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. 2024 May;12(9):e16027.
doi: 10.14814/phy2.16027.

Dynamic cerebral autoregulation is preserved during orthostasis and intrathoracic pressure regulation in healthy subjects: A pilot study

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Dynamic cerebral autoregulation is preserved during orthostasis and intrathoracic pressure regulation in healthy subjects: A pilot study

M Skytioti et al. Physiol Rep. 2024 May.

Abstract

Resistance breathing may restore cardiac output (CO) and cerebral blood flow (CBF) during hypovolemia. We assessed CBF and cerebral autoregulation (CA) during tilt, resistance breathing, and paced breathing in 10 healthy subjects. Blood velocities in the internal carotid artery (ICA), middle cerebral arteries (MCA, four subjects), and aorta were measured by Doppler ultrasound in 30° and 60° semi-recumbent positions. ICA blood flow and CO were calculated. Arterial blood pressure (ABP, Finometer), and end-tidal CO2 (ETCO2) were recorded. ICA blood flow response was assessed by mixed-models regression analysis. The synchronization index (SI) for the variable pairs ABP-ICA blood velocity, ABP-MCA velocities in 0.005-0.08 Hz frequency interval was calculated as a measure of CA. Passive tilting from 30° to 60° resulted in 12% decrease in CO (p = 0.001); ICA blood flow tended to fall (p = 0.04); Resistance breathing restored CO and ICA blood flow despite a 10% ETCO2 drop. ETCO2 and CO contributed to ICA blood flow variance (adjusted R2: 0.9, p < 0.0001). The median SI was low (<0.2) indicating intact CA, confirmed by surrogate date testing. The peak SI was transiently elevated during resistance breathing in the 60° position. Resistance breathing may transiently reduce CA efficiency. Paced breathing did not restore CO or ICA blood flow.

Keywords: cerebral autoregulation; hemodynamics; impedance threshold device; passive tilting; resistance breathing; synchronization index.

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Conflict of interest statement

We confirm that none of the authors has any conflicts of interests.

Figures

FIGURE 1
FIGURE 1
Raw recordings from one subject. 6 bpm‐30°, paced breathing with six breaths per minute in the 30° position; 6 bpm‐60°, paced breathing with six breaths per minute in the 60° position; CO, cardiac output estimate from Finometer; ETCO2, end‐tidal CO2; HR, heart rate; ITD, impedance threshold device; ITD‐30°, impedance threshold device in the 30° position; ITD‐60°, impedance threshold device in the 60° position; MAP, mean arterial blood pressure; Mean MCA Vel, averaged blood velocity in middle cerebral artery; RF, respiratory frequency; SB‐30°, spontaneous breathing in the 30° position; SB‐60°, spontaneous breathing in the 60° position.
FIGURE 2
FIGURE 2
Individual responses of the blood velocities measured in the right and left middle cerebral artery (R‐MCAvel and L‐MCAvel) and of end‐tidal CO2 (ETCO2) changes at the different experimental states. 6 bpm‐30°, paced breathing with six breaths per minute in the 30° position; 6 bpm‐60°, paced breathing with six breaths per minute in the 60° position; ITD‐30°, impedance threshold device in the 30° position; ITD‐60°, impedance threshold device in the 60° position; SB‐30°, spontaneous breathing in the 30° position; SB‐60°, spontaneous breathing in the 60° position. N = 4.
FIGURE 3
FIGURE 3
Predicted internal carotid artery blood flow (ICABF) response to changes in end‐tidal CO2 (ETCO2), cardiac stroke volume calculated from aorta velocity (SVus), and heart rate (HR). Solid line: mean ICABF response. Blue lines: 95% confidence intervals. Horizontal red dotted line: ICABF response at given ETCO2, SVus, and HR. Vertical red dotted lines: values of ETCO2, SVus, and HR.
FIGURE 4
FIGURE 4
Contour plot of wavelet phase coherence (a), plot of the time‐averaged synchronization index γ for actual signals (black line) and for the random permutation surrogates (RP, orange line) (b), and plot of the frequency‐averaged synchronization index over the duration of the experiment (c), for the variable pair arterial blood pressure (ABP)—right middle cerebral artery blood velocity (rMCAvel). N = 1, same subject as in Figure 1. In this subject, ETCO2, CO, and MAP increased during ITD‐60°.
FIGURE 5
FIGURE 5
Contour plot of wavelet phase coherence (a), plot of the time‐averaged synchronization index γ for actual signals (black line), and for the random permutation surrogates (RP, orange line) (b), and plot of the frequency‐averaged synchronization index γ over the duration of the experiment (c), for the variable pair arterial blood pressure (ABP)—internal carotid artery blood velocity (ICAvel). N = 1 (same subject as in Figures 1 and 4). In supplementary material, similar figures from all 10 subjects can be found.
FIGURE 6
FIGURE 6
Contour plots of the wavelet phase coherence and plots of the time‐averaged gamma (γ) synchronization index for actual signals (black line) and for the random permutation surrogates (RP, orange line) over frequency for the variable pairs: (a) End‐tidal CO2 (ETCO2)‐left MCA velocity (LMCAvel) and (b) ETCO2‐right MCA velocity (RMCAvel) from one subject. Moderate values of synchronization are observed at frequencies below 0.03 Hz, indicating a degree of interrelation between MCA blood velocity and ETCO2.

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