Sascha E. Martin

Compliance with CPAP therapy in patients with the sleep apnoea/hypopnoea syndrome.

BACKGROUND--Continuous positive airway pressure (CPAP) therapy is the treatment of choice for the sleep apnoea/hypopnoea syndrome. Compliance with this relatively obtrusive therapy has not been well studied. METHODS--Usage of CPAP was investigated in 54 patients with sleep apnoea/hypopnoea syndrome (median 36 (range 7-129) apnoeas + hypopnoeas/hour slept) over the first 1-3 months after starting CPAP therapy. In all cases CPAP usage was monitored by hidden time clocks that indicated for how long the machines were switched on--that is, the CPAP run time. In 32 patients the time at which the CPAP mask pressure was at the therapeutic level of CPAP pressure set for that patient--that is, the mask time--was also monitored. In all patients objective daytime sleepiness was assessed by multiple sleep latency before and after CPAP therapy. RESULTS--The mean (SE) nightly CPAP run time was 4.7 (0.4) hours. There was no correlation between run time and severity of the sleep apnoea/hypopnoea syndrome as assessed by apnoea + hypopnoea frequency or multiple sleep latency, and no correlation between CPAP usage and improvement in multiple sleep latency. Thirty two patients in whom mask time was recorded had therapeutic CPAP pressures for 89% (3%) of their CPAP run times. Patients who experienced side effects from CPAP used their CPAP machines significantly less than those who did not. CONCLUSIONS--Patients with sleep apnoea/hypopnoea syndrome used CPAP for less than five hours/night on average with no correlation between severity of sleep apnoea/hypopnoea syndrome and CPAP usage. Patients who complained of side effects used their CPAP therapy less. It is recommended that, as a minimum, CPAP run time should be regularly recorded in all patients receiving CPAP therapy.

Randomised placebo controlled trial of daytime function after continuous positive airway pressure (CPAP) therapy for the sleep apnoea/hypopnoea syndrome.

BACKGROUND Patients with the sleep apnoea/hypopnoea syndrome (SAHS) report improved sleepiness, cognitive function, and psychological well being after continuous positive airway pressure (CPAP) therapy, and it is for these daytime features that CPAP is usually given. However, few randomised or controlled studies exist on the effects of CPAP on daytime function. METHODS A prospective, randomised, single blind, placebo controlled, crossover trial of daytime function after CPAP was conducted in 23 patients with SAHS, all with ⩾15 apnoeas+hypopnoeas/hour and ⩾2 symptoms of SAHS. All patients spent four weeks on CPAP therapy and four weeks on oral placebo treatment, following randomisation to treatment order. With ethics committee approval, patients were told the placebo tablet might improve upper airway function. Average effective CPAP use was monitored using hidden time clocks. Assessments of objective and subjective sleepiness, symptoms, cognitive performance, and psychological well being were performed on the last day of each treatment and compared. RESULTS Objective sleepiness measured by sleep onset latency on the multiple sleep latency test improved with CPAP (mean difference from placebo +2.4 min, 95% CI 0.8 to 4.0; p<0.001) as did subjective sleepiness on the Epworth scale (mean difference –6, 95% CI –3 to –9; p = 0.001). Symptom total score also fell with CPAP (mean difference –1.6, 95% CI –2.2 to –1.0; p<0.001). No determinants of these changes with active treatment were identified, and no significant enhancements to cognitive function or psychosocial well being were found in this small sample. CONCLUSIONS These findings provide further evidence for clinically significant benefits to daytime function from CPAP.

Microarousals in patients with sleep apnoea/hypopnoea syndrome

SUMMARY Upper airway obstructions during sleep cause recurrent brief awakenings or microarousals. Standard criteria exist for sleep and respiratory event scoring, however, there are different definitions currently used to score microarousals. We therefore compared three definitions of microarousal (ranging from 1.5‐3 s in duration) and one of awakening (> 15 s). We examined their occurrence at the termination of apnoeas and hypopnoeas and their correlation with daytime sleepiness in patients with sleep apnoea/hypopnoea syndrome (SAHS). Sixty‐three patients (aged 49, SD 10) had overnight polysomnography, multiple sleep latency tests (MSLT) and Epworth Sleepiness Scales (ESS). There were significantly more microarousals by any definition than there were awakenings (P<0.001) and there were more 1.5 s than 3 s microarousals (P<0.001). Significantly more apnoeas and hypopnoeas were terminated by 1.5 s microarousals (83% and 81%) than by 3 s microarousals (75%) (all P<0.001). Apnoea/hypopnoea index (AHI) correlated significantly with objective daytime sleepiness (p = ‐0.30, P<0.01). There were weakly significant relationships between all three microarousal definitions (‐0.24

The effect of clustered versus regular sleep fragmentation on daytime function

Previously, we found that regular sleep fragmentation, similar to that found in patients with sleep apnoea/hypopnoea syndrome (SAHS), impairs daytime function. Apnoeas and hypopnoeas occur in groups in patients with REM or posture related SAHS. Thus, we hypothesised that clustered sleep fragmentation would have a similar impact on daytime function as regular sleep fragmentation. We studied 16 subjects over two pairs of 2 nights and 2 days. The first night of each pair was for acclimatisation. On the second night, subjects either had their sleep fragmented regularly every 90 s, or fragmented every 30 s for 30 min every 90 min, the remaining 60 min being undisturbed. We fragmented sleep with tones to produce a minimum 3 s increase in EEG frequency. During the days following each pair of nights we tested subjects daytime function. Total sleep time (TST) and microarousal frequency were similar on both study nights. We found significantly less stage 2 (55 SD 4, 62±7%; P=0.001) and more slow wave sleep (21 SD 3, 12±6%; P < 0.001) on the clustered night. Mean sleep onset latency was similar on MSLT (clustered 10 SD 5, regular 9±4 min; P=0.7) and MWT (clustered 32 SD 7, regular 30±7 min; P=0.2). There was no difference in subjects mood or cognitive function after either study night. These results suggest that although there is more slow wave sleep (SWS) on the clustered night, similar numbers of sleep fragmenting events produced similar daytime function whether the events were evenly spaced or clustered.

Does sleep enhance the effect of subanesthetic isoflurane on hypoxic ventilation

After surgery, patients may receive little audiovisual stimulation and may sleep.Lack of audiovisual stimulation enhances the suppression of the hypoxic ventilatory response (HVR) by 0.1 minimum alveolar anesthetic concentration (MAC) isoflurane. Sleep also reduces the HVR and may thus increase the risk of hypoxia in patients at this time. We therefore measured the ventilatory response in volunteers to a sustained step hypoxic stimulus (mean arterial oxygen saturation [SaO2] 80% [SEM 0.3] for 20 min) in the presence of 0.1 MAC isoflurane, with subjects in the awake and asleep states. The behavioral states were studied in random order in nine male subjects. The combination of isoflurane and sleep significantly reduced (P < 0.05) normoxic ventilation (6.71 [0.39] vs 8.24 [0.29] L/min) and increased end-tidal PCO2 (PETCO2) (43.1 [0.5] vs 40.4 [0.8] mm Hg) compared with the awake state. However, ventilation was similar in the asleep and awake states during early (15.10 [1.35] vs 15.50 [1.61] L/min) and late (10.45 [0.97] vs 11.03 [0.99] L/min) hypoxia in the presence of isoflurane. Thus sleep did not reduce ventilation during hypoxia in the presence of isoflurane sedation. The increase in PETCO2 during sleep may have offset suppression of the HVR. (Anesth Analg 1995;81:751-6)