Journal articles: 'Dynamic Cerebral Autoregulation'

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Beishon, L., JS Minhas, R. Nogueira, P. Castro, C. Budgeon, M. Aries, S. Payne, TG Robinson, and RB Panerai. "INFOMATAS multi-center systematic review and meta-analysis individual patient data of dynamic cerebral autoregulation in ischemic stroke." International Journal of Stroke 15, no. 7 (February 24, 2020): 807–12. http://dx.doi.org/10.1177/1747493020907003.

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Rationale Disturbances in dynamic cerebral autoregulation after ischemic stroke may have important implications for prognosis. Recent meta-analyses have been hampered by heterogeneity and small samples. Aim and/or hypothesis The aim of study is to undertake an individual patient data meta-analysis (IPD-MA) of dynamic cerebral autoregulation changes post-ischemic stroke and to determine a predictive model for outcome in ischemic stroke using information combined from dynamic cerebral autoregulation, clinical history, and neuroimaging. Sample size estimates To detect a change of 2% between categories in modified Rankin scale requires a sample size of ∼1500 patients with moderate to severe stroke, and a change of 1 in autoregulation index requires a sample size of 45 healthy individuals (powered at 80%, α = 0.05). Pooled estimates of mean and standard deviation derived from this study will be used to inform sample size calculations for adequately powered future dynamic cerebral autoregulation studies in ischemic stroke. Methods and design This is an IPD-MA as part of an international, multi-center collaboration (INFOMATAS) with three phases. Firstly, univariate analyses will be constructed for primary (modified Rankin scale) and secondary outcomes, with key co-variates and dynamic cerebral autoregulation parameters. Participants clustering from within studies will be accounted for with random effects. Secondly, dynamic cerebral autoregulation variables will be validated for diagnostic and prognostic accuracy in ischemic stroke using summary receiver operating characteristic curve analysis. Finally, the prognostic accuracy will be determined for four different models combining clinical history, neuroimaging, and dynamic cerebral autoregulation parameters. Study outcome(s) The outcomes for this study are to determine the relationship between clinical outcome, dynamic cerebral autoregulation changes, and baseline patient demographics, to determine the diagnostic and prognostic accuracy of dynamic cerebral autoregulation parameters, and to develop a prognostic model using dynamic cerebral autoregulation in ischemic stroke. Discussion This is the first international collaboration to use IPD-MA to determine prognostic models of dynamic cerebral autoregulation for patients with ischemic stroke.

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Panerai, Ronney B. "Nonstationarity of dynamic cerebral autoregulation." Medical Engineering & Physics 36, no. 5 (May 2014): 576–84. http://dx.doi.org/10.1016/j.medengphy.2013.09.004.

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Secher, Niels H., and Johannes J. van Lieshout. "Dynamic Cerebral Autoregulation and Monitoring Cerebral Perfusion." Hypertension 56, no. 2 (August 2010): 189–90. http://dx.doi.org/10.1161/hypertensionaha.110.154971.

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Schondorf, Ronald, Reuben Stein, Richard Roberts, Julie Benoit, and William Cupples. "Dynamic cerebral autoregulation is preserved in neurally mediated syncope." Journal of Applied Physiology 91, no. 6 (December 1, 2001): 2493–502. http://dx.doi.org/10.1152/jappl.2001.91.6.2493.

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To test whether cerebral autoregulation is impaired in patients with neurally mediated syncope (NMS), we evaluated 15 normal subjects and 37 patients with recurrent NMS. Blood pressure (BP), heart rate, and cerebral blood velocity (CBV) (transcranial Doppler) were recorded at rest and during 80° head-up tilt (HUT). Static cerebral autoregulation as assessed from the change in cerebrovascular resistance during HUT was the same in NMS and controls. Properties of dynamic cerebral autoregulation were inferred from transfer gain, coherence, and phase of the relationship between BP and CBV estimated from filtered data segments (0.02–0.8 Hz). During the 3 min preceding syncope, dynamic cerebral autoregulation of subjects with NMS did not differ from that of controls nor did it change over the course of HUT in patients with NMS or in control subjects. Dynamic cerebral autoregulation was also unaffected by the degree of orthostatic intolerance as inferred from latency to onset of syncope. We conclude that cerebral autoregulation in patients with recurrent syncope does not differ from that of normal control subjects.

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Nishimura, Naoko, Ken-ichi Iwasaki, Yojiro Ogawa, and Ken Aoki. "Decreased steady-state cerebral blood flow velocity and altered dynamic cerebral autoregulation during 5-h sustained 15% O2 hypoxia." Journal of Applied Physiology 108, no. 5 (May 2010): 1154–61. http://dx.doi.org/10.1152/japplphysiol.00656.2009.

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Effects of hypoxia on cerebral circulation are important for occupational, high-altitude, and aviation medicine. Increased risk of fainting might be attributable to altered cerebral circulation by hypoxia. Dynamic cerebral autoregulation is reportedly impaired immediately by mild hypoxia. However, continuous exposure to hypoxia causes hyperventilation, resulting in hypocapnia. This hypocapnia is hypothesized to restore impaired dynamic cerebral autoregulation with reduced steady-state cerebral blood flow (CBF). However, no studies have examined hourly changes in alterations of dynamic cerebral autoregulation and steady-state CBF during sustained hypoxia. We therefore examined cerebral circulation during 5-h exposure to 15% O2 hypoxia and 21% O2 in 13 healthy volunteers in a sitting position. Waveforms of blood pressure and CBF velocity in the middle cerebral artery were measured using finger plethysmography and transcranial Doppler ultrasonography. Dynamic cerebral autoregulation was assessed by spectral and transfer function analysis. As expected, steady-state CBF velocity decreased significantly from 2 to 5 h of hypoxia, accompanying 2- to 3-Torr decreases in end-tidal CO2 (ETCO2). Furthermore, transfer function gain and coherence in the very-low-frequency range increased significantly at the beginning of hypoxia, indicating impaired dynamic cerebral autoregulation. However, contrary to the proposed hypothesis, indexes of dynamic cerebral autoregulation showed no significant restoration despite ETCO2 reductions, resulting in persistent higher values of very-low-frequency power of CBF velocity variability during hypoxia (214 ± 40% at 5 h of hypoxia vs. control) without significant increases in blood pressure variability. These results suggest that sustained mild hypoxia reduces steady-state CBF and continuously impairs dynamic cerebral autoregulation, implying an increased risk of shortage of oxygen supply to the brain.

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Schondorf, Ronald, Julie Benoit, and Reuben Stein. "Cerebral autoregulation is preserved in postural tachycardia syndrome." Journal of Applied Physiology 99, no. 3 (September 2005): 828–35. http://dx.doi.org/10.1152/japplphysiol.00225.2005.

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To test whether cerebral autoregulation is impaired in patients with postural tachycardia syndrome (POTS), we evaluated 17 healthy control subjects and 27 patients with POTS. Blood pressure, heart rate, and cerebral blood velocity (transcranial Doppler) were recorded at rest and during 80° head-up tilt (HUT). Static cerebral autoregulation, as assessed from the change in cerebrovascular resistance during HUT, was the same in POTS and in controls. The properties of dynamic cerebral autoregulation were inferred from transfer gain, coherence, and phase of the relationship between blood pressure and cerebral blood velocity estimated from filtered data segments (0.02–0.8 Hz). Dynamic cerebral autoregulation of patients with POTS did not differ from that of controls. The patients' dynamic cerebral autoregulation did not change over the course of HUT, despite increased tachycardia suggestive of worsening orthostatic stress. Inflation of military anti-shock trouser pants substantially reduced the tachycardia of patients with POTS without affecting cerebral autoregulation. Symptoms of orthostatic intolerance were reduced in one-half of the patients following military anti-shock trouser pants inflation. We conclude that cerebral perfusion and autoregulation in many patients with POTS do not differ from that of normal control subjects.

