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Dynamic cerebral autoregulation across the cardiac cycle during 8 hr of recovery from acute exercise.

ABSTRACT: Current protocols examining cerebral autoregulation (CA) parameters require participants to refrain from exercise for 12-24 hr, however there is sparse objective evidence examining the recovery trajectory of these measures following exercise across the cardiac cycle (diastole, mean, and systole). Therefore, this study sought to determine the duration acute exercise impacts CA and the within-day reproducibility of these measures. Nine participants performed squat-stand maneuvers at 0.05 and 0.10 Hz at baseline before three interventions: 45-min moderate-continuous exercise (at 50% heart-rate reserve), 30-min high-intensity intervals (ten, 1-min at 85% heart-rate reserve), and a control day (30-min quiet rest). Squat-stands were repeated at hours zero, one, two, four, six, and eight after each condition. Transcranial doppler ultrasound of the middle cerebral artery (MCA) and the posterior cerebral artery (PCA) was used to characterize CA parameters across the cardiac cycle. At baseline, the systolic CA parameters were different than mean and diastolic components (ps < 0.015), however following both exercise protocols in both frequencies this disappeared until hour four within the MCA (ps > 0.079). In the PCA, phase values were affected only following high-intensity intervals until hour four (ps > 0.055). Normalized gain in all cardiac cycle domains remained different following both exercise protocols (ps < 0.005) and across the control day (p < .050). All systolic differences returned by hour six across all measures (ps < 0.034). Future CA studies may use squat-stand maneuvers to assess the cerebral pressure-flow relationship 6 hr after exercise. Finally, CA measures under this paradigm appear to have negligible within-day variation, allowing for reproducible interpretations to be drawn.

SUBMITTER: Burma JS

PROVIDER: S-EPMC7066871 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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Dynamic cerebral autoregulation across the cardiac cycle during 8 hr of recovery from acute exercise.

Burma Joel S JS Copeland Paige P Macaulay Alannah A Khatra Omeet O Wright Alexander D AD Smirl Jonathan D JD

Physiological reports 20200301 5

Current protocols examining cerebral autoregulation (CA) parameters require participants to refrain from exercise for 12-24 hr, however there is sparse objective evidence examining the recovery trajectory of these measures following exercise across the cardiac cycle (diastole, mean, and systole). Therefore, this study sought to determine the duration acute exercise impacts CA and the within-day reproducibility of these measures. Nine participants performed squat-stand maneuvers at 0.05 and 0.10 ...[more]

PMID: 32163235

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Project description:BackgroundClassically, cerebral autoregulation (CA) entails cerebral blood flow (CBF) remaining constant by cerebrovascular tone adapting to fluctuations in mean arterial pressure (MAP) between ∼60 and ∼150 mmHg. However, this is not an on-off mechanism; previous work has suggested that vasomotor tone is proportionally related to CA function. During propofol-based anaesthesia, there is cerebrovascular vasoconstriction, and static CA remains intact. Sevoflurane-based anaesthesia induces cerebral vasodilation and attenuates CA dose-dependently. It is unclear how this translates to dynamic CA across a range of blood pressures in the autoregulatory range.ObjectiveThe aim of this study was to quantify the effect of step-wise increases in MAP between 60 and 100 mmHg, using phenylephrine, on dynamic CA during propofol- and sevoflurane-based anaesthesia.DesignA nonrandomised interventional trial.SettingSingle centre enrolment started on 11 January 2019 and ended on 23 September 2019.PatientsWe studied American Society of Anesthesiologists (ASA) I/II patients undergoing noncardiothoracic, nonneurosurgical and nonlaparoscopic surgery under general anaesthesia.InterventionIn this study, cerebrovascular tone was manipulated in the autoregulatory range by increasing MAP step-wise using phenylephrine in patients receiving either propofol- or sevoflurane-based anaesthesia. MAP and mean middle cerebral artery blood velocity (MCA Vmean ) were measured in ASA I and II patients, anaesthetised with either propofol ( n = 26) or sevoflurane ( n = 28), during 10 mmHg step-wise increments of MAP between 60 and 100 mmHg. Static CA was determined by plotting 2-min averaged MCA Vmean versus MAP. Dynamic CA was determined using transfer function analysis and expressed as the phase lead (°) between MAP and MCA Vmean oscillations, created with positive pressure ventilation with a frequency of 6 min -1 .Main outcomesThe primary outcome of this study was the response of dynamic CA during step-wise increases in MAP during propofol- and sevoflurane-based anaesthesia.ResultsMAP levels achieved per step-wise increments were comparable between anaesthesia regiment (63 ± 3, 72 ± 2, 80 ± 2, 90 ± 2, 100 ± 3 mmHg, and 61 ± 4, 71 ± 2, 80 ± 2, 89 ± 2, 98 ± 4 mmHg for propofol and sevoflurane, respectively). MCA Vmean increased more during step-wise MAP increments for sevoflurane compared to propofol ( P ≤0.001). Dynamic CA improved during propofol (0.73° mmHg -1 , 95% CI 0.51 to 0.95; P ≤ 0.001)) and less pronounced during sevoflurane-based anaesthesia (0.21° mmHg -1 (95% CI 0.01 to 0.42, P = 0.04).ConclusionsDuring general anaesthesia, dynamic CA is dependent on MAP, also within the autoregulatory range. This phenomenon was more pronounced during propofol anaesthesia than during sevoflurane.Trial registrationNCT03816072 ( https://clinicaltrials.gov/ct2/show/NCT03816072 ).

