Wojciech Guminski

Influence of Acute Jugular Vein Compression on the Cerebral Blood Flow Velocity, Pial Artery Pulsation and Width of Subarachnoid Space in Humans

Purpose The aim of this study was to assess the effect of acute bilateral jugular vein compression on: (1) pial artery pulsation (cc-TQ); (2) cerebral blood flow velocity (CBFV); (3) peripheral blood pressure; and (4) possible relations between mentioned parameters. Methods Experiments were performed on a group of 32 healthy 19–30 years old male subjects. cc-TQ and the subarachnoid width (sas-TQ) were measured using near-infrared transillumination/backscattering sounding (NIR-T/BSS), CBFV in the left anterior cerebral artery using transcranial Doppler, blood pressure was measured using Finapres, while end-tidal CO2 was measured using medical gas analyser. Bilateral jugular vein compression was achieved with the use of a sphygmomanometer held on the neck of the participant and pumped at the pressure of 40 mmHg, and was performed in the bend-over (BOPT) and swayed to the back (initial) position. Results In the first group (n = 10) during BOPT, sas-TQ and pulse pressure (PP) decreased (−17.6% and −17.9%, respectively) and CBFV increased (+35.0%), while cc-TQ did not change (+1.91%). In the second group, in the initial position (n = 22) cc-TQ and CBFV increased (106.6% and 20.1%, respectively), while sas-TQ and PP decreases were not statistically significant (−15.5% and −9.0%, respectively). End-tidal CO2 remained stable during BOPT and venous compression in both groups. Significant interdependence between changes in cc-TQ and PP after bilateral jugular vein compression in the initial position was found (r = −0.74). Conclusions Acute bilateral jugular venous insufficiency leads to hyperkinetic cerebral circulation characterised by augmented pial artery pulsation and CBFV and direct transmission of PP into the brain microcirculation. The Windkessel effect with impaired jugular outflow and more likely increased intracranial pressure is described. This study clarifies the potential mechanism linking jugular outflow insufficiency with arterial small vessel cerebral disease.

Technical foundations for noninvasive assessment of changes in the width of the subarachnoid space with near-infrared transillumination-backscattering sounding (NIR-TBSS)

This paper presents technical foundations for a new technique of near-infrared transillumination-backscattering sounding, which is designed to enable noninvasive detection and monitoring of changes in the width of the subarachnoid space (SAS) and magnitude of cerebrovascular pulsation in humans. The key novelty of the technique is elimination of influence of blood flow in the scalp on the signals received from two infrared sensors-proximal and distal. A dedicated digital algorithm is used to estimate on line the ratio of the powers of received signals, referred to as two-sensor distal-to-proximal received power quotient, TQ (t). The propagation duct for NIR radiation reaching the distal sensor is the SAS filled with translucent cerebrospinal fluid. Information on slow fluctuations of the average width of the SAS is contained in the slow-variable part of the TQ (t), called the subcardiac component, and in TQ itself. Variations in frequency and magnitude of faster oscillations of the width of that space around the baseline value, dependent on cerebrovascular pulsation, are reflected in instantaneous frequency and envelope of the fast-variable component. Frequency and magnitude of the cerebrovascular pulsation depend on the action of the heart, so this fast-variable component is referred to as the cardiac component.

Effect of Maximal Apnoea Easy-Going and Struggle Phases on Subarachnoid Width and Pial Artery Pulsation in Elite Breath-Hold Divers

Purpose The aim of the study was to assess changes in subarachnoid space width (sas-TQ), the marker of intracranial pressure (ICP), pial artery pulsation (cc-TQ) and cardiac contribution to blood pressure (BP), cerebral blood flow velocity (CBFV) and cc-TQ oscillations throughout the maximal breath hold in elite apnoea divers. Non-invasive assessment of sas-TQ and cc-TQ became possible due to recently developed method based on infrared radiation, called near-infrared transillumination/backscattering sounding (NIR-T/BSS). Methods The experimental group consisted of seven breath-hold divers (six men). During testing, each participant performed a single maximal end-inspiratory breath hold. Apnoea consisted of the easy-going and struggle phases (characterised by involuntary breathing movements (IBMs)). Heart rate (HR) was determined using a standard ECG. BP was assessed using the photoplethysmography method. SaO2 was monitored continuously with pulse oximetry. A pneumatic chest belt was used to register thoracic and abdominal movements. Cerebral blood flow velocity (CBFV) was estimated by a 2-MHz transcranial Doppler ultrasonic probe. sas-TQ and cc-TQ were measured using NIR-T/BSS. Wavelet transform analysis was performed to assess cardiac contribution to BP, CBFV and cc-TQ oscillations. Results Mean BP and CBFV increased compared to baseline at the end of the easy phase and were further augmented by IBMs. cc-TQ increased compared to baseline at the end of the easy phase and remained stable during the IBMs. HR did not change significantly throughout the apnoea, although a trend toward a decrease during the easy phase and recovery during the IBMs was visible. Amplitudes of BP, CBFV and cc-TQ were augmented. sas-TQ and SaO2 decreased at the easy phase of apnoea and further decreased during the IBMs. Conclusions Apnoea increases intracranial pressure and pial artery pulsation. Pial artery pulsation seems to be stabilised by the IBMs. Cardiac contribution to BP, CBFV and cc-TQ oscillations does not change throughout the apnoea.

