The aim of the study was to assess cardiac and respiratory blood pressure (BP) and subarachnoid space (SAS) width oscillations during the resting state for slow and fast breathing and breathing against inspiratory resistance. Experiments were performed on a group of 20 healthy volunteers (8 males and 12 females; age 25.3 ± 7.9 years; BMI = 22.1 ± 3.2 kg/m 2 ). BP and heart rate (HR) were measured using continuous finger-pulse photoplethysmography. SAS signals were recorded using an SAS monitor. Oxyhaemoglobin saturation (SaO 2 ) and end-tidal CO 2 (EtCO 2 ) were measured using a medical monitoring system. Procedure 1 consisted of breathing spontaneously and at controlled rates of 6 breaths/minute and 6 breaths/minute with inspiratory resistance for 10 minutes. Procedure 2 consisted of breathing spontaneously and at controlled rates of 6, 12 and 18 breaths/minute for 5 minutes. Wavelet analysis with the Morlet mother wavelet was applied for delineation of BP and SAS signals cardiac and respiratory components. Slow breathing diminishes amplitude of cardiac BP and SAS oscillations. The overall increase in BP and SAS oscillations during slow breathing is driven by the respiratory component. Drop in cardiac component of BP amplitude evoked by slow-breathing may be perceived as a cardiovascular protective mechanism to avoid target organ damage. Further studies are warranted to assess long-term effects of slow breathing.

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The paper considers the contribution of conductivity changes undergone in an anisotropical medium to measured resistance. This was achieved by extending the relationship proposed by Geselowitz to anisotropical materials described, therefore, by a conductivity tensor. It was found that each element of a conductivity change tensor contributed to the measured resistance only if a corresponding component of the electrical field was nonzero. Numerical calculations were performed for blood-flow-associated conductivity changes. A special experiment stand was developed which allowed experiments to be performed proving the theoretical results. It was found that the absolute value of resistance change measured in the direction perpendicular to the vessel axis was much smaller than that measured along the vessel axis. The results obtained may explain the fact that the actual change of measured resistance created by changes of conductivity induced by aortic blood flow is lower than expected from simplified models.

The main aim of the study is to establish a relation between different sources of Impedance cardiogram (ICG) as function of spatial distribution of conductivity. A three-dimensional model of a human thorax using the finite element method has been constructed. The model includes 35 horizontal layers consisting of up to 519 pentahedral elements that are automatically divided into tetrahedral ones before calculating the potential distribution. Electrode array configuration proposed by Kubicek et al. (Aerosp. Med. 37: 1208-1212, 1996) has been studied. A relationship proposed by Geselowitz (IEEE Trans. Biomed. Eng. 18: 38-41, 1971) has been used to calculate the sensitivity of the examined electrode array to conductivity changes inside the thorax. This relationship has allowed for the calculation of the contributions to ICG from spatially separated sources when modeling all changes in conductivity simultaneously. It has been confirmed that the main contributions to ICG signal come from ventricles, atria, aorta, and lungs. The relations between these components have been found to be dependent nonlinearly on spatial conductivity distribution. As a result, reliable and reproducible measurements of stroke volume (SV) using ICG are impossible. Nevertheless, ICG can be used to monitor relative changes of SV in all cases where the spatial distribution of conductivity and geometry of the subject, during the examination, is preserved. However, it does not mean that the accuracy of SV measurement will be the same in all these cases.

IntroductionUsing a novel method called near-infrared transillumination backscattering sounding (NIR-T/BSS) that allows for the non-invasive measurement of pial artery pulsation (cc-TQ) and subarachnoid width (sas-TQ) in humans, we assessed the influence of sympathetic activation on the cardiac and respiratory contribution to blood pressure (BP) cc-TQ oscillations in healthy subjects.MethodsThe pial artery and subarachnoid width response to handgrip (HGT) and cold test (CT) were studied in 20 healthy subjects. The cc-TQ and sas-TQ were measured using NIR-T/BSS; cerebral blood flow velocity (CBFV) was measured using Doppler ultrasound of the left internal carotid artery; heart rate (HR) and beat-to-beat mean BP were recorded using a continuous finger-pulse photoplethysmography; respiratory rate (RR), minute ventilation (MV), end-tidal CO2 (EtCO2) and end-tidal O2 (EtO2) were measured using a metabolic and spirometry module of the medical monitoring system. Wavelet transform analysis was used to assess the relationship between BP and cc-TQ oscillations.ResultsHGT evoked an increase in BP (+15.9%; P<0.001), HR (14.7; P<0.001), SaO2 (+0.5; P<0.001) EtO2 (+2.1; P<0.05) RR (+9.2%; P = 0.05) and MV (+15.5%; P<0.001), while sas-TQ was diminished (-8.12%; P<0.001), and a clear trend toward cc-TQ decline was observed (-11.0%; NS). CBFV (+2.9%; NS) and EtCO2 (-0.7; NS) did not change during HGT. CT evoked an increase in BP (+7.4%; P<0.001), sas-TQ (+3.5%; P<0.05) and SaO2(+0.3%; P<0.05). HR (+2.3%; NS), CBFV (+2.0%; NS), EtO2 (-0.7%; NS) and EtCO2 (+0.9%; NS) remained unchanged. A trend toward decreased cc-TQ was observed (-5.1%; NS). The sas-TQ response was biphasic with elevation during the first 40 seconds (+8.8% vs. baseline; P<0.001) and subsequent decline (+4.1% vs. baseline; P<0.05). No change with respect to wavelet coherence and wavelet phase coherence was found between the BP and cc-TQ oscillations.ConclusionsShort sympathetic activation does not affect the cardiac and respiratory contribution to the relationship between BP—cc-TQ oscillations. HGT and CT display divergent effects on the width of the subarachnoid space, an indirect marker of changes in intracranial pressure.