Cerebral Autoregulation and Cerebral Blood Flow Response to Mean Arterial Pressure Challenge Following Induction of General Anaesthesia for Neuroradiology Procedures

 

Dr. Madhusudhana Rao Bathala¹, Dr. Seham Syeda², Dr. Saurabh Bhandge³

 

¹Assistant Professor, Dept. Of Anaesthesiology, Division of Neuroanesthesia and Neurocritical Care, Ramaiah Medical College, Ramaiah University of Applied Sciences, Bengaluru, Karnataka, India

Email Id: drbmadhusudhanrao15@gmail.com 

²Assistant Professor, Dept. Of Anaesthesiology, Division of Neuroanesthesia and Neurocritical Care, Ramaiah Medical College, Ramaiah University of Applied Sciences, Bengaluru, Karnataka, India

Email Id: sehamsyeda@gmail.com 

³Associate Professor, Dept. Of Anaesthesia and Critical Care, Shri Rawatpura Sarkar Institute of Medical Sciences and Research, Atal Nagar Nawa Raipur, Chhattisgarh, IND.

Email Id: Saurabh.bhandge@gmail.com 

 

Corresponding Author

Dr. Madhusudhana Rao Bathala

 

ABSTRACT

Background: Intraoperative hypotension following induction of general anaesthesia is common and has been associated with adverse neurological outcomes. Cerebral autoregulation (CA) normally maintains stable cerebral blood flow (CBF) across a range of arterial pressures; however, anaesthetic agents such as propofol may transiently impair this protective mechanism.

Objectives: To determine the incidence of impaired cerebral autoregulation following induction of general anaesthesia and to evaluate the effect of a mean arterial pressure (MAP) challenge on cerebral blood flow and autoregulatory function.

Methods: In this prospective observational study, 40 adult patients undergoing elective interventional neuroradiology procedures under total intravenous anaesthesia were enrolled. Mean arterial pressure, mean middle cerebral artery blood flow velocity (MCAv_mean), and regional cerebral oxygen saturation (rSO₂) were continuously monitored. Dynamic cerebral autoregulation was assessed using the mean flow index (Mxa).  Mxa value >0.3 was considered indicative of impaired autoregulation. In patients developing hypotension (≥20% reduction from baseline MAP), a norepinephrine-induced MAP challenge was performed.

Results: Following induction of anaesthesia, 53% of patients demonstrated impaired cerebral autoregulation despite comparable demographic characteristics, cardiovascular risk factors, anaesthetic depth, and baseline haemodynamics. In patients with impaired CA, MAP augmentation resulted in significant increases in MCAv_mean and a significant reduction in Mxa, indicating restoration of autoregulation. A strong positive correlation was observed between baseline Mxa and cerebral blood flow variation (ΔCBF) (r = 0.73, p < 0.001).

Conclusion: Patients undergoing neuroradiological procedures frequently exhibit impaired cerebral autoregulation secondary to general anesthesia induced hypotension. Early vasopressor-guided optimization of mean arterial pressure can restore autoregulatory function and improve cerebral perfusion, highlighting the importance of individualized, autoregulation guided hemodynamic strategies.

KEYWORDS: Cerebral autoregulation; Mean arterial pressure; Transcranial Doppler; General anaesthesia; Cerebral blood flow.

How to Cite: Dr. Madhusudhana Rao Bathala1, Dr. Seham Syeda2, Dr. Saurabh Bhandge3, (2026) Cerebral Autoregulation and Cerebral Blood Flow Response to Mean Arterial Pressure Challenge Following Induction of General Anaesthesia for Neuroradiology Procedures, European Journal of Clinical Pharmacy, Vol.8, No.1, pp. 5492-5497

INTRODUCTION

Intraoperative hypotension frequently occurs following induction of general anaesthesia and has been consistently associated with increased postoperative morbidity and mortality, including neurological complications and postoperative delirium [1–3]. Propofol, a widely used induction and maintenance agent, causes dose-dependent reductions in Systemic Vascular Resistance (SVR) and arterial pressure, predisposing patients to hypotension during the early phases of anaesthesia [4].