Effects of acute hypercapnia on the amplitude of cerebrovascular pulsation in humans registered with a non-invasive method.

AIM The aim of the study was to assess non-invasively the effects of acute hypercapnia on the amplitude of cerebrovascular pulsation (CVP) in humans. METHODS Experiments were carried out in four male volunteers aged 25, 26, 31 and 49. Changes in blood flow through the pial arteries were induced using two interventions: (A) breathing a gas mixture containing 5% CO(2) for 2 minutes and (B) intravenous administration of 1g acetazolamide. The amplitude of CVP and width of subarachnoid space (SAS) were measured non-invasively using near-infrared transillumination/backscattering sounding (NIR-T/BSS), while cerebral blood flow was assessed by single photon emission computed tomography (SPECT) and mean blood flow velocity in the left anterior cerebral artery by transcranial Doppler. RESULTS Inhalation of a gas mixture containing 5% CO(2) evoked an increase in the amplitude of CVP (202.5% ± SE 10.1), normalized number of counts (22.6% ± SE 3.5%) and mean blood flow velocity in the left cerebral anterior artery (37.6%± SE 11.7%), while resistive index decreased (-8.7% ± SE 2.3%) and the width of SAS decreased (-8.0 ± SE 0.45). Acetazolamide also produced an increase in the amplitude of CVP (23.7% ± SE 5.4%), normalized number of counts (7.9% ± SE 1.1%), and mean blood flow velocity in the left cerebral anterior artery (62.8% ± SE 13.7%), while resistive index decreased (-7.9% ± SE 1.7%), and the width of SAS decreased (-13.4% ± SE 3.4%). CONCLUSION Acute hypercapnia causes an increase in the amplitude of CVP pulsation in humans. NIR-T/BSS allows for non-invasive bedside monitoring of the amplitude of CVP. NIR-T/BSS is consistent with transcranial Doppler and SPECT.

Wavelet transform analysis to assess oscillations in pial artery pulsation at the human cardiac frequency

Pial artery adjustments to changes in blood pressure (BP) may last only seconds in humans. Using 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) in humans, we aimed to assess the relationship between spontaneous oscillations in BP and cc-TQ at frequencies between 0.5 Hz and 5 Hz. We hypothesized that analysis of very short data segments would enable the estimation of changes in the cardiac contribution to the BP vs. cc-TQ relationship during very rapid pial artery adjustments to external stimuli. BP and pial artery oscillations during baseline (70s and 10s signals) and the response to maximal breath-hold apnea were studied in eighteen healthy subjects. The cc-TQ was measured using NIR-T/BSS; cerebral blood flow velocity, the pulsatility index and the resistive index were measured using Doppler ultrasound of the left internal carotid artery; heart rate and beat-to-beat systolic and diastolic blood pressure were recorded using a Finometer; end-tidal CO2 was measured using a medical gas analyzer. Wavelet transform analysis was used to assess the relationship between BP and cc-TQ oscillations. The recordings lasting 10s and representing 10 cycles with a frequency of ~1 Hz provided sufficient accuracy with respect to wavelet coherence and wavelet phase coherence values and yielded similar results to those obtained from approximately 70cycles (70s). A slight but significant decrease in wavelet coherence between augmented BP and cc-TQ oscillations was observed by the end of apnea. Wavelet transform analysis can be used to assess the relationship between BP and cc-TQ oscillations at cardiac frequency using signals intervals as short as 10s. Apnea slightly decreases the contribution of cardiac activity to BP and cc-TQ oscillations.

Sympathetic Activation Does Not Affect the Cardiac and Respiratory Contribution to the Relationship between Blood Pressure and Pial Artery Pulsation Oscillations in Healthy Subjects

Introduction Using 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. Methods The 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. Results HGT 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. Conclusions Short 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.

Pial artery and subarachnoid width response to apnoea in normal humans.

