Contribution of arterial blood pressure and PaCO2 to the cerebrovascular responses to motor stimulation

2012 ◽  
Vol 302 (2) ◽  
pp. H459-H466 ◽  
Author(s):  
Ronney B. Panerai ◽  
Angela S. M. Salinet ◽  
Thompson G. Robinson
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Moving Average ◽  
Sudden Change ◽  
Elbow Flexion ◽  
Autoregressive Moving Average Model ◽  
Arterial Blood ◽  
Moving Average Model ◽  
Aged Subjects ◽  
End Tidal

Motor stimulation induces a neurovascular response that can be detected by continuous measurement of cerebral blood flow (CBF). Simultaneous changes in arterial blood pressure (ABP) and PaCO2 have been reported, but their influence on the CBF response has not been quantified. Continuous bilateral recordings of CBF velocity (CBFV), ABP, and end-tidal CO2 (ETCO2) were obtained in 10 healthy middle-aged subjects at rest and during 60 s of repetitive, metronome-controlled (1 Hz) elbow flexion. A multivariate autoregressive-moving average model was adopted to quantify the relationship between beat-to-beat changes in ABP, breath-by-breath ETCO2, and the motor stimulus, represented by the metronome on-off signal (inputs), and the CBFV response to stimulation (output). All three inputs contributed to explain CBFV variance following stimulation. For the ipsi- and contralateral hemispheres, ABP explained 20.3 ± 17.3% ( P = 0.0007) and 19.5 ± 17.2% ( P = 0.01) of CBFV variance, respectively. Corresponding values for ETCO2 and metronome signals were 22.0 ± 24.2% ( P = 0.008), 24.0 ± 24.1% ( P = 0.037), 32.7 ± 22.5% ( P = 0.0015), and 43.2 ± 25.1% ( P = 0.013), respectively. Synchronized population averages suggest that the initial sudden change in CBFV was largely due to ABP, while the influence of ETCO2 was more erratic. The component due to elbow flexion showed a well-defined pattern, with rise time slower than the main CBFV change but reaching a stable plateau after 15 s of stimulation. Identifying and removing the influences of ABP and PaCO2 to motor-induced changes in CBF should lead to more robust estimates of neurovascular coupling and better understanding of its physiological covariates.

Active, passive, and motor imagery paradigms: component analysis to assess neurovascular coupling

2013 ◽  
Vol 114 (10) ◽  
pp. 1406-1412 ◽  
Author(s):  
Angela S. M. Salinet ◽  
Thompson G. Robinson ◽  
Ronney B. Panerai
Keyword(s):  
Motor Imagery ◽  
Moving Average ◽  
Neurovascular Coupling ◽  
Neural Activation ◽  
Autoregressive Moving Average Model ◽  
Arterial Blood ◽  
Moving Average Model ◽  
End Tidal ◽  
The Right ◽  
Cognitive Paradigms

The association between neural activity and cerebral blood flow (CBF) has been used to assess neurovascular coupling (NVC) in health and diseases states, but little attention has been given to the contribution of simultaneous changes in peripheral covariates. We used an innovative approach to assess the contributions of arterial blood pressure (BP), PaCO2, and the stimulus itself to changes in CBF velocities (CBFv) during active (MA), passive (MP), and motor imagery (MI) paradigms. Continuous recordings of CBFv, beat-to-beat BP, heart rate, and breath-by-breath end-tidal CO2 (EtCO2) were performed in 17 right-handed subjects before, during, and after motor-cognitive paradigms performed with the right arm. A multivariate autoregressive-moving average model was used to calculate the separate contributions of BP, EtCO2, and the neural activation stimulus (represented by a metronome on-off signal) to the CBFv response during paradigms. Differences were found in the bilateral CBFv responses to MI compared with MA and MP, due to the contributions of stimulation ( P < 0.05). BP was the dominant contributor to the initial peaked CBFv response in all paradigms with no significant differences between paradigms, while the contribution of the stimulus explained the plateau phase and extended duration of the CBFv responses. Separating the neural activation contribution from the influences of other covariates, it was possible to detect differences between three paradigms often used to assess disease-related NVC. Apparently similar CBFv responses to different motor-cognitive paradigms can be misleading due to the contributions from peripheral covariates and could lead to inaccurate assessment of NVC, particularly during MI.