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Ogawa, Yojiro, Ken Aoki, Jitsu Kato, and Ken-ichi Iwasaki. "Differential effects of mild central hypovolemia with furosemide administration vs. lower body suction on dynamic cerebral autoregulation." Journal of Applied Physiology 114, no. 2 (January 15, 2013): 211–16. http://dx.doi.org/10.1152/japplphysiol.00741.2012.

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Diuretic-induced mild hypovolemia with hemoconcentration reportedly improves dynamic cerebral autoregulation, whereas central hypovolemia without hemoconcentration induced by lower body negative pressure (LBNP) has no effect or impairs dynamic cerebral autoregulation. This discrepancy may be explained by different blood properties, by degrees of central hypovolemia, or both. We investigated the effects of equivalent central hypovolemia induced by furosemide administration or LBNP application on dynamic cerebral autoregulation to test our hypothesis that mild central hypovolemia due to furosemide administration enhances dynamic cerebral autoregulation in contrast to LBNP. Seven healthy male subjects received 0.4 mg/kg furosemide and LBNP, with equivalent decreases in central venous pressure (CVP). Dynamic cerebral autoregulation was assessed by spectral and transfer function analysis between beat-to-beat mean arterial blood pressure (MAP) and mean cerebral blood flow velocity (MCBFV). CVP decreased by ∼3–4 mmHg with both furosemide administration (∼26 mg) and LBNP (approximately −20 mmHg). Steady state MCBFV remained unchanged with both techniques, whereas MAP increased significantly with furosemide administration. Coherence and transfer function gain in the low and high frequency ranges with hypovolemia due to furosemide administration were significantly lower than those due to LBNP (ANOVA interaction effects, P < 0.05), although transfer function gain in the very low frequency range did not change. Our results suggest that although the decreases in CVP were equivalent between furosemide administration and LBNP, the resultant central hypovolemia differentially affected dynamic cerebral autoregulation. Mild central hypovolemia with hemoconcentration resulting from furosemide administration may enhance dynamic cerebral autoregulation compared with LBNP.

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WHITE, R. P., P. VALLANCE, and H. S. MARKUS. "Effect of inhibition of nitric oxide synthase on dynamic cerebral autoregulation in humans." Clinical Science 99, no. 6 (November 21, 2000): 555–60. http://dx.doi.org/10.1042/cs0990555.

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Cerebral blood flow is maintained constant over a range of cerebral perfusion pressures by cerebral autoregulation. Impaired cerebral autoregulation may be important in the pathogenesis of cerebral ischaemia. The mechanisms mediating normal cerebral autoregulation in humans are poorly understood. We used a recently described transcranial Doppler technique, which allows non-invasive measurement of dynamic cerebral autoregulation, to test the hypothesis that nitric oxide mediates cerebral autoregulation. The rate of rise of middle cerebral artery blood flow velocity, compared with that of arterial blood pressure, was determined following a stepwise fall in arterial blood pressure, in order to calculate an autoregulatory index. The effect of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) on dynamic autoregulation was compared with that of noradrenaline titrated to result in a similar rise in blood pressure. Six healthy subjects were studied in each group. The mean (S.D.) change in autoregulatory index following noradrenaline at a similar pressor dose was significantly greater than the change following the L-NMMA bolus: 1.1 (1.2) compared with -0.8 (0.8) for the left middle cerebral artery (P = 0.002), and 1.1 (0.8) compared with -0.8 (0.8) for the right middle cerebral artery (P = 0.002). There was no difference in the mean (S.D.) blood pressure increase resulting from the two agents: L-NMMA, 19.7 (7.4) mmHg; noradrenaline, 15.5 (4.8) mmHg (P = 0.281). These results suggest that nitric oxide mediates at least part of the dynamic phase of cerebral autoregulation in humans. Reduced nitric oxide release may play a role in the impaired cerebral autoregulation seen in patients with, or at risk of, cerebral ischaemia.

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Parthasarathy, Ashwin B., Kimberly P. Gannon, Wesley B. Baker, Christopher G. Favilla, Ramani Balu, Scott E. Kasner, Arjun G. Yodh, John A. Detre, and Michael T. Mullen. "Dynamic autoregulation of cerebral blood flow measured non-invasively with fast diffuse correlation spectroscopy." Journal of Cerebral Blood Flow & Metabolism 38, no. 2 (December 12, 2017): 230–40. http://dx.doi.org/10.1177/0271678x17747833.

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Cerebral autoregulation (CA) maintains cerebral blood flow (CBF) in the presence of systemic blood pressure changes. Brain injury can cause loss of CA and resulting dysregulation of CBF, and the degree of CA impairment is a functional indicator of cerebral tissue health. Here, we demonstrate a new approach to noninvasively estimate cerebral autoregulation in healthy adult volunteers. The approach employs pulsatile CBF measurements obtained using high-speed diffuse correlation spectroscopy (DCS). Rapid thigh-cuff deflation initiates a chain of responses that permits estimation of rates of dynamic autoregulation in the cerebral microvasculature. The regulation rate estimated with DCS in the microvasculature (median: 0.26 s−1, inter quartile range: 0.19 s−1) agrees well (R = 0.81, slope = 0.9) with regulation rates measured by transcranial Doppler ultrasound (TCD) in the proximal vasculature (median: 0.28 s−1, inter quartile range: 0.10 s−1). We also obtained an index of systemic autoregulation in concurrently measured scalp microvasculature. Systemic autoregulation begins later than cerebral autoregulation and exhibited a different rate (0.55 s−1, inter quartile range: 0.72 s−1). Our work demonstrates the potential of diffuse correlation spectroscopy for bedside monitoring of cerebral autoregulation in the microvasculature of patients with brain injury.

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Elting, Jan Willem J., Jeanette Tas, Marcel JH Aries, Marek Czosnyka, and Natasha M. Maurits. "Dynamic cerebral autoregulation estimates derived from near infrared spectroscopy and transcranial Doppler are similar after correction for transit time and blood flow and blood volume oscillations." Journal of Cerebral Blood Flow & Metabolism 40, no. 1 (October 24, 2018): 135–49. http://dx.doi.org/10.1177/0271678x18806107.

