A wearable system developed to monitor people suffering from vasovagal syncope.

A wearable system for monitoring non-invasively signals invaluable when examining person suffering from vasovagal syncope is presented in the paper. Following signals are continuously recorded: electrocardiogram, photopletysmogram, impedance cardiogram and electrodermal resistance.

A Meta-Analysis of Pulse Arrival Time Based Blood Pressure Estimation.

The paper presents a preliminary meta-analysis of the sample correlation between pulse arrival time (PAT) and blood pressure (BP). The aim of the study was to verify sample correlation coefficient between PAT and BP using an affine model $ BP = a . PAT+b $ for systolic and diastolic blood pressure. The databases included in the search were the IEEE Xplore Digital Library, Springer Link and Google Scholar. Only papers from 2005 to 2017 wereincluded into analysis. The random-effects model was considered. The resulting sample correlation coefficient was equal to -0.82 (95 % CI; -0.89, -0.72) for systolic blood pressure and -0.64 (95% CI, -0.74 -0.51) for diastolic one. Egger's regression test showed that there was no evidence of publication bias. Obtained 95% CI intervals for sample correlation coefficients for SBP and DBP are almost separate, which may indicate different relation between PAT and BP for systolic and diastolic pressure.

Acute hypoxia diminishes the relationship between blood pressure and subarachnoid space width oscillations at the human cardiac frequency.

BACKGROUND: Acute hypoxia exerts strong effects on the cardiovascular system. Heart-generated pulsatile cerebrospinal fluid motion is recognised as a key factor ensuring brain homeostasis. We aimed to assess changes in heart-generated coupling between blood pressure (BP) and subarachnoid space width (SAS) oscillations during hypoxic exposure. METHODS: Twenty participants were subjected to a controlled decrease in oxygen saturation (SaO2 = 80%) for five minutes. BP and heart rate (HR) were measured using continuous finger-pulse photoplethysmography, oxyhaemoglobin saturation with an ear-clip sensor, end-tidal CO2 with a gas analyser, and cerebral blood flow velocity (CBFV), pulsatility and resistive indices with Doppler ultrasound. Changes in SAS were recorded with a recently-developed method called near-infrared transillumination/backscattering sounding. Wavelet transform analysis was used to assess the relationship between BP and SAS oscillations. RESULTS: Gradual increases in systolic, diastolic BP and HR were observed immediately after the initiation of hypoxic challenge (at fifth minute +20.1%, +10.2%, +16.5% vs. baseline, respectively; all P<0.01), whereas SAS remained intact (P = NS). Concurrently, the CBFV was stable throughout the procedure, with the only increase observed in the last two minutes of deoxygenation (at the fifth minute +6.8% vs. baseline, P<0.05). The cardiac contribution to the relationship between BP and SAS oscillations diminished immediately after exposure to hypoxia (at the fifth minute, right hemisphere -27.7% and left hemisphere -26.3% vs. baseline; both P<0.05). Wavelet phase coherence did not change throughout the experiment (P = NS). CONCLUSIONS: Cerebral haemodynamics seem to be relatively stable during short exposure to normobaric hypoxia. Hypoxia attenuates heart-generated BP SAS coupling.