Pressure is not flow: Rethinking blood pressure as a surrogate for cerebral blood flow during general anesthesia
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Background
Mean arterial pressure (MAP) is pharmacologically augmented in selected perioperative and critical care settings, including acute neurological conditions and after cardiac arrest, with the aim of improving cerebral perfusion, although it remains uncertain whether higher arterial pressure translates into increased cerebral blood flow (CBF). We investigated the CBF response to MAP augmentation with norepinephrine (NE), a commonly used vasopressor in perioperative and critical care settings, during propofol-based general anesthesia.
Methods
In this prospective within-subject interventional study, 16 neurologically intact patients with ASA physical status I–II undergoing elective surgery were studied using phase-contrast magnetic resonance imaging. CBF was quantified in the awake state and during propofol-based general anesthesia before and after NE-induced MAP augmentation. During general anesthesia, NE was titrated to increase MAP by approximately 25% from baseline. Concurrent systemic hemodynamics were assessed.
Results
General anesthesia was associated with a 50.1% (interquartile range, 42.1–55.7%) reduction in CBF and a 24.2% (20.3–29.2%) reduction in MAP compared with the awake state (both P<0.001). During general anesthesia, NE-induced MAP augmentation increased MAP by 25.7% (21.9–32.0%; P<0.001), whereas CBF remained unchanged (P=1.000). Cardiac output remained unchanged (P=0.163), whereas systemic vascular resistance index and cerebrovascular resistance increased by 40.0% (28.7–45.2%) and 36.2% (17.7–42.8%), respectively (both P<0.001). Changes in CBF during MAP augmentation were not associated with concurrent changes in MAP, cardiac output, or systemic vascular resistance index.
Conclusions
In neurologically intact patients undergoing propofol-based general anesthesia, clinically relevant NE-induced MAP augmentation did not increase CBF despite an approximately 50% lower CBF than in the awake state. These findings challenge the assumption that pharmacological elevation of an otherwise adequate MAP improves cerebral perfusion in this setting. While maintaining adequate arterial pressure remains essential, further MAP augmentation should not be assumed to increase CBF.
Clinical Trial Registration: https://clinicaltrials.gov/study/NCT06855407 ; NCT06855407 .
Clinical Perspective
What Is New?
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Norepinephrine-induced augmentation of mean arterial pressure by approximately 26% during propofol-based general anesthesia did not increase cerebral blood flow in neurologically intact patients.
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Cerebral blood flow was approximately 50% lower during general anesthesia than in the awake state and remained at this lower level during mean arterial pressure augmentation.
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Cardiac output remained unchanged, whereas systemic and cerebrovascular resistance increased during norepinephrine-induced mean arterial pressure augmentation.
What Are the Clinical Implications?
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Pharmacological augmentation of an otherwise adequate mean arterial pressure should not be assumed to increase cerebral blood flow during propofol-based general anesthesia.
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Mean arterial pressure alone may therefore be an inadequate surrogate for cerebral blood flow when setting hemodynamic targets during general anesthesia.
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Maintaining adequate arterial pressure remains essential, but further pharmacological pressure augmentation should be distinguished from the treatment of hypotension.