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We analysed mean arterial blood pressure, cerebral blood flow velocity, oxygenated haemoglobin and deoxygenated haemoglobin signals to estimate dynamic cerebral autoregulation. We compared macrovascular (mean arterial blood pressure-cerebral blood flow velocity) and microvascular (oxygenated haemoglobin-deoxygenated haemoglobin) dynamic cerebral autoregulation estimates during three different conditions: rest, mild hypocapnia and hypercapnia. Microvascular dynamic cerebral autoregulation estimates were created by introducing the constant time lag plus constant phase shift model, which enables correction for transit time, blood flow and blood volume oscillations (TT-BF/BV correction). After TT-BF/BV correction, a significant agreement between mean arterial blood pressure-cerebral blood flow velocity and oxygenated haemoglobin-deoxygenated haemoglobin phase differences in the low frequency band was found during rest (left: intraclass correlation=0.6, median phase difference 29.5° vs. 30.7°, right: intraclass correlation=0.56, median phase difference 32.6° vs. 39.8°) and mild hypocapnia (left: intraclass correlation=0.73, median phase difference 48.6° vs. 43.3°, right: intraclass correlation=0.70, median phase difference 52.1° vs. 61.8°). During hypercapnia, the mean transit time decreased and blood volume oscillations became much more prominent, except for very low frequencies. The transit time related to blood flow oscillations was remarkably stable during all conditions. We conclude that non-invasive microvascular dynamic cerebral autoregulation estimates are similar to macrovascular dynamic cerebral autoregulation estimates, after TT-BF/BV correction is applied. These findings may increase the feasibility of non-invasive continuous autoregulation monitoring and guided therapy in clinical situations.

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Ogoh, Shigehiko, Ai Hirasawa, Jun Sugawara, Hidehiro Nakahara, Shinya Ueda, J. Kevin Shoemaker, and Tadayoshi Miyamoto. "The effect of an acute increase in central blood volume on the response of cerebral blood flow to acute hypotension." Journal of Applied Physiology 119, no. 5 (September 1, 2015): 527–33. http://dx.doi.org/10.1152/japplphysiol.00277.2015.

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The purpose of the present study was to examine whether the response of cerebral blood flow to an acute change in perfusion pressure is modified by an acute increase in central blood volume. Nine young, healthy subjects voluntarily participated in this study. To measure dynamic cerebral autoregulation during normocapnic and hypercapnic (5%) conditions, the change in middle cerebral artery mean blood flow velocity was analyzed during acute hypotension caused by two methods: 1) thigh-cuff occlusion release (without change in central blood volume); and 2) during the recovery phase immediately following release of lower body negative pressure (LBNP; −50 mmHg) that initiated an acute increase in central blood volume. In the thigh-cuff occlusion release protocol, as expected, hypercapnia decreased the rate of regulation, as an index of dynamic cerebral autoregulation (0.236 ± 0.018 and 0.167 ± 0.025 s−1, P = 0.024). Compared with the cuff-occlusion release, the acute increase in central blood volume (relative to the LBNP condition) with LBNP release attenuated dynamic cerebral autoregulation ( P = 0.009). Therefore, the hypercapnia-induced attenuation of dynamic cerebral autoregulation was not observed in the LBNP release protocol ( P = 0.574). These findings suggest that an acute change in systemic blood distribution modifies dynamic cerebral autoregulation during acute hypotension.

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Berg, Ronan M. G., Ronni R. Plovsing, Andreas Ronit, Damian M. Bailey, Niels-Henrik Holstein-Rathlou, and Kirsten Møller. "Disassociation of static and dynamic cerebral autoregulatory performance in healthy volunteers after lipopolysaccharide infusion and in patients with sepsis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 11 (December 1, 2012): R1127—R1135. http://dx.doi.org/10.1152/ajpregu.00242.2012.

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Sepsis is frequently complicated by brain dysfunction, which may be associated with disturbances in cerebral autoregulation, rendering the brain susceptible to hypoperfusion and hyperperfusion. The purpose of the present study was to assess static and dynamic cerebral autoregulation 1) in a human experimental model of the systemic inflammatory response during early sepsis and 2) in patients with advanced sepsis. Cerebral autoregulation was tested using transcranial Doppler ultrasound in healthy volunteers ( n = 9) before and after LPS infusion and in patients with sepsis ( n = 16). Static autoregulation was tested by norepinephrine infusion and dynamic autoregulation by transfer function analysis (TFA) of spontaneous oscillations between mean arterial blood pressure and middle cerebral artery blood flow velocity in the low frequency range (0.07–0.20 Hz). Static autoregulatory performance after LPS infusion and in patients with sepsis was similar to values in healthy volunteers at baseline. In contrast, TFA showed decreased gain and an increased phase difference between blood pressure and middle cerebral artery blood flow velocity after LPS (both P < 0.01 vs. baseline); patients exhibited similar gain but lower phase difference values ( P < 0.01 vs. baseline and LPS), indicating a slower dynamic autoregulatory response. Our findings imply that static and dynamic cerebral autoregulatory performance may disassociate in sepsis; thus static autoregulation was maintained both after LPS and in patients with sepsis, whereas dynamic autoregulation was enhanced after LPS and impaired with a prolonged response time in patients. Hence, acute surges in blood pressure may adversely affect cerebral perfusion in patients with sepsis.

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Christiansen, Claus, Ronni Plovsing, Andreas Ronit, Niels-Henrik Holstein-Rathlou, Stig Yndgaard, Kirsten Møller, and Ronan Berg. "Dynamic Cerebral Autoregulation after Cardiopulmonary Bypass." Thoracic and Cardiovascular Surgeon 64, no. 07 (October 26, 2015): 569–74. http://dx.doi.org/10.1055/s-0035-1566128.

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ZHANG, R. "ENHANCED DYNAMIC CEREBRAL AUTOREGULATION DURING SPACEFLIGHT." Medicine & Science in Sports & Exercise 31, Supplement (May 1999): S193. http://dx.doi.org/10.1097/00005768-199905001-00871.

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Summors, Andrew C., Arun K. Gupta, and Basil F. Matta. "Dynamic Cerebral Autoregulation During Sevoflurane Anesthesia." Anesthesia & Analgesia 88, no. 2 (February 1999): 341–45. http://dx.doi.org/10.1213/00000539-199902000-00022.

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Summors, Andrew C., Arun K. Gupta, and Basil F. Matta. "Dynamic Cerebral Autoregulation During Sevoflurane Anesthesia." Anesthesia & Analgesia 88, no. 2 (February 1999): 341–45. http://dx.doi.org/10.1097/00000539-199902000-00022.

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Vavilala, M. S., D. W. Newell, E. Junger, C. M. Douville, R. Aaslid, F. P. Rivara, and A. M. Lam. "Dynamic cerebral autoregulation in healthy adolescents." Acta Anaesthesiologica Scandinavica 46, no. 4 (April 2002): 393–97. http://dx.doi.org/10.1034/j.1399-6576.2002.460411.x.

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Oehm, E., M. Reinhard, C. Keck, T. Els, J. Spreer, and A. Hetzel. "Impaired dynamic cerebral autoregulation in eclampsia." Ultrasound in Obstetrics and Gynecology 22, no. 4 (August 1, 2003): 395–98. http://dx.doi.org/10.1002/uog.183.

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Bajwa, Garima, Ram Dantu, and Arvind Nana. "Quantifying Dynamic Cerebral Autoregulation using Electroencephalograms." Archives of Physical Medicine and Rehabilitation 96, no. 10 (October 2015): e69. http://dx.doi.org/10.1016/j.apmr.2015.08.231.

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Sheriff, Faheem, Pedro Castro, Mariel Kozberg, Sarah LaRose, Andrew Monk, Elsa Azevedo, Karen Li, et al. "Dynamic Cerebral Autoregulation Post Endovascular Thrombectomy in Acute Ischemic Stroke." Brain Sciences 10, no. 9 (September 16, 2020): 641. http://dx.doi.org/10.3390/brainsci10090641.