scholarly journals Cerebrovascular effects of the thigh cuff maneuver

2015 ◽  
Vol 308 (7) ◽  
pp. H688-H696 ◽  
Author(s):  
R. B. Panerai ◽  
N. P. Saeed ◽  
T. G. Robinson
Keyword(s):  
Cerebral Blood Flow Velocity ◽  
Moving Average ◽  
Autoregressive Moving Average ◽  
Strongly Correlated ◽  
Mean Values ◽  
Autoregressive Moving Average Model ◽  
Arterial Blood ◽  
Moving Average Model ◽  
Area Product ◽  
End Tidal

Arterial hypotension can be induced by sudden release of inflated thigh cuffs (THC), but its effects on the cerebral circulation have not been fully described. In nine healthy subjects [aged 59 (9) yr], bilateral cerebral blood flow velocity (CBFV) was recorded in the middle cerebral artery (MCA), noninvasive arterial blood pressure (BP) in the finger, and end-tidal CO2 (ETCO2) with nasal capnography. Three THC maneuvers were performed in each subject with cuff inflation 20 mmHg above systolic BP for 3 min before release. Beat-to-beat values were extracted for mean CBFV, BP, ETCO2, critical closing pressure (CrCP), resistance-area product (RAP), and heart rate (HR). Time-varying estimates of the autoregulation index [ARI( t)] were also obtained using an autoregressive-moving average model. Coherent averages synchronized by the instant of cuff release showed significant drops in mean BP, CBFV, and RAP with rapid return of CBFV to baseline. HR, ETCO2, and ARI( t) were transiently increased, but CrCP remained relatively constant. Mean values of ARI( t) for the 30 s following cuff release were not significantly different from the classical ARI [right MCA 5.9 (1.1) vs. 5.1 (1.6); left MCA 5.5 (1.4) vs. 4.9 (1.7)]. HR was strongly correlated with the ARI( t) peak after THC release (in 17/22 and 21/24 recordings), and ETCO2 was correlated with the subsequent drop in ARI( t) (19/22 and 20/24 recordings). These results suggest a complex cerebral autoregulatory response to the THC maneuver, dominated by myogenic mechanisms and influenced by concurrent changes in ETCO2 and possible involvement of the autonomic nervous system and baroreflex.

scholarly journals Directional sensitivity of dynamic cerebral autoregulation in squat-stand maneuvers

2018 ◽  
Vol 315 (4) ◽  
pp. R730-R740 ◽  
Author(s):  
Ronney B. Panerai ◽  
Sam C. Barnes ◽  
Mintu Nath ◽  
Naomi Ball ◽  
Thompson G. Robinson ◽  
...  
Keyword(s):  
Cerebral Autoregulation ◽  
Moving Average ◽  
Nonlinear Behavior ◽  
Directional Sensitivity ◽  
Autoregressive Moving Average Model ◽  
Arterial Blood ◽  
Cerebral Blood Velocity ◽  
Young Subjects ◽  
End Tidal ◽  
Dynamic Cerebral Autoregulation

Dynamic cerebral autoregulation (CA), the transient response of cerebral blood flow (CBF) to rapid changes in arterial blood pressure (BP), is usually modeled as a linear mechanism. We tested the hypothesis that dynamic CA can display nonlinear behavior resulting from differential efficiency dependent on the direction of BP changes. Cerebral blood velocity (CBV) (transcranial Doppler), heart rate (HR) (three-lead ECG), continuous BP (Finometer), and end-tidal CO2 (capnograph) were measured in 10 healthy young subjects during 15 squat-stand maneuvers (SSM) with a frequency of 0.05 Hz. The protocol was repeated with a median (interquartile range) of 44 (35–64) days apart. Dynamic CA was assessed with the autoregulation index (ARI) obtained from CBV step responses estimated with an autoregressive moving-average model. Mean BP, HR, and CBV were different (all P < 0.001) between squat and stand, regardless of visits. ARI showed a strong interaction ( P < 0.001) of SSM with the progression of transients; in general, the mean ARI was higher for the squat phase compared with standing. The changes in ARI were partially explained by concomitant changes in CBV ( P = 0.023) and pulse pressure ( P < 0.001), but there was no evidence that ARI differed between visits ( P = 0.277). These results demonstrate that dynamic CA is dependent on the direction of BP change, but further work is needed to confirm if this finding can be generalized to other physiological conditions and also to assess its dependency on age, sex and pathology.