 

Cerebral autoregulation (CA) is a critical physiological mechanism that maintains relatively constant cerebral blood flow (CBF) across a wide range of systemic blood pressures [5]. When autoregulation is intact, cerebral arterioles adjust their tone in response to changes in perfusion pressure, thereby protecting the brain from both hypoperfusion or hyperperfusion. However, general anaesthesia, abrupt haemodynamic changes, and underlying cerebrovascular disease may impair this mechanism [6–8]. Importantly, systemic blood pressure values alone may not accurately reflect the adequacy of cerebral perfusion [12,13].

 

Dynamic cerebral autoregulation can be assessed using the mean flow index (Mxa), derived from the correlation between spontaneous fluctuations in mean arterial pressure (MAP) and cerebral blood flow velocity [14,22]. Elevated Mxa values indicate pressure-passive cerebral circulation and impaired autoregulatory capacity. The present study aimed to evaluate the prevalence of impaired cerebral autoregulation following induction of general anaesthesia for neuroradiology procedures and to assess the cerebrovascular response to a targeted MAP challenge.

 

MATERIALS AND METHODS

Study Design and Patients

This prospective, single-centre observational study was conducted in adult patients (aged ≥18 years) undergoing elective interventional neuroradiology procedures, including diagnostic cerebral angiography, intracranial aneurysm coiling, arteriovenous malformation embolization, and tumor embolization, under general anaesthesia. Institutional Ethics Committee approval was obtained, and written informed consent was secured from all participants. All identifying patient information was removed to ensure confidentiality, and consent was obtained for publication of anonymized data. 

 

Total intravenous anaesthesia was induced using propofol and remifentanil via target-controlled infusion. Anaesthetic depth was monitored using processed electroencephalography (Patient State Index), with values maintained between 25 and 50. End-tidal carbon dioxide, non-invasive arterial blood pressure monitoring, core temperature, and oxygen saturation were maintained within normal physiological ranges.

Continuous intraarterial blood pressure monitoring was performed. Cerebral blood flow velocity was measured in the middle cerebral artery using transcranial Doppler ultrasound. Regional cerebral oxygen saturation was monitored using near-infrared spectroscopy.{ brands of the monitor used ]

· Cerebral autoregulation was quantified using the mean flow index (Mxa), calculated as the Pearson correlation coefficient between MAP and MCAv_mean over multiple epochs. Mxa >0.3 was considered indicative of impaired autoregulation (22,23).

o Epoch length

o Sampling frequency

o Signal preprocessing (filtering, artifact rejection)
are not described.

Given that Mxa is a methodology-sensitive index, lack of detail limits reproducibility.

 

In patients who developed hypotension (≥20% reduction from baseline MAP), norepinephrine infusion was started to restore MAP. Changes in MCAv_mean, Mxa, and ΔCBF were analysed before and after the MAP challenge. [ add when was baseline MAP measured ·  “Baseline MAP” is used repeatedly, but timing is unclear:

· Pre-induction awake baseline?

· After arterial line placement but before propofol?

This distinction is crucial because autoregulation indices are sensitive to baseline state.

MAP challenge is described conceptually but lacks protocol clarity:

· Target MAP?

· Rate of norepinephrine escalation?

· Duration between pre- and post-challenge measurements?

Clearly define ΔCBF mathematically in Methods and standardize units.

Clarify whether TCD monitoring was unilateral or bilateral.

Specify probe fixation method (important for signal stability).

rSO₂ device brand and sensor location should be stated.

Rationale for sample size, or

Explicit statement that this was an exploratory hypothesis-generating study.

 

Statistical Analysis

Continuous variables were expressed as mean ± SD or median [IQR]. Comparisons were performed using appropriate parametric or non-parametric tests. Correlations were analysed using Pearson’s coefficient. A p-value <0.05 was considered statistically significant.

 

RESULTS

Patient Characteristics

Forty patients were included in the final analysis. The median age was 58 years, and 57% were female. Baseline demographic characteristics, cardiovascular risk factors, and haemodynamic parameters were comparable between patients with preserved cerebral autoregulation (CA+) and those with impaired autoregulation (CA−).

 

 

 

 

Table 1. Baseline demographic and clinical characteristics

CA+: preserved cerebral autoregulation; CA−: impaired cerebral autoregulation; NS: non-significant.