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The development of the endovascular thrombectomy (EVT) technique has revolutionized acute stroke management for patients with large vessel occlusions (LVOs). The impact of successful recanalization using an EVT on autoregulatory profiles is unknown. A more complete understanding of cerebral autoregulation in the context of EVT may assist with post-procedure hemodynamic optimization to prevent complications. We examined cerebral autoregulation in 107 patients with an LVO in the anterior circulation (proximal middle cerebral artery (M1/2) and internal cerebral artery (ICA) terminus) who had been treated using an EVT. Dynamic cerebral autoregulation was assessed at multiple time points, ranging from less than 24 hours to 5 days following last seen well (LSW) time, using transcranial Doppler ultrasound recordings and transfer function analysis. Complete (Thrombolysis in Cerebral Infarction (TICI) 3) recanalization was associated with a more favorable autoregulation profile compared with TICI 2b or poorer recanalization (p < 0.05), which is an effect that was present after accounting for differences in the infarct volumes. Less effective autoregulation in the first 24 h following the LSW time was associated with increased rates of parenchymal hematoma types 1 and 2 hemorrhagic transformations (PH1–PH2). These data suggest that patients with incomplete recanalization and poor autoregulation (especially within the first 24 h post-LSW time) may warrant closer blood pressure monitoring and control in the first few days post ictus.

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Claassen, Jurgen AHR, Aisha SS Meel-van den Abeelen, David M. Simpson, and Ronney B. Panerai. "Transfer function analysis of dynamic cerebral autoregulation: A white paper from the International Cerebral Autoregulation Research Network." Journal of Cerebral Blood Flow & Metabolism 36, no. 4 (January 18, 2016): 665–80. http://dx.doi.org/10.1177/0271678x15626425.

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Cerebral autoregulation is the intrinsic ability of the brain to maintain adequate cerebral perfusion in the presence of blood pressure changes. A large number of methods to assess the quality of cerebral autoregulation have been proposed over the last 30 years. However, no single method has been universally accepted as a gold standard. Therefore, the choice of which method to employ to quantify cerebral autoregulation remains a matter of personal choice. Nevertheless, given the concept that cerebral autoregulation represents the dynamic relationship between blood pressure (stimulus or input) and cerebral blood flow (response or output), transfer function analysis became the most popular approach adopted in studies based on spontaneous fluctuations of blood pressure. Despite its sound theoretical background, the literature shows considerable variation in implementation of transfer function analysis in practice, which has limited comparisons between studies and hindered progress towards clinical application. Therefore, the purpose of the present white paper is to improve standardisation of parameters and settings adopted for application of transfer function analysis in studies of dynamic cerebral autoregulation. The development of these recommendations was initiated by (but not confined to) the Cerebral Autoregulation Research Network (CARNet – www.car-net.org ).

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Deegan, B. M., E. R. Devine, M. C. Geraghty, E. Jones, G. ÓLaighin, and J. M. Serrador. "The relationship between cardiac output and dynamic cerebral autoregulation in humans." Journal of Applied Physiology 109, no. 5 (November 2010): 1424–31. http://dx.doi.org/10.1152/japplphysiol.01262.2009.

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Cerebral autoregulation adjusts cerebrovascular resistance in the face of changing perfusion pressures to maintain relatively constant flow. Results from several studies suggest that cardiac output may also play a role. We tested the hypothesis that cerebral blood flow would autoregulate independent of changes in cardiac output. Transient systemic hypotension was induced by thigh-cuff deflation in 19 healthy volunteers (7 women) in both supine and seated positions. Mean arterial pressure (Finapres), cerebral blood flow (transcranial Doppler) in the anterior (ACA) and middle cerebral artery (MCA), beat-by-beat cardiac output (echocardiography), and end-tidal Pco2 were measured. Autoregulation was assessed using the autoregulatory index (ARI) defined by Tiecks et al. (Tiecks FP, Lam AM, Aaslid R, Newell DW. Stroke 26: 1014–1019, 1995). Cerebral autoregulation was better in the supine position in both the ACA [supine ARI: 5.0 ± 0.21 (mean ± SE), seated ARI: 3.9 ± 0.4, P = 0.01] and MCA (supine ARI: 5.0 ± 0.2, seated ARI: 3.8 ± 0.3, P = 0.004). In contrast, cardiac output responses were not different between positions and did not correlate with cerebral blood flow ARIs. In addition, women had better autoregulation in the ACA ( P = 0.046), but not the MCA, despite having the same cardiac output response. These data demonstrate cardiac output does not appear to affect the dynamic cerebral autoregulatory response to sudden hypotension in healthy controls, regardless of posture. These results also highlight the importance of considering sex when studying cerebral autoregulation.

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Kato, Tomokazu, Takuya Kurazumi, Toru Konishi, Chiharu Takko, Yojiro Ogawa, and Ken-ichi Iwasaki. "Effects of −10° and −30° head-down tilt on cerebral blood velocity, dynamic cerebral autoregulation, and noninvasively estimated intracranial pressure." Journal of Applied Physiology 132, no. 4 (April 1, 2022): 938–46. http://dx.doi.org/10.1152/japplphysiol.00283.2021.

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This appears to be the first study to evaluate steady-state cerebral blood flow (CBF), dynamic cerebral autoregulation, and intracranial pressure (ICP) during −30° head-down tilt (HDT) compared with those during −10° HDT using noninvasive measurements. The results suggest that steady-state CBF and dynamic cerebral autoregulation are preserved despite the higher ICP during short-term −30° HDT compared with −10° HDT.

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Iwasaki, Ken-Ichi, Rong Zhang, Julie H. Zuckerman, Yojiro Ogawa, Lærke H. Hansen, and Benjamin David Levine. "Impaired Dynamic Cerebral Autoregulation at Extreme High Altitude Even after Acclimatization." Journal of Cerebral Blood Flow & Metabolism 31, no. 1 (June 23, 2010): 283–92. http://dx.doi.org/10.1038/jcbfm.2010.88.

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Cerebral blood flow (CBF) increases and dynamic cerebral autoregulation is impaired by acute hypoxia. We hypothesized that progressive hypocapnia with restoration of arterial oxygen content after altitude acclimatization would normalize CBF and dynamic cerebral autoregulation. To test this hypothesis, dynamic cerebral autoregulation was examined by spectral and transfer function analyses between arterial pressure and CBF velocity variabilities in 11 healthy members of the Danish High-Altitude Research Expedition during normoxia and acute hypoxia (10.5% O2) at sea level, and after acclimatization (for over 1 month at 5,260 m at Chacaltaya, Bolivia). Arterial pressure and CBF velocity in the middle cerebral artery (transcranial Doppler), were recorded on a beat-by-beat basis. Steady-state CBF velocity increased during acute hypoxia, but normalized after acclimatization with partial restoration of SaO2 (acute, 78%±2%; chronic, 89%±1%) and progression of hypocapnia (end-tidal carbon dioxide: acute, 34±2 mm Hg; chronic, 21±1 mm Hg). Coherence (0.40±0.05 Units at normoxia) and transfer function gain (0.77±0.13 cm/s per mm Hg at normoxia) increased, and phase (0.86±0.15 radians at normoxia) decreased significantly in the very-low-frequency range during acute hypoxia (gain, 141%±24%; coherence, 136%±29%; phase, −25%±22%), which persisted after acclimatization (gain, 136%±36%; coherence, 131%±50%; phase, −42%±13%), together indicating impaired dynamic cerebral autoregulation in this frequency range. The similarity between both acute and chronic conditions suggests that dynamic cerebral autoregulation is impaired by hypoxia even after successful acclimatization to an extreme high altitude.

