Summary
In a prospective study of 16 neurologically intact patients under propofol-based general anesthesia, norepinephrine raised mean arterial pressure by about 26% without increasing cerebral blood flow. The findings apply to this study setting and do not directly establish how pressure augmentation affects patients with acute neurological conditions.
A prospective study of 16 neurologically intact patients found that raising mean arterial pressure with norepinephrine during propofol-based general anesthesia did not increase cerebral blood flow. The medRxiv preprint reports that blood flow to the brain was about half the awake level under anesthesia, even after the pressure-raising intervention.
The result bears on a common clinical rationale for raising arterial pressure: that a higher pressure will improve blood supply to the brain. The study measured pressure and flow separately, and found that they did not move together in this group of patients.
How the study measured pressure and flow
Researchers studied 16 patients with American Society of Anesthesiologists physical status I–II who were neurologically intact and undergoing elective surgery. In this prospective within-subject study, each patient was measured while awake and during propofol-based general anesthesia. The team used phase-contrast magnetic resonance imaging to quantify cerebral blood flow (CBF), and assessed systemic haemodynamics alongside it.
During anesthesia, the researchers titrated norepinephrine, a vasopressor used to raise blood pressure, to increase mean arterial pressure (MAP) by approximately 25% from baseline. MAP is an average measure of arterial pressure over the cardiac cycle; CBF measures the volume of blood reaching the brain. They are related measures, but pressure alone does not describe flow, which also depends on vascular resistance.
Pressure rose while cerebral blood flow did not
Compared with the awake state, general anesthesia was associated with a 50.1% reduction in CBF (interquartile range, 42.1–55.7%) and a 24.2% reduction in MAP (20.3–29.2%). Both changes had P<0.001.
After norepinephrine was given during anesthesia, MAP rose by 25.7% (21.9–32.0%; P<0.001). CBF remained unchanged (P=1.000). Cardiac output also remained unchanged (P=0.163), while the systemic vascular resistance index increased by 40.0% and cerebrovascular resistance by 36.2% (both P<0.001). These measurements show that the higher arterial pressure was not accompanied by greater measured brain blood flow in this experiment.
The findings challenge the assumption that pharmacologically raising an otherwise adequate MAP necessarily improves cerebral perfusion during propofol-based anesthesia. They do not mean that maintaining adequate arterial pressure is unimportant; the authors distinguish pressure maintenance from further pressure augmentation as a means of increasing CBF.
The study is a small intervention in neurologically intact patients having elective surgery. MAP is also raised in some perioperative and critical-care settings, including acute neurological conditions and after cardiac arrest, but those patients and circumstances were not studied here. Whether the same pressure-flow relationship applies in those settings remains a separate clinical question.