局部脑氧饱和度在监测脑血流自动调节中的应用

脑血流自动调节（cerebral autoregulation, CA）是维持脑血流量相对稳定从而维持脑氧供需平衡的重要机制,明确患者CA能力有助于评估患者预后;维持患者MAP在CA范围内有助于维持重要器官的灌注。但目前还没有理想的监测方式用于患者CA监测,无创局部脑氧饱和度（regional cerebral oxy...     

Effects of desflurane on cerebral autoregulation

The aim of this study was to determine the effects of desflurane,at 1 and 1.5 MAC, on cerebral autoregulation. Data were analysedfrom eight patients undergoing non-neurosurgical procedure.The blood flow velocity in the middle cerebral artery was measuredby transcranial Doppler ultrasound and cerebral autoregulationwas assessed by the transient hyperaemic response test. Partialpressure of the end-tidal carbon dioxide (PE'_CO2) and mean arterialpressure were measured throughout the study. Anaesthesia wasinduced with propofol and was maintained with desflurane atend-tidal concentrations of 7.4% (1 MAC) or 10.8% (1.5 MAC).The order of administration of the desflurane concentrationswas determined randomly and a period of 15 min was allowed forequilibration at each concentration. The transient hyperaemicresponse tests were performed before induction of anaesthesiaand after equilibration with each concentration of desflurane.An infusion of phenylephrine was used to maintain pre-inductionmean arterial pressure and ventilation was adjusted to maintainthe pre-induction value of PE'_CO2 throughout the study. Twoindices derived from the transient hyperaemic response test(the transient hyperaemic response ratio and the strength ofautoregulation) were used to assess cerebral autoregulation.Desflurane resulted in a marked and significant impairment incerebral autoregulation; at concentrations of 1.5 MAC, autoregulationwas almost abolished. Br J Anaesth 2001; 87: 193–7     

Effect of ketanserin on cerebral blood flow autoregulation in healthy volunteers

Summary The effect of a clinically relevant dose of ketanserin (10 mg as a bolus followed by an infusion of 6mg/h) on cerebral blood flow (CBF) and CBF autoregulation was examined in 12 healthy volunteers. Changes in CBF were estimated by the cerebral arteriovenous-oxygen saturation difference method, while mean arterial blood pressure (MABP) was increased by norepinephrine and decreased by ganglionic blockade (trimethaphan camphosulphonate) combined with lower body negative pressure one hour after the infusion of ketanserin. During ketanserin infusion, MABP fell insignificantly by 2.5 mmHg (6 to –2), while CBF rose insignificantly by 5 ml/100 g/min. Autoregulation was preserved in all volunteers. CO₂-correction factors from 0 to 4.6% CBF/0.1 kPa were used. The lower limit of CBF autoregulation was 82 mmHg (80–86) with an SE of 3 mmHg (1–5) similar to a previous control group of healthy volunteers. Aside from a major decrease in MABP in one subject, no adverse side effects were observed.The present study shows that CBF autoregulation is maintained during ketanserin infusion.     

Cerebral autoregulation in children during sevoflurane anaesthesia

Introduction. Little is known about cerebral autoregulationin children. The aim of this study was to examine cerebral autoregulationin children. Methods. Cerebral autoregulation testing was performed duringless than 1 MAC sevoflurane anaesthesia in children (from 6months to 14 yr) and in adults (18–41 yr). Mean middlecerebral artery flow velocities (V_MCA) were measured using transcranialDoppler ultrasonography. Mean arterial pressure (MAP) was increasedto whichever was greater: 20% above baseline or (i) 80 mm Hgfor less than 9 yr, (ii) 90 mm Hg for 9–14 yr, and (iii)100 mm Hg for adults. Cerebral autoregulation was consideredintact if the autoregulatory index was     

Preservation of static and dynamic cerebral autoregulation after mild hypothermic cardiopulmonary bypass