scholarly journals Multiple-input nonlinear modelling of cerebral haemodynamics using spontaneous arterial blood pressure, end-tidal CO 2  and heart rate measurements

2016 ◽  
Vol 374 (2067) ◽  
pp. 20150180 ◽  
Author(s):  
V. Z. Marmarelis ◽  
G. D. Mitsis ◽  
D. C. Shin ◽  
R. Zhang
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Prediction Error ◽  
Cerebral Blood Flow Velocity ◽  
Cerebral Arteries ◽  
Cerebral Haemodynamics ◽  
Functional Connection ◽  
Arterial Blood ◽  
End Tidal

In order to examine the effect of changes in heart rate (HR) upon cerebral perfusion and autoregulation, we include the HR signal recorded from 18 control subjects as a third input in a two-input model of cerebral haemodynamics that has been used previously to quantify the dynamic effects of changes in arterial blood pressure and end-tidal CO 2 upon cerebral blood flow velocity (CBFV) measured at the middle cerebral arteries via transcranial Doppler ultrasound. It is shown that the inclusion of HR as a third input reduces the output prediction error in a statistically significant manner, which implies that there is a functional connection between HR changes and CBFV. The inclusion of nonlinearities in the model causes further statistically significant reduction of the output prediction error. To achieve this task, we employ the concept of principal dynamic modes (PDMs) that yields dynamic nonlinear models of multi-input systems using relatively short data records. The obtained PDMs suggest model-driven quantitative hypotheses for the role of sympathetic and parasympathetic activity (corresponding to distinct PDMs) in the underlying physiological mechanisms by virtue of their relative contributions to the model output. These relative PDM contributions are subject-specific and, therefore, may be used to assess personalized characteristics for diagnostic purposes.

Ventilatory response to isocapnic hyperoxia

1995 ◽  
Vol 78 (2) ◽  
pp. 696-701 ◽  
Author(s):  
H. Becker ◽  
O. Polo ◽  
S. G. McNamara ◽  
M. Berthon-Jones ◽  
C. E. Sullivan
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Minute Ventilation ◽  
Normobaric Hyperoxia ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Blood Gas Analyses ◽  
End Tidal ◽  
Arterial Po2

Breathing O2 for up to 1 h has been shown to either not influence or slightly increase (6–13%) minute ventilation. However, end-tidal PCO2 was not kept constant in these experiments. In nine healthy men, we studied the ventilatory, blood pressure, and heart rate responses to 30 min of normobaric hyperoxia (50% O2) at isocapnic conditions. Hyperoxia led to a 60% increase in mean minute ventilation (P = 0.002), largely due to an increase in mean tidal volume from 0.66 +/- 0.04 (SE) to 0.88 +/- 0.05 liter (P = 0.007). Fifteen minutes after the termination of hyperoxia, minute ventilation was still increased (P = 0.02) compared with baseline, although it was reduced compared with hyperoxia (P = 0.02). Arterial blood gas analyses in six subjects before and during hyperoxia showed an increase in arterial PO2 and O2 saturation but no change in arterial PCO2 or pH. Hyperoxia induced no changes in arterial blood pressure or heart rate. We conclude that 1) isocapnic hyperoxia stimulates respiration markedly, an effect that is approximately five times higher than previously measured; 2) the increase in ventilation induced by hyperoxia does not affect arterial blood pressure and heart rate; and 3) in experiments using hyperoxia, its effect on breathing and subsequently on PCO2 has to be taken into account.

