scholarly journals Dynamic cerebral autoregulation during cognitive task: effect of hypoxia

2018 ◽  
Vol 124 (6) ◽  
pp. 1413-1419 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Hiroki Nakata ◽  
Tadayoshi Miyamoto ◽  
Damian Miles Bailey ◽  
Manabu Shibasaki

Changes in cerebral blood flow (CBF) subsequent to alterations in the partial pressures of oxygen and carbon dioxide can modify dynamic cerebral autoregulation (CA). While cognitive activity increases CBF, the extent to which it impacts CA remains to be established. In the present study we determined whether dynamic CA would decrease during a cognitive task and whether hypoxia would further compound impairment. Fourteen young healthy subjects performed a simple Go/No-go task during normoxia and hypoxia (inspired O2 fraction = 12%), and the corresponding relationship between mean arterial pressure (MAP) and mean middle cerebral artery blood velocity (MCA Vmean) was examined. Dynamic CA and steady-state changes in MCA V in relation to changes in arterial pressure were evaluated with transfer function analysis. While MCA Vmean increased during the cognitive activity ( P < 0.001), hypoxia did not cause any additional changes ( P = 0.804 vs. normoxia). Cognitive performance was also unaffected by hypoxia (reaction time, P = 0.712; error, P = 0.653). A decrease in the very low- and low-frequency phase shift (VLF and LF; P = 0.021 and P = 0.01) and an increase in LF gain were observed ( P = 0.037) during cognitive activity, implying impaired dynamic CA. While hypoxia also increased VLF gain ( P < 0.001), it failed to cause any additional modifications in dynamic CA. Collectively, our findings suggest that dynamic CA is impaired during cognitive activity independent of altered systemic O2 availability, although we acknowledge the interpretive complications associated with additional competing, albeit undefined, inputs that could potentially distort the MAP-MCA Vmean relationship. NEW & NOTEWORTHY During normoxia, cognitive activity while increasing cerebral perfusion was shown to attenuate dynamic cerebral autoregulation (CA) yet failed to alter reaction time, thereby questioning its functional significance. No further changes were observed during hypoxia, suggesting that impaired dynamic CA occurs independently of altered systemic O2 availability. However, impaired dynamic CA may reflect a technical artifact, given the confounding influence of additional inputs that could potentially distort the mean arterial pressure-mean middle cerebral artery blood velocity relationship.

2013 ◽  
Vol 34 (2) ◽  
pp. 228-234 ◽  
Author(s):  
Sushmita Purkayastha ◽  
Otite Fadar ◽  
Aujan Mehregan ◽  
David H Salat ◽  
Nicola Moscufo ◽  
...  

White matter hyperintensities (WMH) in elderly individuals with vascular diseases are presumed to be due to ischemic small vessel diseases; however, their etiology is unknown. We examined the cross-sectional relationship between cerebrovascular hemodynamics and white matter structural integrity in elderly individuals with vascular risk factors. White matter hyperintensity volumes, fractional anisotropy (FA), and mean diffusivity (MD) were obtained from MRI in 48 subjects (75±7years). Pulsatility index (PI) and dynamic cerebral autoregulation (dCA) was assessed using transcranial Doppler ultrasound of the middle cerebral artery. Dynamic cerebral autoregulation was calculated from transfer function analysis (phase and gain) of spontaneous blood pressure and flow velocity oscillations in the low (LF, 0.03 to 0.15 Hz) and high (HF, 0.16 to 0.5 Hz) frequency ranges. Higher PI was associated with greater WMH ( P<0.005). Higher phase across all frequency ranges was associated with greater FA and lower MD ( P<0.005). Lower gain was associated with higher FA in the LF range ( P=0.001). These relationships between phase and FA were significant in the territories limited to the middle cerebral artery as well as across the entire brain. Our results show a strong relationship between impaired cerebrovascular hemodynamics (PI and dCA) and loss of cerebral white matter structural integrity (WMH and DTI metrics) in elderly individuals.


1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P&lt;0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.