Project description:Dynamic cerebral autoregulation (DCA) is the continuous counterregulation of cerebral blood flow to fluctuations in blood pressure. DCA can become impaired after acute stroke, but it remains unclear to what extent and over what interval this occurs.We included 28 patients (NIHSS = 12 ± 6.5, age = 68.4 ± 17.1, 16F) with acute large-vessel ischemic stroke in the middle cerebral artery territory and 29 healthy controls (mean age 54.9 ± 9, 16F). DCA was assessed by simultaneous measurement of blood pressure together with blood flow velocities using finger plethysmography/arterial catheter and transcranial Doppler over three 10-minute recordings on days 0-2, 3-6 and ?7 days after stroke. Transfer function analysis was applied to calculate average phase shift (PS) in the low frequency range (0.06-0.12 Hz). Less PS indicated poorer autoregulation. The affected side was compared with the unaffected side and controls. Univariate comparisons of data were performed using t tests at single time points, and generalized estimating equations with an exchangeable correlation matrix to examine the change in PS over time.At mean 1.3 ± 0.5 days after stroke the average PS in the affected hemisphere was 29.6 ± 10.5 vs. 42.5 ± 13 degrees in the unaffected hemisphere (p = 0.004). At 4.1 ± 1 days, the PS in affected and unaffected hemisphere was 23.2 ± 19.1 vs. 41.7 ± 18.5 degrees, respectively (p = 0.003). At mean 9.75 ± 2.2 days stroke there was no difference between the affected and the unaffected hemisphere (53.2 ± 28.2 vs. 50.7 ± 29.2 degrees, p = 0.69). Control subjects had an average PS = 47.9 ± 16.8, significantly different from patients' affected hemisphere at the first two measurements (p = 0.001), but not the third (p = 0.37). The PS in controls remained unchanged on repeat testing after an average 19.1 days (48.4 ± 17.1, p = 0.61). Using the last recording as the reference, the average PS in the affected hemisphere was -23.54 (-44.1, -3) degrees lower on recording one (p = 0.025), and -31.6 (-56.1, -7.1) degrees lower on recording two (p < 0.011). Changes in the unaffected hemisphere over time were nonsignificant.These data suggest that dynamic cerebral autoregulation is impaired in the affected hemisphere throughout the first week after large-vessel ischemic stroke, and then normalizes by week two. These findings may have important implications for acute blood pressure management after stroke.