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Rangel-Castilla, Leonardo, Jaime Gasco, Haring J. W. Nauta, DaviD O. Okonkwo, and Claudia S. Robertson. "Cerebral pressure autoregulation in traumatic brain injury." Neurosurgical Focus 25, no. 4 (October 2008): E7. http://dx.doi.org/10.3171/foc.2008.25.10.e7.

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An understanding of normal cerebral autoregulation and its response to pathological derangements is helpful in the diagnosis, monitoring, management, and prognosis of severe traumatic brain injury (TBI). Pressure autoregulation is the most common approach in testing the effects of mean arterial blood pressure on cerebral blood flow. A gold standard for measuring cerebral pressure autoregulation is not available, and the literature shows considerable disparity in methods. This fact is not surprising given that cerebral autoregulation is more a concept than a physically measurable entity. Alterations in cerebral autoregulation can vary from patient to patient and over time and are critical during the first 4–5 days after injury. An assessment of cerebral autoregulation as part of bedside neuromonitoring in the neurointensive care unit can allow the individualized treatment of secondary injury in a patient with severe TBI. The assessment of cerebral autoregulation is best achieved with dynamic autoregulation methods. Hyperventilation, hyperoxia, nitric oxide and its derivates, and erythropoietin are some of the therapies that can be helpful in managing cerebral autoregulation. In this review the authors summarize the most important points related to cerebral pressure autoregulation in TBI as applied in clinical practice, based on the literature as well as their own experience.

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Gong, Xi-ping, Yao Li, Wei-jian Jiang, and Yongjun Wang. "Impaired dynamic cerebral autoregulation in middle cerebral artery stenosis." Neurological Research 28, no. 1 (January 2006): 76–81. http://dx.doi.org/10.1179/016164106x91915.

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Skow, Rachel J., Lawrence Labrecque, Jade A. Rosenberger, Patrice Brassard, Craig D. Steinback, and Margie H. Davenport. "Prenatal exercise and cardiovascular health (PEACH) study: impact of acute and chronic exercise on cerebrovascular hemodynamics and dynamic cerebral autoregulation." Journal of Applied Physiology 132, no. 1 (January 1, 2022): 247–60. http://dx.doi.org/10.1152/japplphysiol.00446.2021.

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These data represent the first assessments of dynamic cerebral autoregulation in pregnancy using a sit-to-stand. We used a randomized controlled trial to show dynamic cerebral autoregulation is not impacted by gestational age or by chronic exercise. However, there are larger decreases in blood pressure and cerebral blood velocity following sit-to-stand after acute exercise without adverse events. These data highlight the adaptability of the cerebral circulation during pregnancy to accommodate large changes in the cardiovascular system.

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Kim, Yu-Sok, Rogier V. Immink, Wim J. Stok, John M. Karemaker, Niels H. Secher, and Johannes J. van Lieshout. "Dynamic cerebral autoregulatory capacity is affected early in Type 2 diabetes." Clinical Science 115, no. 8 (September 12, 2008): 255–62. http://dx.doi.org/10.1042/cs20070458.

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Type 2 diabetes is associated with an increased risk of endothelial dysfunction and microvascular complications with impaired autoregulation of tissue perfusion. Both microvascular disease and cardiovascular autonomic neuropathy may affect cerebral autoregulation. In the present study, we tested the hypothesis that, in the absence of cardiovascular autonomic neuropathy, cerebral autoregulation is impaired in subjects with DM+ (Type 2 diabetes with microvascular complications) but intact in subjects with DM− (Type 2 diabetes without microvascular complications). Dynamic cerebral autoregulation and the steady-state cerebrovascular response to postural change were studied in subjects with DM+ and DM−, in the absence of cardiovascular autonomic neuropathy, and in CTRL (healthy control) subjects. The relationship between spontaneous changes in MCA Vmean (middle cerebral artery mean blood velocity) and MAP (mean arterial pressure) was evaluated using frequency domain analysis. In the low-frequency region (0.07–0.15 Hz), the phase lead of the MAP-to-MCA Vmean transfer function was 52±10 ° in CTRL subjects, reduced in subjects with DM− (40±6 °; P<0.01 compared with CTRL subjects) and impaired in subjects with DM+ (30±5 °; P<0.01 compared with subjects with DM−), indicating less dampening of blood pressure oscillations by affected dynamic cerebral autoregulation. The steady-state response of MCA Vmean to postural change was comparable for all groups (−12±6% in CTRL subjects, −15±6% in subjects with DM− and −15±7% in subjects with DM+). HbA1c (glycated haemoglobin) and the duration of diabetes, but not blood pressure, were determinants of transfer function phase. In conclusion, dysfunction of dynamic cerebral autoregulation in subjects with Type 2 diabetes appears to be an early manifestation of microvascular disease prior to the clinical expression of diabetic nephropathy, retinopathy or cardiovascular autonomic neuropathy.

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Panerai, R. B., S. T. Deverson, P. Mahony, P. Hayes, and D. H. Evans. "Effect of CO2on dynamic cerebral autoregulation measurement." Physiological Measurement 20, no. 3 (August 1, 1999): 265–75. http://dx.doi.org/10.1088/0967-3334/20/3/304.

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Ogoh, Shigehiko, Christian Selmer, Oivind Jans, Paul J. Fadel, Rong Zhang, Niels H. Secher, and Peter B. Raven. "Dynamic Cerebral Autoregulation During Exercise in Humans." Medicine & Science in Sports & Exercise 36, Supplement (May 2004): S25. http://dx.doi.org/10.1249/00005768-200405001-00118.

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Panerai, Ronney B., Michelle Moody, Penelope J. Eames, and John F. Potter. "Dynamic cerebral autoregulation during brain activation paradigms." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 3 (September 2005): H1202—H1208. http://dx.doi.org/10.1152/ajpheart.00115.2005.

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Dynamic cerebral autoregulation (CA) describes the transient response of cerebral blood flow (CBF) to rapid changes in arterial blood pressure (ABP). We tested the hypothesis that the efficiency of dynamic CA is increased by brain activation paradigms designed to induce hemispheric lateralization. CBF velocity [CBFV; bilateral, middle cerebral artery (MCA)], ABP, ECG, and end-tidal Pco2 were continuously recorded in 14 right-handed healthy subjects (21–43 yr of age), in the seated position, at rest and during 10 repeated presentations (30 s on-off) of a word generation test and a constructional puzzle. Nonstationarities were not found during rest or activation. Transfer function analysis of the ABP-CBFV (i.e., input-output) relation was performed for the 10 separate 51.2-s segments of data during activation and compared with baseline data. During activation, the coherence function below 0.05 Hz was significantly increased for the right MCA recordings for the puzzle tasks compared with baseline values (0.36 ± 0.16 vs. 0.26 ± 0.13, P < 0.05) and for the left MCA recordings for the word paradigm (0.48 ± 0.23 vs. 0.29 ± 0.16, P < 0.05). In the same frequency range, significant increases in gain were observed during the puzzle paradigm for the right (0.69 ± 0.37 vs. 0.46 ± 0.32 cm·s−1·mmHg−1, P < 0.05) and left (0.61 ± 0.29 vs. 0.45 ± 0.24 cm·s−1·mmHg−1, P < 0.05) hemispheres and during the word tasks for the left hemisphere (0.66 ± 0.31 vs. 0.39 ± 0.15 cm·s−1·mmHg−1, P < 0.01). Significant reductions in phase were observed during activation with the puzzle task for the right (−0.04 ± 1.01 vs. 0.80 ± 0.86 rad, P < 0.01) and left (0.11 ± 0.81 vs. 0.57 ± 0.51 rad, P < 0.05) hemispheres and with the word paradigm for the right hemisphere (0.05 ± 0.87 vs. 0.64 ± 0.59 rad, P < 0.05). Brain activation also led to changes in the temporal pattern of the CBFV step response. We conclude that transfer function analysis suggests important changes in dynamic CA during mental activation tasks.

