Search

Introduction: There is no clear relationship between the severity of obstructive sleep apneas (OSA) and the degree of sleepiness. We analysed if any polysomography (PSG) based parameter is related with either subjective or objective sleepiness measures by sleepiness scales and pupillographic sleepiness test (PST). Methods: We included 105 patients. Following PSG patients indicated perceived sleepiness by the Stanford Sleepiness (SSS), Epworth sleepiness (ESS) and the visual analogue scale (VAS). The PST was applied as an objective assessment of sleepiness. Beside the total pupillary unrest index (PUI) we analysed the percentage of time spend with normal (%PUI 0-6.5), marginal (%PUI 6,6-9,7) and sleepy PUI values (%PUI => 9,8). Patients were divided in sleepy or non sleepy according to an ESS value ≥ 10 or an PUI ≥ 9,8%. Results: We found an increased PUI in 32 patients (33%). 37 patients demonstrated an increased ESS and 17 an increased SSS. There was no direct correlation between the values of the PST and the subjective sleepiness scales. PSG parameters were not significantly different between the sleepy and non sleep patients. We analysed subjective and objective sleepiness in patients with an AHI Conclusion: In this study we do not find any correlation between severity of OSA and sleepiness. Patients with sleep disturbances find it often difficult to distinguish between fatigue and real sleepiness, which might explain the missing correlation between subjective and objective sleepiness.

Introduction: Sleep onset (SO) is associated with a decrease in heart rate (HR), systolic and diastolic blood pressure (Sys, Dia). These changes are reduced by obstructive sleep apneas (OSA). There is little evidence if obesity alone influences the hemodynamic parameters (HP) at SO. Methods: We investigated 40 patients with a BMI > 30 kg/m2 via polysomnography and Nexfin-HD® recordings. Group A: 16 patients without OSA; Group B: 24 patients with OSA. Sys, Dia, mean blood pressure (MAP), HR, stroke volume (SV) and cardiac output (CO) were analyzed 5 min before (P0) and 20 min after SO (P1). The student t-test for independent samples was applied with a significance level of p Results: SO was not associated with any significant decrease in HP. However, variation of HP was different between the two groups. It decreased in Group A: Sys: -0,6 mmHg; Dia: -0,1 mmHg; HR: -0,6 bpm, SV: -0,7 ml and CO: -0,2 L/min. MAP increased by 0.04 mmHg. All HP increased significantly in group B with Sys: +2,3 mmHg, Dia: +0,8 mmHg, HR: +0,2, MAP: +1,4 mmHg, SV: +1,1 ml and CO: +0,2 L/min and reached signficance when compared to group A. Discussion: SO was not associated with a significant decrease in any investigated HP. Perhaps obesity alone attenuates the physiological reduction of the sympathetic activity at SO. The higher variation of hemodynamic parameters in OSA indicates its impact on the cardiovascular stability.