Background. Dysfunction of cerebral autoregulation might contributeto neurological morbidity after cardiac surgery. In this study,our aim was to assess the preservation of cerebral autoregulationafter cardiac surgery involving cardiopulmonary bypass (CPB). Methods. Dynamic and static components of cerebral autoregulationwere evaluated in 12 patients undergoing coronary artery bypassgraft surgery, anaesthetized with midazolam, fentanyl, and propofol,and using mild hypothermic CPB (31–33°C). Arterialpressure (ABP), central venous pressure (CVP), and blood flowvelocity in the middle cerebral artery (CBFV) were recorded.The cerebral perfusion pressure (CPP) was calculated as a differencebetween mean ABP and CVP. Rapid decrease of CPP was caused bya sudden change of patients' position from Trendelenburg toreverse Trendelenburg. Cerebral vascular resistance (CVR) wascalculated by dividing CPP by CBFV. Index of static cerebralautoregulation (CAstat) was calculated as the change of CVRrelated to change of CPP during the manoeuvre. Dynamic rateof autoregulation (RoRdyn) was determined as the change in CVRper second during the first 4 s immediately after a decreasein CPP, related to the change of CPP. Measurements were obtainedafter induction of anaesthesia, and 15, 30, and 45 min aftertermination of CPB. Results. No significant changes were found in CAstat or RoRdynafter CPB. Significant changes in CVR could be explained byconcomitant changes in body temperature and haematocrit. Conclusion. Autoregulation of cerebral blood flow remains preservedafter mild hypothermic CPB.      

Cerebral blood flow autoregulation in experimental subarachnoid haemorrhage in rat

Summary Haemodynamic instability is of great importance in clinical management of patients with subarachnoid haemorrhage (SAH). The significance of angiographically demonstrable vasospasm for disturbances of cerebral blood flow (CBF) and cerebral autoregulation has not yet been clarified.The present study was designed to describe disturbances of cerebral autoregulation during the timecourse of experimental SAH (eSAH) in rats. A second aim of the study was to relate the results to a reported timecourse of angiographic vasospasm in the same animal model. Previous studies have shown that the timecourse of angiographically visible vasospasm in eSAH is biphasic with maximal spasm at 10 min and 2 days after induction of eSAH. At 5 days, the vasospasms have resolved.CBF was measured using a¹³³-Xenon intracarotid injection method which allowed serial measurements of mean hemispheric CBF during controlled manipulations of arterial blood pressure. In this way, an autoregulation curve could be constructed.The present study shows that autoregulation is severely disturbed or even totally absent at 2 and 5 days after eSAH. Thus there seems to be no direct correlation between presence of angiographic vasospasm and impairment of autoregulation, or that the impairment of autoregulation is more protracted than the presence of cerebral vasospasm, presuming a correlation exist.     

A bedside test for cerebral autoregulation using transcranial Doppler ultrasound

Summary Although disorders of cerebral autoregulation are commonly seen in neurosurgical disease, there is currently no test of autoregulation in widespread use that may be performed safely at the bedside. The presence of autoregulation, however, can be seen in the brief hyperemic response in the middle cerebral artery distribution following a transient manual carotid artery compression in the neck. This transient hyperemic response (THR) is readily measured with transcranial Doppler techniques, and therefore might serve as a qualitative marker of cerebral autoregulation.To evaluate the THR as a clinical tool, carotid compressions were performed during 172 TCD studies on 79 patients with neurosurgical disorders and on 10 patients without cerebral disease. The results were correlated with clinical status (e.g., Hunt-Hess Grade for subarachnoid hemorrhage and Glasgow Coma Score for trauma). There were no complications arising from the compressions. A separate assessment of autoregulation was made from TCD recordings obtained intraoperatively during 16 procedures and correlated to the pre-operative THRs. Autoregulation was further assessed in 4 patients during a hypotensive challenge, and again compared to the THRs.A strong correlation was seen between the THR results and clinical status. The THR was also strongly correlated with the intraoperative assessments, and all 4 patients receiving hypotensive challenges had abnormal THRs and demonstrated evidence of poor autoregulation during the challenge. None of the control patients had abnormal THRs.The THR arising from transient artery compression is readily detected with TCD techniques and correlates well with clinical status and other indicators of autoregulatory ability. The THR test can be safely performed at the bedside, uses noninvasive technology, and may emerge as a useful marker of cerebral autoregulation.     

Cerebral autoregulation following prophylactic and delayed experimental STA-MCA bypass