 

Cerebral Autoregulation After Induction

Following induction of general anaesthesia, the mean MAP decreased to approximately 67 mmHg. Impaired cerebral autoregulation (Mxa >0.3) was identified in 21 patients (53%). No significant differences were observed between CA+ and CA− groups in terms of age, anaesthetic depth, end-tidal CO₂, temperature, or rSO₂ values.

 

Table 2. Monitoring parameters following anaesthesia induction

CA+: preserved cerebral autoregulation; CA−: impaired cerebral autoregulation; NS: non-significant; p-value <0.05 was considered statistically significant.

 

Effect of Mean Arterial Pressure Challenge

Twenty-two patients required a MAP challenge. In patients with impaired CA, MAP augmentation resulted in a significant increase in MCAv_mean and a marked reduction in Mxa, indicating restoration of autoregulatory function. In contrast, patients with preserved CA demonstrated minimal changes in cerebral blood flow parameters.

 

Table 3. Cerebrovascular response to MAP challenge

CA+: preserved cerebral autoregulation; CA−: impaired cerebral autoregulation; p-value <0.05 was considered statistically significant.

 

Relationship Between Mxa and ΔCBF

A strong positive correlation was observed between baseline Mxa and ΔCBF (r = 0.73, p < 0.001), demonstrating that patients with more severely impaired autoregulation experienced greater increases in cerebral blood flow in response to MAP augmentation.

 

DISCUSSION

The present study demonstrates that impairment of cerebral autoregulation (CA) is a frequent occurrence following induction of general anaesthesia for neuroradiology procedures, affecting more than half of the studied population. This finding is clinically important, as cerebral autoregulation is a key protective mechanism that maintains stable cerebral blood flow (CBF) across a wide range of systemic blood pressures (1,2). Disruption of this mechanism renders cerebral perfusion pressure-dependent, increasing vulnerability to perioperative cerebral hypoperfusion or hyperperfusion.

 

Incidence and Clinical Relevance of Impaired Cerebral Autoregulation

In this cohort, 53% of patients exhibited impaired CA as defined by an Mxa value greater than 0.3 following induction of anaesthesia. This incidence is higher than traditionally anticipated in patients without overt traumatic brain injury or raised intracranial pressure. However, similar rates of autoregulatory impairment have been reported in patients undergoing cardiac surgery, carotid endarterectomy, and procedures requiring deep anaesthesia or rapid haemodynamic manipulation (3–5).

 

The high prevalence observed may be attributable to the combined effects of anaesthetic agents, abrupt reductions in mean arterial pressure (MAP), and pre-existing cerebrovascular pathology. Propofol, the primary induction agent used in this study, is known to reduce systemic vascular resistance and arterial pressure while also exerting direct cerebrovascular effects (6,7). Although cerebral metabolic rate is reduced under propofol anaesthesia, autoregulatory capacity may be transiently impaired during periods of haemodynamic instability, particularly immediately after induction (8).

 

Lack of Predictive Value of Conventional Risk Factors

A notable observation in this study was the absence of significant differences in age, cardiovascular risk factors, baseline blood pressure, anaesthetic depth, or regional cerebral oxygen saturation between patients with preserved and impaired CA. These findings are consistent with prior investigations demonstrating that interindividual variability in cerebral autoregulatory limits is substantial and poorly predicted by demographic or clinical characteristics alone (9,10).

 

Chronic hypertension has traditionally been thought to shift the autoregulatory curve rightward, necessitating higher perfusion pressures to maintain adequate CBF (11). However, several studies have shown that acute intraoperative autoregulatory failure may occur independently of baseline blood pressure or hypertensive status (12,13). This reinforces the limitation of population-based blood pressure targets and highlights the inadequacy of using MAP thresholds alone as surrogates for cerebral perfusion adequacy.

 

Effect of Mean Arterial Pressure Challenge

The MAP challenge performed in hypotensive patients represents one of the most clinically relevant components of this study. In patients with impaired CA, augmentation of MAP using norepinephrine resulted in a significant increase in MCAv_mean and a marked reduction in Mxa values, indicating partial or complete restoration of autoregulatory function. These findings suggest that many patients with impaired CA were operating below their lower limit of autoregulation (LLA) following induction.