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Oeinck, Maximilian, Florian Neunhoeffer, Klaus-Juergen Buttler, Stephan Meckel, Bernhard Schmidt, Marek Czosnyka, Cornelius Weiller, and Matthias Reinhard. "Dynamic Cerebral Autoregulation in Acute Intracerebral Hemorrhage." Stroke 44, no. 10 (October 2013): 2722–28. http://dx.doi.org/10.1161/strokeaha.113.001913.

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Background and Purpose— Cerebral autoregulation (CA) is not universally impaired in acute intracerebral hemorrhage (ICH); however, the dynamic components of CA are probably more vulnerable. This study, therefore, evaluates the time course of dynamic CA in acute ICH and its relationship to clinical outcome. Methods— Twenty-six patients with ICH were studied on days 1, 3, and 5 after ictus. Dynamic CA was measured from spontaneous fluctuations in blood pressure and middle cerebral artery flow velocity by transfer function phase (reflecting rapidity of CA) and gain (reflecting damping characteristics of CA) in the low frequency range. Results were compared with those from 55 controls and related with clinical factors and 90-day outcome (modified Rankin scale). Results— Phase did not fluctuate significantly over time, nor did it differ between sides or differ from controls. Gain was always higher in patients than in controls but showed no significant association with outcome or other clinical factors. At day 1, poorer ipsilateral phase was associated with lower blood pressure and higher ICH volume. Poorer phase always coincided with lower Glasgow Coma Scale values. Poorer ipsilateral phase on day 5 was related with poorer clinical outcome according to multivariate analysis ( P =0.013). Conclusions— Dynamic temporal characteristics of CA (phase) are not generally altered in acute ICH. Poorer individual phase values are, however, associated with larger ICH volume, lower blood pressure, and worsened outcome. Dampening characteristics of CA (gain) are generally impaired in acute ICH but not related to clinical factors or outcome.

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Noack, Frank, Melanie Christ, Sven-Axel May, Ralf Steinmeier, and Ute Morgenstern. "Assessment of dynamic changes in cerebral autoregulation." Biomedizinische Technik/Biomedical Engineering 52, no. 1 (February 2007): 31–36. http://dx.doi.org/10.1515/bmt.2007.007.

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Ogoh, Shigehiko, Christian Selmer, Oivind Jans, Paul J. Fadel, Rong Zhang, Niels H. Secher, and Peter B. Raven. "Dynamic Cerebral Autoregulation During Exercise in Humans." Medicine & Science in Sports & Exercise 36, Supplement (May 2004): S25. http://dx.doi.org/10.1097/00005768-200405001-00118.

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Boylan, Geraldine B., Kevin Young, Ronney B. Panerai, Janet M. Rennie, and David H. Evans. "Dynamic Cerebral Autoregulation in Sick Newborn Infants." Pediatric Research 48, no. 1 (July 2000): 12–17. http://dx.doi.org/10.1203/00006450-200007000-00005.

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Tutaj, Marcin, Clive M. Brown, Miroslaw Brys, Harald Marthol, Martin J. Hecht, Matthias Dutsch, Georg Michelson, and Max J. Hilz. "Dynamic cerebral autoregulation is impaired in glaucoma." Journal of the Neurological Sciences 220, no. 1-2 (May 2004): 49–54. http://dx.doi.org/10.1016/j.jns.2004.02.002.

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Chen, Jie, Jia Liu, Lian Duan, Ren Xu, Yi-Qin Han, Wei-Hai Xu, Li-Ying Cui, and Shan Gao. "Impaired Dynamic Cerebral Autoregulation in Moyamoya Disease." CNS Neuroscience & Therapeutics 19, no. 8 (June 3, 2013): 638–40. http://dx.doi.org/10.1111/cns.12130.

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Carey, Brian J., Penelope J. Eames, Melanie J. Blake, Ronney B. Panerai, and John F. Potter. "Dynamic Cerebral Autoregulation Is Unaffected by Aging." Stroke 31, no. 12 (December 2000): 2895–900. http://dx.doi.org/10.1161/01.str.31.12.2895.

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Ogawa, Yojiro, Ken-ichi Iwasaki, Ken Aoki, Wakako Kojima, Jitsu Kato, and Setsuro Ogawa. "Dexmedetomidine Weakens Dynamic Cerebral Autoregulation as Assessed by Transfer Function Analysis and the Thigh Cuff Method." Anesthesiology 109, no. 4 (October 1, 2008): 642–50. http://dx.doi.org/10.1097/aln.0b013e3181862a33.

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Background Dexmedetomidine, which is often used in intensive care units in patients with compromised circulation, might induce further severe decreases in cerebral blood flow (CBF) with temporal decreases in arterial pressure induced by various stimuli if dynamic cerebral autoregulation is not improved. Therefore, the authors hypothesized that dexmedetomidine strengthens dynamic cerebral autoregulation. Methods Fourteen healthy male subjects received placebo, low-dose dexmedetomidine (loading, 3 microg x kg(-1) x h(-1) for 10 min; maintenance, 0.2 microg x kg(-1) x h(-1) for 60 min), and high-dose dexmedetomidine (loading, 6 microg x kg(-1) x h(-1) for 10 min; maintenance, 0.4 microg x kg(-1) x h(-1) for 60 min) infusions in a randomized, double-blind, crossover study. After 70 min of drug administration, dynamic cerebral autoregulation was estimated by transfer function analysis between arterial pressure variability and CBF velocity variability, and the thigh cuff method. Results Compared with placebo, steady state CBF velocity and mean blood pressure significantly decreased during administration of dexmedetomidine. Transfer function gain in the very-low-frequency range increased and phase in the low-frequency range decreased significantly, suggesting alterations in dynamic cerebral autoregulation in lower frequency ranges. Moreover, the dynamic rate of regulation and percentage restoration in CBF velocity significantly decreased when a temporal decrease in arterial pressure was induced by thigh cuff release. Conclusion Contrary to the authors' hypothesis, the current results of two experimental analyses suggest together that dexmedetomidine weakens dynamic cerebral autoregulation and delays restoration in CBF velocity during conditions of decreased steady state CBF velocity. Therefore, dexmedetomidine may lead to further sustained reductions in CBF during temporal decreases in arterial pressure.

