decreased from 0.8 per 100,000 km (untreated) to 0.15 per 100,000 km with nCPAP treatment. Variables that were considered to be likely to increase accident risk (sleeping spells, fatigue, vigilance test reaction time, daytime sleep latency) also improved with treatment.We conclude that treatment of sleep-disordered breathing by nasal continuous positive airway pressure is related to reduction in patient motor vehicle accident rates, probably due to the reversal of excessive daytime sleepiness. Eur Respir J., 1996Respir J., , 9, 2606 This study is part of the research project 2.9107: "Sleep related breathing disorders and traffic security", carried out on behalf of the "Bundesanstalt für Straβenwesen".

Arterial blood pressure patterns in 12 men with sleep apnea and arterial hypertension were studied at baseline and after 6 months’ therapy with nasal continuous positive airway pressure (nCPAP). Preexisting antihypertensive medication was discontinued 1 week before baseline measurements. Weight did not change during the study period; body mass index was 29.3 (range, 25.4–38.5) vs. 29.3 (25.0–38.5). During therapy the apnea index decreased from 58 (range 30–73) to 2 (range 0–7) apneic episodes per hour (p < 0.01). Intra-arterial systolic (BP sys.) and diastolic (BP dias.) blood pressure and heart rate decreased during therapy (p < 0.001). Mean values ± 95 % confidence intervals were as follows: BP sys., 147.1 ( ± 1.6) mm Hg vs. 126.4 ( ± 1.5) mm Hg; BP dias., 81.6 ( ± 0.8) mm Hg vs. 69.4 ( ± 0.6) mm Hg; heart rate, 68.8 ( ± 0.7) beats/min vs. 65.4 ( ± 0.7) beats/min. Furthermore, the variability of these parameters decreased during therapy: variability BPsys.,53.8( ± 1.1) mm Hg vs. 25.6 ( ± 1.1) mm Hg; variability BP dias., 35.6 ( ± 0.7) mm Hg vs. 17.9 ( ± 0.7) mm Hg; variability of heart rate, 28.1 ( ± 0.7) beats/min vs. 14.9 ( ± 0.7) beats/min (p < 0.001). During treatment we found that blood pressure scores already dropped during the awake phase, with a further decrease during non-REM and REM sleep (p < 0.001). Our results, which demonstrate the reversibility of high blood pressure upon treatment of sleep apnea, indicate that sleep apnea can be an etiological factor in hypertension. Sleep apnea should therefore be considered in the differential diagnosis of arterial hypertension.