Summary Cerebral autoregulation is impaired in ischaemic regions. We hypothesized that pre-existing STA-MCA bypass would be superior to delayed revascularization in maintaining ipsilateral rCBF and preserving cerebral autoregulation following experimental stroke. Two series of dogs were tested to evaluate this hypothesis, but which was disproved for the chosen experimental conditions.In the first, eight dogs underwent craniotomy, STA-MCA bypass, and radiolabeled microsphere rCBF determinations. Blood pressure was manipulated with intravenous adenosine and levarterenol. Ischaemic zone rCBF was measured at MAP 60 mm Hg (97.2 ml·min^–1·100 g^–1) and MAP 140 mm Hg (113.6) (p=NS), in the intact arterial system with the patent bypass in place. An hemispheric ipsilateral ischaemic lesion was then created, and three further microsphere rCBF determinations were made at MAP 60 mm Hg (41.7ml·min^–1·100 g^–1), MAP 100 mm Hg (52.6) and MAP 140 mm Hg (58.3). There were no significant differences between these measurements (ANOVA p=NS).In a second series of five animals the bypass was placed and the stroke lesion created first. Ischaemic zone rCBF was then measured at MAP 60 mm Hg (35 ml·min^–1·100 g^–1) and MAP 140 mm Hg (44 ml·min^–1·100 g^–1) (p=NS), with the patent bypass in place. The bypass was then clamped for 15 minutes and profound ischaemia confirmed (5 ml·min^–1·100 g^–1, p < 0.05). Three further microspherer CBF determinations were made following bypass reopening at MAP 60 mm Hg (29 ml·min^–1·100 g^–1), MAP 100 mm Hg (33 ml·min^–1·100 g^–1) and MAP 140 mm Hg (36 ml·min^–1·100 g^–1). There were no significant differences between these measurements (ANOVA p=NS).In the first series hypertension did not significantly affect rCBF in the intact system. The risk of a prophylactic bypass producing deleterious flow increases thus appears minimal. In both series no significant rCBF changes occurred despite extremes of blood pressure in the post-occlusive hemisphere protected by a pre-existing bypass. In the second series ischaemic zone rCBF was not significantly affected by hypo- or hypertension even following fifteen minutes of profound ischaemia with delayed revascularization.Both prophylactic and delayed revascularization were effective in preserving ischaemic zone autoregulatory function, disproving our hypothesis. These data support the continued utility of prophylactic or delayed STA-MCA bypass in clinical situations when the potential for acute vascular injury is high.     

Influence of external cardiac pacing on cerebral oxygenation measured by near‐infrared spectroscopy in children after cardiac surgery

Background: The brain of children in the early period after repair of congenital heart defects with cardiopulmonary bypass (CPB) may be more vulnerable to hemodynamic changes because of impaired cerebral autoregulation. During postoperative testing of the external temporary safety pacer, we performed desynchronizing ventricular pacing (VVI) while monitoring cerebral oxygenation using near‐infrared spectroscopy (NIRS). Methods: We prospectively investigated 11 children (6 girls, 5 boys). Mean age was 6.1 months (±3.8 months) and mean weight: 5.3 kg (±1.5 kg). We performed measurements at four study steps: baseline I, VVI pacing, baseline II and atrial pacing (AOO) to exclude effects of higher heart rate. We continuously measured the effects on hemodynamic and respiratory parameters as well as on cerebral tissue oxygenation index (TOI). Hemoglobin difference (HbD) was calculated as a parameter for cerebral blood flow (CBF). Results: Ventricular pacing leads to a significant decrease in arterial blood pressure and central venous saturation accompanied by an immediate and significant decrease in TOI (63.3% ± 7.6% to 61.5% ± 8.4% [P < 0.05]) and HbD (0.51 ± 1.8 μmol·l⁻¹ to −2.9 ± 4.7 μmol·l⁻¹ [P < 0.05]). Conclusion: Cardiac desynchronization after CPB seems to reduce CBF and cerebral oxygenation in children.     

Effects of remifentanil/propofol in comparison with isoflurane on dynamic cerebrovascular autoregulation in humans

BACKGROUND: This study investigates the effects of remifentanil and propofol in comparison to isoflurane on dynamic cerebrovascular autoregulation in humans. METHODS: In 16 awake patients dynamic cerebrovascular autoregulation was measured using transcranial Doppler sonography (TCD). Thereafter patients were intubated, ventilated with O2/air (FiO2=0.33) and randomly assigned to one of the following anesthetic protocols: group 1 (n=8): 0.5 microg x kg(-1) x min(-1) remifentanil combined with a propofol-target plasma concentration of 1.5 microg x ml(-1) group 2 (n=8): 1.8 % isoflurane (1.5 MAC). Following 20 min of equilibration the autoregulatory challenge was repeated. Arterial blood gases and body temperature were maintained constant over time. Statistics: Mann-Whitney U-test and Wilcoxon signed-rank test. RESULTS: Dynamic autoregulation was intact in all patients prior to induction of anesthesia expressed by an autoregulatory index (ARI) of 5.4+/-1.21 (mean+/-SD, group 1) and 5.9+/-0.98 (mean+/-SD, group 2). With remifentanil/propofol anesthesia dynamic autoregulation was similar to the awake state (group 1: ARI=4.9+/-0.88). In contrast, autoregulatory response was delayed with 1.5 MAC isoflurane (group 2, ARI=2.1+/-0.92) (P<0.05). CONCLUSION: These data show that dynamic cerebrovascular autoregulation is maintained with remifentanil-based total intravenous anesthesia. This is consistent with the view that narcotics (and hypnotics) do not alter the physiologic cerebrovascular responses to changes in MAP. In contrast, 1.5 MAC isoflurane delays cerebrovascular autoregulation compared to the awake state.     