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Moir, M. Erin, Stephen A. Klassen, Baraa K. Al-Khazraji, Emilie Woehrle, Sydney O. Smith, Brad J. Matushewski, Duško Kozić, Željko Dujić, Otto F. Barak, and J. Kevin Shoemaker. "Impaired dynamic cerebral autoregulation in trained breath-hold divers." Journal of Applied Physiology 126, no. 6 (June 1, 2019): 1694–700. http://dx.doi.org/10.1152/japplphysiol.00210.2019.

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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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Reinhard, Matthias, Zora Waldkircher, Jens Timmer, Cornelius Weiller, and Andreas Hetzel. "Cerebellar Autoregulation Dynamics in Humans." Journal of Cerebral Blood Flow & Metabolism 28, no. 9 (May 21, 2008): 1605–12. http://dx.doi.org/10.1038/jcbfm.2008.48.

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Knowledge on autoregulation of cerebellar blood flow in humans is scarce. This study investigated whether cerebellar autoregulation dynamics and CO2 reactivity differ from those of the supratentorial circulation. In 56 healthy young adults, transcranial Doppler (TCD) monitoring of the posterior inferior cerebellar artery (PICA) and, simultaneously, of the contralateral middle cerebral artery (MCA) was performed. Autoregulation dynamics were assessed by the correlation coefficient method (indices Dx and Mx) from spontaneous blood pressure fluctuations and by transfer function analysis (phase and gain) from respiratory-induced 0.1 Hz blood pressure oscillations. CO2 reactivity was measured via inhalation of air mixed with 7% CO2. The autoregulatory indices Dx and Mx did not differ between the cerebellar (PICA) and cerebral (MCA) vasculature. Phase and gain, which describe faster aspects of autoregulation, showed slightly better values in the PICA compared with the MCA (higher phase, P = 0.005; lower gain, P = 0.007). Correlation between absolute autoregulation values in the PICA and the MCA was significant ( P < 0.001). The TCD CO2 reactivity was significantly lower in the PICA ( P < 0.001), which could be influenced by an assumed PICA dilation under hypercapnia. In conclusion, dynamic autoregulation in the human cerebellum is well operating and has slightly faster regulatory properties than the anterior cerebral circulation.

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Nishimura, Naoko, Ken-ichi Iwasaki, Yojiro Ogawa, and Shigeki Shibata. "Oxygen Administration, Cerebral Blood Flow Velocity, and Dynamic Cerebral Autoregulation." Aviation, Space, and Environmental Medicine 78, no. 12 (December 1, 2007): 1121–27. http://dx.doi.org/10.3357/asem.2177.2007.

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Reinhard, Matthias, Leonie Lorenz, Linda Sommerlade, Arthur Allignol, Horst Urbach, Cornelius Weiller, and Karl Egger. "Impaired dynamic cerebral autoregulation in patients with cerebral amyloid angiopathy." Brain Research 1717 (August 2019): 60–65. http://dx.doi.org/10.1016/j.brainres.2019.04.014.

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Moir, M. Erin, Stephen A. Klassen, Mair Zamir, and J. Kevin Shoemaker. "Rapid changes in vascular compliance contribute to cerebrovascular adjustments during transient reductions in blood pressure in young, healthy adults." Journal of Applied Physiology 129, no. 1 (July 1, 2020): 27–35. http://dx.doi.org/10.1152/japplphysiol.00272.2020.

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Historically, dynamic cerebral autoregulation has been characterized by adjustments in cerebrovascular resistance following systematic changes in blood pressure. However, with the use of Windkessel modeling approaches, this study revealed rapid and large increases in cerebrovascular compliance that preceded reductions in cerebrovascular resistance following standing-induced blood pressure reductions. Importantly, the rapid cerebrovascular compliance response contributed to preservation of systolic blood velocity during the transient hypotensive phase. These results broaden our understanding of dynamic cerebral autoregulation.

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Ogoh, Shigehiko, Mads K. Dalsgaard, Chie C. Yoshiga, Ellen A. Dawson, David M. Keller, Peter B. Raven, and Niels H. Secher. "Dynamic cerebral autoregulation during exhaustive exercise in humans." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 3 (March 2005): H1461—H1467. http://dx.doi.org/10.1152/ajpheart.00948.2004.

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We investigated whether dynamic cerebral autoregulation is affected by exhaustive exercise using transfer-function gain and phase shift between oscillations in mean arterial pressure (MAP) and middle cerebral artery (MCA) mean blood flow velocity ( Vmean). Seven subjects were instrumented with a brachial artery catheter for measurement of MAP and determination of arterial Pco2 (PaCO2) while jugular venous oxygen saturation (SvO2) was determined to assess changes in whole brain blood flow. After a 10-min resting period, the subjects performed dynamic leg-cycle ergometry at 168 ± 5 W (mean ± SE) that was continued to exhaustion with a group average time of 26.8 ± 5.8 min. Despite no significant change in MAP during exercise, MCA Vmean decreased from 70.2 ± 3.6 to 57.4 ± 5.4 cm/s, SvO2 decreased from 68 ± 1 to 58 ± 2% at exhaustion, and both correlated to PaCO2 (5.5 ± 0.2 to 3.9 ± 0.2 kPa; r = 0.47; P = 0.04 and r = 0.74; P < 0.001, respectively). An effect on brain metabolism was indicated by a decrease in the cerebral metabolic ratio of O2 to [glucose + one-half lactate] from 5.6 to 3.8 ( P < 0.05). At the same time, the normalized low-frequency gain between MAP and MCA Vmean was increased ( P < 0.05), whereas the phase shift tended to decrease. These findings suggest that dynamic cerebral autoregulation was impaired by exhaustive exercise despite a hyperventilation-induced reduction in PaCO2.

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Kainerstorfer, Jana M., Angelo Sassaroli, Kristen T. Tgavalekos, and Sergio Fantini. "Cerebral Autoregulation in the Microvasculature Measured with Near-Infrared Spectroscopy." Journal of Cerebral Blood Flow & Metabolism 35, no. 6 (February 11, 2015): 959–66. http://dx.doi.org/10.1038/jcbfm.2015.5.

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Cerebral autoregulation (CA) is the mechanism that allows the brain to maintain a stable blood flow despite changes in blood pressure. Dynamic CA can be quantified based on continuous measurements of systemic mean arterial pressure (MAP) and global cerebral blood flow. Here, we show that dynamic CA can be quantified also from local measurements that are sensitive to the microvasculature. We used near-infrared spectroscopy (NIRS) to measure temporal changes in oxy- and deoxy-hemoglobin concentrations in the prefrontal cortex of 11 human subjects. A novel hemodynamic model translates those changes into changes of cerebral blood volume and blood flow. The interplay between them is described by transfer function analysis, specifically by a high-pass filter whose cutoff frequency describes the autoregulation efficiency. We have used pneumatic thigh cuffs to induce MAP perturbation by a fast release during rest and during hyperventilation, which is known to enhance autoregulation. Based on our model, we found that the autoregulation cutoff frequency increased during hyperventilation in comparison to normal breathing in 10 out of 11 subjects, indicating a greater autoregulation efficiency. We have shown that autoregulation can reliably be measured noninvasively in the microvasculature, opening up the possibility of localized CA monitoring with NIRS.

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Wilson, Luke C., James D. Cotter, Jui-Lin Fan, Rebekah A. I. Lucas, Kate N. Thomas, and Philip N. Ainslie. "Cerebrovascular reactivity and dynamic autoregulation in tetraplegia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 4 (April 2010): R1035—R1042. http://dx.doi.org/10.1152/ajpregu.00815.2009.