 

Previous studies have demonstrated that restoring MAP above the LLA improves cerebral perfusion and reduces pressure-dependent fluctuations in CBF (14–16). The present findings extend this concept to neuroradiology patients and emphasize that autoregulatory failure after induction is often functional and reversible rather than fixed.

 

In contrast, patients with preserved CA exhibited minimal changes in MCAv_mean following MAP augmentation, consistent with intact autoregulatory buffering. Interestingly, a small subset of patients demonstrated worsening Mxa values following aggressive MAP elevation, suggesting possible overshoot beyond the upper limit of autoregulation (ULA). This observation aligns with the concept of a narrow optimal perfusion window and underscores the risk of indiscriminate vasopressor-driven blood pressure escalation (17).

 

Relationship Between Static and Dynamic Autoregulation Metrics

A strong positive correlation was observed between baseline Mxa and cerebral blood flow variation (ΔCBF) during the MAP challenge. Patients with higher Mxa values experienced larger increases in CBF in response to pressure augmentation, indicating greater pressure dependency of cerebral perfusion.

 

Mxa is a well-validated index of dynamic cerebral autoregulation derived from the correlation between spontaneous fluctuations in MAP and cerebral blood flow velocity (18,19). The present findings support its physiological relevance and demonstrate its concordance with a more intuitive, flow-based measure such as ΔCBF. Similar relationships have been reported in neurocritical care and cardiac surgery populations, where impaired autoregulation has been associated with pressure-passive cerebral circulation and worse neurological outcomes (20–22).

 

Importantly, ΔCBF and Mxa identified autoregulatory impairment even when MAP values remained within conventionally accepted limits. This finding further challenges the reliance on absolute or relative blood pressure thresholds for intraoperative cerebral protection.

 

Implications for Intraoperative Blood Pressure Management

Current guidelines for intraoperative blood pressure management largely recommend maintaining MAP above fixed absolute values or within a percentage of baseline (23). However, these recommendations do not account for patient-specific autoregulatory limits and may fail to prevent cerebral hypoperfusion in susceptible individuals.

 

The present study supports a growing body of evidence advocating for individualized, autoregulation-guided haemodynamic management. Autoregulation-guided MAP targeting has been shown to reduce postoperative delirium and organ dysfunction in cardiac surgery patients (15,24). Given the vulnerability of neuroradiology patients to cerebral ischemia, this approach may be particularly beneficial in this population.

 

Integrating cerebral autoregulation monitoring into routine anaesthetic practice could enable clinicians to identify patients at risk of cerebral hypoperfusion early and tailor vasopressor therapy accordingly. While technical and logistical challenges remain, advances in non-invasive monitoring technologies may facilitate broader implementation in the future.

 

Add a dedicated limitations paragraph, including:

· Single-centre design

· Small sample size

· Surrogate outcome (MCAv ≠ absolute CBF)

· Lack of postoperative neurological outcomes

 

CONCLUSION

Impaired cerebral autoregulation is common following induction of general anaesthesia in patients undergoing neuroradiology procedures. Autoregulation failure appears to be functional and reversible in many patients, as targeted MAP augmentation restores cerebral blood flow regulation. These findings support the concept of individualized, autoregulation-guided haemodynamic management to optimize cerebral perfusion and potentially improve neurological outcomes.

References :

1. Wesselink EM, Kappen TH, Torn HM, Slooter AJC, van Klei WA. Intraoperative hypotension and the risk of postoperative adverse outcomes: a systematic review. Br J Anaesth. (2018) 121(4):706–21. doi: 10.1016/j.bja.2018.04.036

PubMed Abstract | Cross Ref Full Text | Google Scholar

2. Sessler DI, Sigl JC, Kelley SD, Chamoun NG, Manberg PJ, Saager L, et al. Hospital stay and mortality are increased in patients having a “triple low” of low blood pressure, low bispectral index, and low minimum alveolar concentration of volatile anesthesia. Anesthesiology. (2012) 116(6):1195–203. doi: 10.1097/ALN.0b013e31825683dc