Phase shift and correlation coefficient measurement of cerebral autoregulation during deep breathing in traumatic brain injury (TBI)

Summary Background. Impairment of cerebral autoregulation is known to adversely affect outcome following traumatic brain injury (TBI). The phase shift (PS) method of cerebral autoregulation (CA) assessment describes the time lag between fluctuations in arterial blood pressure (ABP) and cerebral blood flow velocity (CBFV) in the middle cerebral artery. An alternative method (Mx-ABP) is based on the statistical correlation between ABP and CBFV waveforms over time. We compared these two indices in a cohort of severely head injured patients undergoing controlled, 6-breaths-per-minute ventilation. Methods. PS and Mx-ABP were calculated from 33 recordings of CBFV and MAP in 22 patients with TBI. Spearman’s correlation coefficient was used to assess the agreement between PS and Mx-ABP. The relationship between ICP slow wave amplitude, MAP slow wave amplitude and mean ICP was also examined. Findings. Mean values for Mx-ABP and PS were 0.44 ± 0.27, and 49 ± 26 (degrees), respectively. PS correlated significantly with Mx-ABP (r = −0.648, p < 0.001). A Bland-Altman plot of normalised Mx-ABP and Phase Shift values showed no significant bias or relationship (mean difference = 0.0004, r = −0.037, p = 0.852). During the test procedure, ICP fluctuated in an approximately sinusoidal fashion, with a mean amplitude of 4.96 ± 2.72 mmHg (peak to peak). The magnitude of ICP fluctuation during deep breathing correlated weakly but significantly with mean ICP (r = 0.391, p < 0.05) and with the amplitude of ABP fluctuations (r = 0.625, p < 0.0005). Conclusions. Phase shift and Mx-ABP in TBI are well correlated. Deep breathing presents as an effective tool with which to assess autoregulation using the phase shift method. Correspondence: Philip M. Lewis, BappSc, Scientific Officer, Department of Neurosurgery, Alfred Hospital, P.O. Box 315, Prahran, VIC 3181, Australia.     

Racemic ketamine does not abolish cerebrovascular autoregulation in the pig

BACKGROUND: Little is known about the influence of racemic ketamine on autoregulation of cerebral blood flow (CBF), and available reports regarding its influence on cerebral hemodynamics are contradictory. This study was designed to evaluate cerebrovascular responses to changes in the mean arterial pressure (MAP) during ketamine anesthesia. METHODS: In eight normoventilated pigs anesthesia was induced with propofol and maintained by i.v. infusion of ketamine (15.0 mg kg(-1) x h(-1)) during measurements. The intra-arterial xenon clearance technique was used to calculate CBF. Balloon-tipped catheters were introduced in the inferior caval vein and mid-aorta, and increases or decreases by up to 40% in mean arterial pressure (MAP) in random order were achieved by titrated inflation of these balloon catheters. Cerebral blood flow was determined at each MAP level. Regression coefficients of linear pressure-flow curves were calculated in all animals. RESULTS: From the mean baseline level (101 mmHg) MAP was reduced by 20% and 40%, and increased by 26% and 43%. The maximal mean increase and decrease in MAP induced a 12% increase and a 15% decrease, respectively, of CBF from the mean baseline level (52.6 ml.100 g(-1) x min1). The 95% confidence interval (-0.02; 0.38) of the mean regression coefficient of individual pressure-flow curves does not include the regression coefficient (0.64) of a linear correlation between MAP and CBF including origo (correlation coefficient 0.99), which indicates complete lack of cerebrovascular autoregulation. CONCLUSIONS: We conclude that autoregulation of CBF is not abolished during continuous ketamine infusion in normoventilated pigs and that previous divergent conclusions are unlikely to be associated with severe impairment of cerebrovascular autoregulation.     