Background: Little is known about intracranial pressure (ICP)-cerebral haemodynamic interplay during repetitive apnoea. A recently developed method based on near-infrared transillumination/backscattering sounding (NIR-T/BSS) noninvasively measures changes in pial artery pulsation (cc-TQ) as well as subarachnoid width (sas-TQ) in humans. Method: We tested the complex response of the pial artery and subarachnoid width to apnoea using this method. The pial artery and subarachnoid width response to consecutive apnoeas lasting 30, 60 s and maximal breath-hold (91.1 ± 23.1 s) were studied in 20 healthy volunteers. The cc-TQ and sas-TQ were measured using NIR-T/BSS; cerebral blood flow velocity (CBFV), pulsatility index and resistive index were measured using Doppler ultrasound of the left internal carotid artery; heart rate (HR) and beat-to-beat SBP and DBP blood pressure were recorded using a Finometer; end-tidal CO2 (EtCO2) was measured using a medical gas analyser. Results: Apnoea evoked a multiphasic response in blood pressure, pial artery compliance and ICP. First, SBP declined, which was accompanied by an increase in cc-TQ and sas-TQ. Directly after these changes, SBP exceeded baseline values, which was followed by a decline in cc-TQ and the return of sas-TQ to baseline. During these initial changes, CBFV remained stable. Towards the end of the apnoea, BP, cc-TQ and CBFV increased, whereas pulsatility index, resistive index and sas-TQ declined. Changes in sas-TQ were linked to changes in EtCO2, HR and SBP. Conclusion: Apnoea is associated with ICP swings, closely reflecting changes in EtCO2, HR and peripheral BP. The baroreflex influences the pial artery response.

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.

Human subarachnoid space width oscillations in the resting state

Abnormal cerebrospinal fluid (CSF) pulsatility has been implicated in patients suffering from various diseases, including multiple sclerosis and hypertension. CSF pulsatility results in subarachnoid space (SAS) width changes, which can be measured with near-infrared transillumination backscattering sounding (NIR-T/BSS). The aim of this study was to combine NIR-T/BSS and wavelet analysis methods to characterise the dynamics of the SAS width within a wide range of frequencies from 0.005 to 2 Hz, with low frequencies studied in detail for the first time. From recordings in the resting state, we also demonstrate the relationships between SAS width in both hemispheres of the brain, and investigate how the SAS width dynamics is related to the blood pressure (BP). These investigations also revealed influences of age and SAS correlation on the dynamics of SAS width and its similarity with the BP. Combination of NIR-T/BSS and time-frequency analysis may open up new frontiers in the understanding and diagnosis of various neurodegenerative and ageing related diseases to improve diagnostic procedures and patient prognosis.

[PP.17.01] INCREASED INSPIRATORY RESISTANCE AFFECTS THE CARDIAC CONTRIBUTION TO THE RELATIONSHIP BETWEEN BLOOD PRESSURE AND PIAL ARTERY PULSATION OSCILLATIONS

Objective: There is increasing evidence that heart performance directly influences cerebral perfusion. We hypothesised that increased inspiratory resistance would affect the cardiac contribution to the relationship between blood pressure and pial artery pulsation oscillations. Design and method: Experiments were performed in a group of 20 healthy volunteers undergoing controlled intermittent Mueller Manoeuvers. Blood pressure and heart rate were measured using continuous finger-pulse photoplethysmography; oxyhaemoglobin saturation with an ear-clip sensor; end-tidal CO2 with a gas analyser; cerebral blood flow velocity, pulsatility and resistive indices with Doppler ultrasound. Changes in the pial artery pulsation and in the width of subarachnoid space were recorded with a new method called near-infrared transillumination/backscattering sounding. Wavelet transform analysis was used to assess the relationship between blood pressure and pial artery pulsation oscillations. Results: Initiating Mueller manoeuvers evoked pial artery pulsation decline (by 18% vs. baseline; P < 0.001), blood pressure and heart rate increase (by 6% P < 0.001, and 3% P < 0.05, respectively). By the end of Mueller manoeuvers, pial artery pulsation and heart rate did not change, but blood pressure was elevated (by 12% vs. baseline; P < 0.001). A decrease in wavelet coherence between blood pressure and pial artery pulsation oscillations at cardiac frequency found in the first half of the Mueller manoeuvers was followed by recovery by the end of Mueller manoeuvers (Tab.). Wavelet phase coherence was high at baseline and did not change throughout the Mueller manoeuvers (Tab.). Tab.: Effects of a 60 s Mueller manoeuvres series on WCO and WPCO between BP and cc-TQpial artery pulsation. Figure. No caption available. Caption: *P < 0.05; **P < 0.01; ***P < 0.001; WCO – wavelet coherence; WPCO – wavelet phase coherence; cc-TQ – cardiac component of transillumination quotient (pial artery pulsation); left – left hemisphere; right – right hemisphere; SD – standard deviation. Conclusions: Increased inspiratory resistance is associated with swings in the cardiac contribution to the dynamic relationship between blood pressure and pial artery pulsation oscillations. Impaired cardiac performance seen during Mueller manoeuvers may be transmitted to the cerebral microcirculation.