PubMed Abstract | Cross Ref Full Text | Google Scholar

3. Futier E, Lefrant JY, Guinot PG, Godet T, Lorne E, Cuvillon P, et al. Effect of individualized vs standard blood pressure management strategies on postoperative organ dysfunction among high-risk patients undergoing major surgery: a randomized clinical trial. JAMA. (10 2017) 318(14):1346–57. doi: 10.1001/jama.2017.14172

PubMed Abstract | Cross Ref Full Text | Google Scholar

4. Su H, Eleveld DJ, Struys MMRF, Colin PJ. Mechanism-based pharmacodynamic model for propofol haemodynamic effects in healthy volunteers⋆. Br J Anaesth. (2022) 128(5):806–16. doi: 10.1016/j.bja.2022.01.022

PubMed Abstract | Cross Ref Full Text | Google Scholar

5. Claassen JAHR, Thijssen DHJ, Panerai RB, Faraci FM. Regulation of cerebral blood flow in humans: physiology and clinical implications of autoregulation. Physiol Rev. (2021) 101(4):1487–559. doi: 10.1152/physrev.00022.2020

PubMed Abstract | Cross Ref Full Text | Google Scholar

6. Birch AA, Dirnhuber MJ, Hartley-Davies R, Iannotti F, Neil-Dwyer G. Assessment of autoregulation by means of periodic changes in blood pressure. Stroke. (1995) 26(5):834–7. doi: 10.1161/01.STR.26.5.834

PubMed Abstract | Cross Ref Full Text | Google Scholar

7. Diehl RR, Linden D, Lücke D, Berlit P. Phase relationship between cerebral blood flow velocity and blood pressure. A clinical test of autoregulation. Stroke 26(10):1801–4. doi: 10.1161/01.STR.26.10.1801

PubMed Abstract | Cross Ref Full Text | Google Scholar

8. Diehl RR, Linden D, Lücke D, Berlit P. Spontaneous blood pressure oscillations and cerebral autoregulation. Clin Auton Res Off J Clin Auton Res Soc. (1998) 8(1):7–12. doi: 10.1007/BF02267598

Cross Ref Full Text | Google Scholar

9. Chaix I, Manquat E, Liu N, Casadio MC, Ludes P, Tantot A, et al. Impact of hypotension on cerebral perfusion during general anesthesia induction: a prospective observational study in adults. Acta Anaesthesiol Scand. (2020) 64(5):592–601. doi: 10.1111/aas.13537

PubMed Abstract | Cross Ref Full Text | Google Scholar

10. . Burkhart CS, Rossi A, Dell-Kuster S, Gamberini M, Möckli A, Siegemund M, et al. Effect of age on intraoperative cerebrovascular autoregulation and near-infrared spectroscopy-derived cerebral oxygenation. Br J Anaesth. (2011) 107(5):742–8. doi: 10.1093/bja/aer252

PubMed Abstract | Cross Ref Full Text | Google Scholar

11. Bijker JB, van Klei WA, Kappen TH, van Wolfswinkel L, Moons KGM, Kalkman CJ. Incidence of intraoperative hypotension as a function of the chosen definition: literature definitions applied to a retrospective cohort using automated data collection. Anesthesiology. (2007) 107(2):213–20. doi: 10.1097/01.anes.0000270724.40897.8e

PubMed Abstract | Cross Ref Full Text | Google Scholar

12. Brady K, Joshi B, Zweifel C, Smielewski P, Czosnyka M, Easley RB, et al. Real-time continuous monitoring of cerebral blood flow autoregulation using near-infrared spectroscopy in patients undergoing cardiopulmonary bypass. Stroke. (2010) 41(9):1951–6. doi: 10.1161/STROKEAHA.109.575159

PubMed Abstract | Cross Ref Full Text | Google Scholar

13. Cardim D, Robba C, Matta B, Tytherleigh-Strong G, Kang N, Schmidt B, et al. Cerebrovascular assessment of patients undergoing shoulder surgery in beach chair position using a multiparameter transcranial Doppler approach. J Clin Monit Comput. (2019) 33(4):615–25. doi: 10.1007/s10877-018-0211-7