Applied cerebral physiology

This article reviews cerebral metabolism and blood flow, and the pressure dynamics within the cranial cavity. The brain functions within the confines of the cranial cavity and it is important to understand the dynamics of the parenchyma, cerebrospinal fluid and blood in relation to intracranial pressure (ICP) and metabolic needs. It requires an uninterrupted supply of oxygen and glucose to maintain its basal energy requirements and these are increased during periods of enhanced activity. Cerebral blood flow (CBF) is therefore critical for normal cerebral function. Its control is dictated by local intrinsic metabolic needs as well as extraneous factors such as arterial blood pressure, arterial carbon dioxide and oxygen tension, temperature and neural factors; all of which can be measured to guide therapy.     

A prospective,observational study of cerebrovascular autoregulation and its association with delirium following cardiac surgery

This aim of this prospective observational cohort study was to evaluate any association between postoperatively impaired cerebrovascular autoregulation and the onset of delirium following cardiac surgery. Previous studies have shown that impaired intra-operative cerebrovascular autoregulation during cardiopulmonary bypass is associated with delirium. However, postoperative changes in cerebrovascular autoregulation and its association with delirium have not been investigated. One-hundred and eight consecutive adult cardiac surgical patients without baseline cognitive dysfunction or aphasia were included in the study. Cerebrovascular autoregulation was assessed by the Pearson correlation between near-infrared spectroscopy-derived cerebral tissue oxygen saturation and mean arterial pressure to derive the tissue oximetry index. Cerebrovascular autoregulation was monitored for a minimum of 90 min on postoperative day 0 and postoperative day 1. Delirium was assessed throughout intensive care unit admission using the confusion assessment method for the intensive care unit. We observed delirium in 24 of the 108 patients studied. The mean (SD) tissue oximetry index was higher in delirious patients on postoperative day 0 compared with non-delirious patients; 0.270 (0.199) vs. 0.180 (0.142), p = 0.044, but not on postoperative day 1; 0.130 (0.160) vs. 0.150 (0.130), p = 0.543. All patients showed improvement in tissue oximetry index on postoperative day 1 compared with postoperative day 0. Logistic regression analysis demonstrated tissue oximetry index on postoperative day 0 to be independently associated with delirium; odds ratio 1.05 (95%CI 1.01–1.10), p = 0.043. In conclusion, we found an association between impaired cerebrovascular autoregulation, measured by near-infrared spectroscopy, and delirium in the early postoperative period.     

Indomethacin and cerebral autoregulation in severe head injured patients: a transcranial Doppler study

Summary Objective. To assess the effect of indomethacin on cerebral autoregulation, systemic and cerebral haemodynamics, in severe head trauma patients. Design. Prospective, controlled clinical trial, with repeated measurements. Settings. A 12-bed adult general intensive care unit in a third level referral university hospital. Patients. 16 severely head injured patients, 14 males, age range 17–60. Interventions. Indomethacin was administrated as a load plus continuous infusion. Indomethacin reactivity was assessed as the estimated cerebral blood flow change elicited by the load. Dynamic and static cerebral autoregulation tests were performed before indomethacin administration, and during its infusion. Measurements and main results. Systemic and cerebral haemodynamic changes were assessed through continuous monitoring of mean arterial pressure, transcranial Doppler cerebral blood flow velocity, intracranial pressure, cerebral perfusion pressure, and jugular venous oxygen saturation. Indomethacin loading dose was immediately followed by a cerebral blood flow median decrease of 36 or 29% (p = ns) evaluated by two different methods, by an ICP decrease and by an AVDO₂ increase from 3.52 to 6.15 mL/dL (p = 0.002). Dynamic autoregulation increased from a median of 28 to 57% (p<0.05) during indomethacin infusion; static autoregulation also increased, from a median of 72 to 89% (p = ns). Conclusions. Indomethacin decreased intracranial pressure and cerebral blood flow, and increased cerebral perfusion pressure, while maintaining tissue properties of further extracting O₂. The increase in both autoregulatory values reveals an enhancement of cerebral microvasculature reactivity under indomethacin, during hypertensive and – especially – during hypotensive situations.     