Cerebral blood flow responses to changes in oxygen and carbon dioxide in humans

2002 ◽  
Vol 80 (8) ◽  
pp. 819-827 ◽  
Author(s):  
Andrea Vovk ◽  
David A Cunningham ◽  
John M Kowalchuk ◽  
Donald H Paterson ◽  
James Duffin
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
Arterial Blood Pressure ◽  
Cerebral Artery ◽  
Mean Arterial Blood Pressure ◽  
Transcranial Doppler Ultrasound ◽  
Arterial Blood ◽  
End Tidal

This study characterized cerebral blood flow (CBF) responses in the middle cerebral artery to PCO2ranging from 30 to 60 mmHg (1 mmHg = 133.322 Pa) during hypoxia (50 mmHg) and hyperoxia (200 mmHg). Eight subjects (25 ± 3 years) underwent modified Read rebreathing tests in a background of constant hypoxia or hyperoxia. Mean cerebral blood velocity was measured using a transcranial Doppler ultrasound. Ventilation (VE), end-tidal PCO2 (PETCO2), and mean arterial blood pressure (MAP) data were also collected. CBF increased with rising PETCO2 at two rates, 1.63 ± 0.21 and 2.75 ± 0.27 cm·s–1·mmHg–1 (p < 0.05) during hypoxic and 1.69 ± 0.17 and 2.80 ± 0.14 cm·s–1·mmHg–1 (p < 0.05) during hyperoxic rebreathing. VE also increased at two rates (5.08 ± 0.67 and 10.89 ± 2.55 L·min–1·mmHg–1 and 3.31 ± 0.50 and 7.86 ± 1.43 L·min–1·mmHg–1) during hypoxic and hyperoxic rebreathing. MAP and PETCO2 increased linearly during both hypoxic and hyperoxic rebreathing. The breakpoint separating the two-component rise in CBF (42.92 ± 1.29 and 49.00 ± 1.56 mmHg CO2 during hypoxic and hyperoxic rebreathing) was likely not due to PCO2 or perfusion pressure, since PETCO2 and MAP increased linearly, but it may be related to VE, since both CBF and VE exhibited similar responses, suggesting that the two responses may be regulated by a common neural linkage. Key words: brain blood flow, middle cerebral artery, ventilation, mean arterial blood pressure.

scholarly journals Rapid Declines in Systolic Blood Pressure Are Associated With an Increase in Pulse Transit Time

2020 ◽  
Author(s):  
Sebastian Schaanning ◽  
Nils Kristian Skjærvold
Keyword(s):  
Blood Pressure ◽  
Linear Regression ◽  
Systolic Blood Pressure ◽  
Arterial Blood Pressure ◽  
Transit Time ◽  
Medical Information ◽  
Moving Average ◽  
Pulse Transit Time ◽  
Non Invasive ◽  
Arterial Blood

Abstract Background : Substantial investigation has been made into the correlation between Pulse Transit Time (PTT) and Blood Pressure (BP), as a possible route to achieve continuous non-invasive measurement of BP (cNIBP). We investigated whether PTT-trends could model BP-trends during episodes of rapid declines in Systolic Blood Pressure (SBP). Methods: From the freely available Medical Information Mart for Intensive Care (MIMIC-III) waveform database, we identified subjects who experienced a reduction in SBP from ≥ 120mmHg to ≤ 90 mmHg during a period of ≤ 15 minutes, for whom complete peak detection was possible. SBP was extracted from the Arterial Blood Pressure (ABP) waveform, and PTT was calculated from the R-peak of the ECG to the peak of the ABP waveform. Both SBP and PTT were processed using a moving average filter, yielding the variables SBP AV and PTT-RA AV . A moving average of continuous heart rate (HR AV ) was also analysed as a negative control to assess the effect of averaging. The intra-individual association between variables was assessed per subject using linear regression. Results: 511 patients were included for the main analysis. Median correlation coefficients (r) obtained from linear regression versus SBP AV were as follows: PTT-RA AV -0.93 (IQR -0.98 to -0.76), HR AV 0.46 (IQR -0.16 to 0.83). Regression slopes for the relationship between SBP AV and PTT-RA AV displayed a median of -2.46 mmHg/ms (IQR -3.47 mmHg/ms to -1.61 mmHg/ms). In supplementary analysis, results did not differ substantially when widening inclusion criteria, but the results were not always consistent within subjects across episodes of hypotension. Conclusions: In a large cohort of critically ill patients experiencing episodes of rapid declines in systolic blood pressure, there was a moderate-strong intra-individual correlation between averaged systolic blood pressure and averaged pulse transit time as measured from ECG R-peak to the peak of the arterial blood pressure waveform. Our findings encourage further investigation into using the pulse transit time for non-invasive real-time detection of hypotension.

Sign in / Sign up

Export Citation Format

Share Document