PubMed Abstract | Cross Ref Full Text | Google Scholar

14. Skow RJ, Brothers RM, Claassen JAHR, Day TA, Rickards CA, Smirl JD, et al. On the use and misuse of cerebral hemodynamics terminology using transcranial Doppler ultrasound: a call for standardization. Am J Physiol Heart Circ Physiol. (2022) 323(2):H350–7. doi: 10.1152/ajpheart.00107.2022

PubMed Abstract | Cross Ref Full Text | Google Scholar

15. Brown CH, Neufeld KJ, Tian J, Probert J, LaFlam A, Max L, et al. Effect of targeting mean arterial pressure during cardiopulmonary bypass by monitoring cerebral autoregulation on postsurgical delirium among older patients: a nested randomized clinical trial. JAMA Surg. (2019) 154(9):819. doi: 10.1001/jamasurg.2019.1163

PubMed Abstract | Cross Ref Full Text | Google Scholar

16. Nilsson P. Early vascular aging (EVA): consequences and prevention. Vasc Health Risk Manag. (2008) 4:547–52. doi: 10.2147/VHRM.S1094

PubMed Abstract | Cross Ref Full Text | Google Scholar

17. Kotsis V, Stabouli S, Karafillis I, Nilsson P. Early vascular aging and the role of central blood pressure. J Hypertens. (2011) 29(10):1847–53. doi: 10.1097/HJH.0b013e32834a4d9f

PubMed Abstract | Cross Ref Full Text | Google Scholar

18. Amar J, Ruidavets JB, Chamontin B, Drouet L, Ferriéres J. Arterial stiffness and cardiovascular risk factors in a population-based study. J Hypertens. (2001) 19(3):381–87. doi: 10.1097/00004872-200103000-00005

PubMed Abstract | Cross Ref Full Text | Google Scholar

19. Petersen NH, Ortega-Gutierrez S, Reccius A, Masurkar A, Huang A, Marshall RS. Comparison of non-invasive and invasive arterial blood pressure measurement for assessment of dynamic cerebral autoregulation. Neurocrit Care. (2014) 20(1):60–8. doi: 10.1007/s12028-013-9898-y

Cross Ref Full Text | Google Scholar

20. Mets B. Should norepinephrine, rather than phenylephrine, be considered the primary vasopressor in anesthetic practice? Anesth Analg. (2016) 122(5):1707–14. doi: 10.1213/ANE.0000000000001239

PubMed Abstract | Cross Ref Full Text | Google Scholar

21. Vallée F, Passouant O, Le Gall A, Joachim J, Mateo J, Mebazaa A, et al. Norepinephrine reduces arterial compliance less than phenylephrine when treating general anesthesia-induced arterial hypotension. Acta Anaesthesiol Scand. (2017) 61(6):590–600. doi: 10.1111/aas.12905

Cross Ref Full Text | Google Scholar

22. Czosnyka M, Smielewski P, Kirkpatrick P, Menon DK, Pickard JD. Monitoring of cerebral autoregulation in head-injured patients. Stroke. (1996) 27(10):1829–34. doi: 10.1161/01.STR.27.10.1829

PubMed Abstract | Cross Ref Full Text | Google Scholar

23. Sorrentino E, Budohoski KP, Kasprowicz M, Smielewski P, Matta B, Pickard JD, et al. Critical thresholds for transcranial Doppler indices of cerebral autoregulation in traumatic brain injury. Neurocrit Care. (2011) 14(2):188–93. doi: 10.1007/s12028-010-9492-5

PubMed Abstract | Cross Ref Full Text | Google Scholar

24. Manquat E, Ravaux H, Kindermans M, Joachim J, Serrano J, Touchard C, et al. Impact of impaired cerebral blood flow autoregulation on electroencephalogram signals in adults undergoing propofol anaesthesia: a pilot study. BJA Open. (2022) 1:100004. doi: 10.1016/j.bjao.2022.100004

Cross Ref Full Text | Google Scholar

25. Olsen MH, Riberholt CG, Mehlsen J, Berg RM, Møller K. Reliability and validity of the mean flow index (Mx) for assessing cerebral autoregulation in humans: a systematic review of the methodology. J Cereb Blood Flow Metab. (2022) 42(1):27–38. doi: 10.1177/0271678X211052588

PubMed Abstract | Cross Ref Full Text | Google Scholar