Angiotensin converting enzyme inhibition,CBF autoregulation,and ICP in patients with normal-pressure hydrocephalus

Summary Fourteen patients with normal pressure hydrocephalus had the autoregulation of cerebral blood flow (CBF) and intracranial pressure (ICP) investigated. In 8 of the patients the effect of Captopril on ICP and CBF was also investigated. The mean arterial blood pressure (MABP) was 109 mmHg (intra-arterially), and ICP was 11 mmHg (intraventricularly). Changes in global CBF were estimated by the arterio-venous oxygen difference method. The autoregulation of CBF was present in 13 of the patients (p < 0.01). The lower limit of CBF autoregulation was 86% of the baseline perfusion pressure. One hour after 50 mg of captopril perorally, MABP was reduced 16 mmHg, and ICP and CBF were unchanged. The autoregulation was maintained and the lower limit was decreased 19 mmHg. Thus patients would be expected to benefit from captopril treatment in hypotensive anaesthesia.     

Effect of adenosine-induced hypotension on the cerebral autoregulation in the anesthetized pig

The influence on cerebral blood flow (CBF) and autoregulation of systemic adenosine infusion, at doses that produced a 29 +/- 4% (0.28 +/- 0.06 mg/kg/min) or a 55 +/- 2% (0.49 +/- 0.07 mg/kg/min) reduction of mean arterial blood pressure (MABP), was evaluated in 12 normoventilated fentanyl/N2) anesthetized pigs. CBF was determined as sagittal sinus outflow and recorded continuously by an electromagnetic technique. Autoregulation was evaluated by two formal tests: infusion of angiotensin for elevation of MABP, and reduction of myocardial filling pressure by caval block for graded MABP decrease before, during and after adenosine infusion. CBF as well as cerebral metabolic rate of oxygen were unaffected during both levels of hypotension and were not significantly altered after the hypotension. Signs of impaired autoregulation were found during the angiotensin test as well as during the caval block at light hypotension (92 +/- 3 mmHg, 12.3 +/- 0.4 kPa), while autoregulation was completely abolished at moderate hypotension (59 +/- 2 mmHg, 7.9 +/- 0.3 kPa). After termination of adenosine-induced hypotension, autoregulation was restored in all animals within 60 min. It is concluded that systemically administered adenosine preserves CBF, even at low MABP levels, by a direct cerebral vasodilatory effect. However, the cerebral autoregulatory mechanisms are impaired or abolished in a dose-dependent and reversible manner.     

Effect of xenon on cerebral autoregulation in pigs

There are little data on the effect of anaesthetic concentrations of xenon on cerebral pressure autoregulation. In this study, we have investigated the effect of 79% xenon inhalation on cerebral pressure autoregulation and CO2 response in pigs. Ten pigs were randomly allocated to receive xenon 79% or halothane anaesthesia, respectively, in a crossover designed study. Halothane was used to validate the experimental set-up. Transcranial Doppler was performed to determine the mean flow velocities in the middle cerebral artery (vMCA) during defined cerebral perfusion pressures and during normo-, hyper- and hypoventilation. The results showed that the inhalation of 79% xenon preserved cerebral autoregulation during conditions of normo-, hyper- and hypoventilation and at different cerebral perfusion pressures in pigs. These results suggest that with the inhalation of xenon, in the highest concentration suitable for a safe clinical use, cerebral autoregulation is preserved.     

Implementation of cerebral autoregulation into computational fluid dynamics studies of cardiopulmonary bypass

Peri‐ or postoperative neurological complications are among the main risks for patients undergoing extracorporeal circulatory support (ECC). Two of the main reasons are an increased risk for strokes and altered flow conditions leading to cerebral hypoperfusion. This is strongly affected by cerebral autoregulation, which is the body's intrinsic ability to provide sufficient cerebral blood flow (CBF) despite changes in cerebral perfusion pressure (CPP). This complex mechanism has been mainly neglected in numerical studies, which have often been applied for analysis of ECC. In this study, a mathematical model is presented to implement cerebral autoregulation into computational fluid dynamics (CFD) studies. CFD simulations of cardiopulmonary bypass (CPB) were performed in a 3D model of the cardiovascular system, with flow variations between 4.5–6 L/min. Cerebral outlets were modeled using an equation to calculate CBF based on CPP. Assuming full regulation, CBF was kept constant for CPP between 80 and 120 mm Hg. A deviation in CBF of 20% occurred for CPP between 55–80 mm Hg and 120–145 mm Hg, respectively. The level of regulation was varied to take possible impairment of cerebral autoregulation into account. Furthermore, chronic hypertension was modeled by increasing the baseline CPP. Results indicate that even for full autoregulation, CBF is decreased during CPB. It is even lower for impaired autoregulation and hypertensive patients, demonstrating the strong impact of autoregulation on CBF. It is therefore imperative to include this mechanism into CFD studies. The presented model can help to improve CPB support conditions based on patient‐specific autoregulation parameters.