Project description:Objective: Cerebral autoregulation limits the variability of cerebral blood flow (CBF) in the presence of systemic arterial blood pressure (ABP) changes. Monitoring cerebral autoregulation is important in the Neurocritical Care Unit (NCCU) to assess cerebral health. Here, our goal is to identify optimal frequency-domain near-infrared spectroscopy (FD-NIRS) parameters and apply a hemodynamic model of coherent hemodynamics spectroscopy (CHS) to assess cerebral autoregulation in healthy adult subjects and NCCU patients. Methods: In five healthy subjects and three NCCU patients, ABP oscillations at a frequency around 0.065 Hz were induced by cyclic inflation-deflation of pneumatic thigh cuffs. Transfer function analysis based on wavelet transform was performed to measure dynamic relationships between ABP and oscillations in oxy- (O), deoxy- (D), and total- (T) hemoglobin concentrations measured with different FD-NIRS methods. In healthy subjects, we also obtained the dynamic CBF-ABP relationship by using FD-NIRS measurements and the CHS model. In healthy subjects, an interval of hypercapnia was performed to induce cerebral autoregulation impairment. In NCCU patients, the optical measurements of autoregulation were linked to individual clinical diagnoses. Results: In healthy subjects, hypercapnia leads to a more negative phase difference of both O and D oscillations vs. ABP oscillations, which are consistent across different FD-NIRS methods and are highly correlated with a more negative phase difference CBF vs. ABP. In the NCCU, a less negative phase difference of D vs. ABP was observed in one patient as compared to two others, indicating a better autoregulation in that patient. Conclusions: Non-invasive optical measurements of induced phase difference between D and ABP show the strongest sensitivity to cerebral autoregulation. The results from healthy subjects also show that the CHS model, in combination with FD-NIRS, can be applied to measure the CBF-ABP dynamics for a better direct measurement of cerebral autoregulation.

Project description:Breath-hold divers (BHD) experience repeated bouts of severe hypoxia and hypercapnia with large increases in blood pressure. However, the impact of long-term breath-hold diving on cerebrovascular control remains poorly understood. The ability of cerebral blood vessels to respond rapidly to changes in blood pressure represents the property of dynamic autoregulation. The current investigation tested the hypothesis that breath-hold diving impairs dynamic autoregulation to a transient hypotensive stimulus. Seventeen BHD (3 women, 11?±?9 yr of diving) and 15 healthy controls (2 women) completed two or three repeated sit-to-stand trials during spontaneous breathing and poikilocapnic conditions. Heart rate (HR), finger arterial blood pressure (BP), and cerebral blood flow velocity (BFV) from the right middle cerebral artery were measured continuously with three-lead electrocardiography, finger photoplethysmography, and transcranial Doppler ultrasonography, respectively. End-tidal carbon dioxide partial pressure was measured with a gas analyzer. Offline, an index of cerebrovascular resistance (CVRi) was calculated as the quotient of mean BP and BFV. The rate of the drop in CVRi relative to the change in BP provided the rate of regulation [RoR; (?CVRi/?T)/?BP]. The BHD demonstrated slower RoR than controls (P ? 0.001, d?=?1.4). Underlying the reduced RoR in BHD was a longer time to reach nadir CVRi compared with controls (P = 0.004, d?=?1.1). In concert with the longer CVRi response, the time to reach peak BFV following standing was longer in BHD than controls (P = 0.01, d?=?0.9). The data suggest impaired dynamic autoregulatory mechanisms to hypotension in BHD. NEW & NOTEWORTHY Impairments in dynamic cerebral autoregulation to hypotension are associated with breath-hold diving. Although weakened autoregulation was observed acutely in this group during apneic stress, we are the first to report on chronic adaptations in cerebral autoregulation. Impaired vasomotor responses underlie the reduced rate of regulation, wherein breath-hold divers demonstrate a prolonged dilatory response to transient hypotension. The slower cerebral vasodilation produces a longer perturbation in cerebral blood flow velocity, increasing the risk of cerebral ischemia.

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Dynamic cerebral autoregulation across the cardiac cycle during 8 hr of recovery from acute exercise.

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Dynamic cerebral autoregulation across the cardiac cycle during 8 hr of recovery from acute exercise.

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