2020 ◽  
Author(s):  
Lawrence Labrecque ◽  
Jonathan Smirl ◽  
Patrice Brassard

Hysteresis in the cerebral pressure-flow relationship describes the superior ability of the cerebrovasculature to buffer cerebral blood flow changes when mean arterial pressure (MAP) acutely increases compared to when it decreases. This phenomenon can be evaluated by comparing the relative change in middle cerebral artery mean blood velocity (MCAv) per relative change in MAP (%ΔMCAv/%ΔMAP) during either acute increases or decreases in MAP induced by repeated squat-stands (RSS). However, no real baseline can be employed for this particular protocol as there is no true stable reference point. Herein, we characterized the %ΔMCAv/%ΔMAP metric using the greatest MAP oscillations induced by RSS without using an independent baseline value. We also examined whether %ΔMCAv/%ΔMAP during each RSS transition were comparable between each other over the 5-min period. %ΔMCAv/%ΔMAP was calculated using the minimum to maximum MCAv and MAP for each RSS performed at 0.05 Hz and 0.10 Hz. We compared averaged %ΔMCAv/%ΔMAP during MAP increases and decreases in 74 healthy subjects [9 women; 32 ± 13 years]. %ΔMCAv/%ΔMAP was lower for MAP increases than MAP decreases (0.05 Hz: 1.25 ± 0.22 vs. 1.35 ± 0.27 %/%, p<0.0001; 0.10Hz: 1.31 ± 0.24 vs. 1.60 ± 0.50 %/%, p<0.0001). For both frequency and MAP direction, time during RSS had no effect on %ΔMCAv/%ΔMAP. This novel analytical method supports the use of the RSS model to evaluate the directional behavior of the pressure-flow relationship. These results contribute to the importance of considering the direction of MAP changes when evaluating dynamic cerebral autoregulation.


2007 ◽  
Vol 106 (1) ◽  
pp. 56-64 ◽  
Author(s):  
Timothy J. McCulloch ◽  
Christopher L. Thompson ◽  
Martin J. Turner

Background Intravenous and inhalational anesthetic agents have differing effects on cerebral hemodynamics: Sevoflurane causes some vasodilation, whereas propofol does not. The authors hypothesized that these differences affect internal carotid artery pressure (ICAP) and the apparent zero flow pressure (critical closing pressure) during carotid endarterectomy. Vasodilation is expected to increase blood flow, reduce ICAP, and reduce apparent zero flow pressure. Methods In a randomized crossover study, the gradient between systemic arterial pressure and ICAP during carotid clamping was measured while changing between sevoflurane and propofol in 32 patients. Middle cerebral artery blood velocity, recorded by transcranial Doppler, and ICAP waveforms were analyzed to determine the apparent zero flow pressure. Results ICAP increased when changing from sevoflurane to propofol, causing the mean gradient between arterial pressure and ICAP to decrease by 10 mmHg (95% confidence interval, 6-14 mmHg; P&lt;0.0001). Changing from propofol to sevoflurane had the opposite effect: The pressure gradient increased by 5 mmHg (95% confidence interval, 2-7 mmHg; P=0.002). Ipsilateral middle cerebral artery blood velocity decreased when changing from sevoflurane to propofol. Cerebral steal was detected in one patient after changing from propofol to sevoflurane. The apparent zero flow pressure (mean+/-SD) was 22+/-10 mmHg with sevoflurane and 30+/-14 mmHg with propofol (P&lt;0.01). There was incomplete drug crossover due to the limited duration of carotid clamping. Conclusions Compared with sevoflurane, ipsilateral ICAP and apparent zero flow pressure are both higher with propofol. Vasodilatation associated with sevoflurane can cause cerebral steal.


2003 ◽  
Vol 94 (4) ◽  
pp. 1335-1344 ◽  
Author(s):  
Frank Pott ◽  
Johannes J. Van Lieshout ◽  
Kojiro Ide ◽  
Per Madsen ◽  
Niels H. Secher

Lifting of a heavy weight may lead to “blackout” and occasionally also to cerebral hemorrhage, indicating pronounced consequences for the blood flow through the brain. We hypothesized that especially strenuous respiratory straining (a Valsalva-like maneuver) associated with intense static exercise would lead to a precipitous rise in mean arterial and central venous pressures and, in turn, influence the middle cerebral artery blood velocity (MCA V mean) as a noninvasive indicator of changes in cerebral blood flow. In 10 healthy subjects, MCA V mean was evaluated in response to maximal static two-legged exercise performed either with a concomitantly performed Valsalva maneuver or with continued ventilation and also during a Valsalva maneuver without associated exercise ( n = 6). During static two-legged exercise, the largest rise for mean arterial pressure and MCA V meanwas established at the onset of exercise performed with a Valsalva-like maneuver (by 42 ± 5 mmHg and 31 ± 3% vs. 22 ± 6 mmHg and 25 ± 6% with continued ventilation; P < 0.05). Profound reductions in MCA V mean were observed both after exercise with continued ventilation (−29 ± 4% together with a reduction in the arterial CO2 tension by −5 ± 1 Torr) and during the maintained Valsalva maneuver (−21 ± 3% together with an elevation in central venous pressure to 40 ± 7 mmHg). Responses to performance of the Valsalva maneuver with and without exercise were similar, reflecting the deterministic importance of the Valsalva maneuver for the central and cerebral hemodynamic response to intense static exercise. Continued ventilation during intense static exercise may limit the initial rise in arterial pressure and may in turn reduce the risk of hemorrhage. On the other hand, blackout during and after intense static exercise may reflect a reduction in cerebral blood flow due to expiratory straining and/or hyperventilation.


2007 ◽  
Vol 180 (3) ◽  
pp. 517-523 ◽  
Author(s):  
M. Reinhard ◽  
E. Wehrle-Wieland ◽  
M. Roth ◽  
W. D. Niesen ◽  
J. Timmer ◽  
...  

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