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Humans with spinal cord injury have impaired cardiovascular function proportional to the level and completeness of the lesion. The effect on cerebrovascular function is unclear, especially for high-level lesions. The purpose of this study was to evaluate the integrity of dynamic cerebral autoregulation (CA) and the cerebrovascular reactivity in chronic tetraplegia (Tetra). After baseline, steady-state hypercapnia (5% CO2) and hypocapnia (controlled hyperventilation) were used to assess cerebrovascular reactivity in 6 men with Tetra (C5–C7 lesion) and 14 men without [able-bodied (AB)]. Middle cerebral artery blood flow velocity (MCAv), cerebral oxygenation, arterial blood pressure (BP), heart rate (HR), cardiac output (Q̇; model flow), partial pressure of end-tidal CO2 (PetCO2), and plasma catecholamines were measured. Dynamic CA was assessed by transfer function analysis of spontaneous fluctuations in BP and MCAv. MCAv pulsatility index (MCAv PI) was calculated as (MCAvsystolic − MCAvdiastolic)/MCAvmean and standardized by dividing by mean arterial pressure (MAP). Resting BP, total peripheral resistance, and catecholamines were lower in Tetra ( P < 0.05), and standardized MCAv PI was ∼36% higher in Tetra ( P = 0.003). Resting MCAv, cerebral oxygenation, HR, and PetCO2 were similar between groups ( P > 0.05). Although phase and transfer function gain relationships in dynamic CA were maintained with Tetra ( P > 0.05), coherence in the very low-frequency range (0.02–0.07 Hz) was ∼21% lower in Tetra ( P = 0.006). Full (hypo- and hypercapnic) cerebrovascular reactivity to CO2 was unchanged with Tetra ( P > 0.05). During hypercapnia, standardized MCAv PI reactivity was enhanced by ∼78% in Tetra ( P = 0.016). Despite impaired cardiovascular function, chronic Tetra involves subtle changes in dynamic CA and cerebrovascular reactivity to CO2. Changes are evident in coherence at baseline and MCAv PI during baseline and hypercapnic states in chronic Tetra, which may be indicative of cerebrovascular adaptation.

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EAMES, Penelope J., John F. POTTER, and Ronney B. PANERAI. "Assessment of cerebral autoregulation from ectopic heartbeats." Clinical Science 109, no. 1 (June 23, 2005): 109–15. http://dx.doi.org/10.1042/cs20050009.

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Transfer function analysis of spontaneous fluctuations in BP (blood pressure) and CBFV (cerebral blood flow velocity) has been widely used to study dynamic CA (cerebral autoregulation). The inverse Fourier transform and its integral, giving the impulse and step responses, have been used to gain perspective of the state of dynamic CA from the frequency and time domains respectively. The occurrence of ectopic heartbeats in the data has usually been treated as an artefact. Data containing multiple ectopic heartbeats were selected from a data set compiled for an acute stroke study which also included bilateral middle CBFV, concurrent surface ECG and non-invasive beat-to-beat BP recordings. Transfer function analysis and impulse and step responses were calculated from these data by (i) retaining ectopic heartbeats, (ii) after removal of ectopic heartbeats and replacement by linear interpolation, and (iii) using a narrow window of data surrounding selected ectopic heartbeats. Coherent averaging of the raw data of the selected ectopic heartbeats also allowed direct visualization of the relationship between BP changes and CBFV. The impulse and step responses were similar in shape whether or not ectopic heartbeats had been removed and showed characteristics of active dynamic CA. Removal of ectopic heartbeats from the CBFV and BP tracings, by linear interpolation or other methods, is not necessary to provide reliable estimates of dynamic autoregulation in subjects with ectopic heartbeat rates of up to eight per min. Additionally, impulse-like disturbances of BP induced by single-beat ectopic heartbeats provide enough information to characterize the autoregulatory response of the subject in agreement with more traditional methods of dynamic autoregulation assessment.

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Jünger, Elisabeth C., David W. Newell, Gerald A. Grant, Anthony M. Avellino, Saadi Ghatan, Colleen M. Douville, Arthur M. Lam, Rune Aaslid, and H. Richard Winn. "Cerebral autoregulation following minor head injury." Neurosurgical Focus 2, no. 1 (January 1997): E1. http://dx.doi.org/10.3171/foc.1997.2.1.1.

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The purpose of this study was to determine whether patients with minor head injury experience impairments in cerebral autoregulation. Twenty-nine patients with minor head injuries defined by Glasgow Coma Scale (GCS) scores of 13 to 15 underwent testing of dynamic cerebral autoregulation within 48 hours of their injury using continuous transcranial Doppler velocity recordings and blood pressure recordings. Twenty-nine age-matched normal volunteers underwent autoregulation testing in the same manner to establish comparison values. The function of the autoregulatory response was assessed by the cerebral blood flow velocity response to induced rapid brief changes in arterial blood pressure and measured as the autoregulation index (ARI).Eight (28%) of the 29 patients with minor head injury demonstrated poorly functioning or absent cerebral autoregulation versus none of the controls, and this difference was highly significant (p = 0.008). A significant correlation between lower blood pressure and worse autoregulation was found by regression analysis in head-injured patients (r = 0.6, p < 0.001); however, lower blood pressure did not account for the autoregulatory impairment in all patients. Within this group of head-injured patients there was no correlation between ARI and initial GCS or 1-month Glasgow Outcome Scale scores. This study indicates that a significant number of patients with minor head injury may have impaired cerebral autoregulation and may be at increased risk for secondary ischemic neuronal damage.

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Jünger, Elisabeth C., David W. Newell, Gerald A. Grant, Anthony M. Avellino, Saadi Ghatan, Colleen M. Douville, Arthur M. Lam, Rune Aaslid, and H. Richard Winn. "Cerebral autoregulation following minor head injury." Journal of Neurosurgery 86, no. 3 (March 1997): 425–32. http://dx.doi.org/10.3171/jns.1997.86.3.0425.

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✓ The purpose of this study was to determine whether patients with minor head injury experience impairments in cerebral autoregulation. Twenty-nine patients with minor head injuries defined by Glasgow Coma Scale (GCS) scores of 13 to 15 underwent testing of dynamic cerebral autoregulation within 48 hours of their injury using continuous transcranial Doppler velocity recordings and blood pressure recordings. Twenty-nine age-matched normal volunteers underwent autoregulation testing in the same manner to establish comparison values. The function of the autoregulatory response was assessed by the cerebral blood flow velocity response to induced rapid brief changes in arterial blood pressure and measured as the autoregulation index (ARI). Eight (28%) of the 29 patients with minor head injury demonstrated poorly functioning or absent cerebral autoregulation versus none of the controls, and this difference was highly significant (p = 0.008). A significant correlation between lower blood pressure and worse autoregulation was found by regression analysis in head-injured patients (r = 0.6, p < 0.001); however, lower blood pressure did not account for the autoregulatory impairment in all patients. Within this group of head-injured patients there was no correlation between ARI and initial GCS or 1-month Glasgow Outcome Scale scores. This study indicates that a significant number of patients with minor head injury may have impaired cerebral autoregulation and may be at increased risk for secondary ischemic neuronal damage.

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Journal articles on the topic 'Dynamic Cerebral Autoregulation'

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