Cerebral Autoregulation

Most organ systems have some form of autoregulation to provide a steady supply of blood flow and oxygen to maintain normal physiologic function. This autoregulation is largely driven by chemical mediators to “couple” metabolic demand with blood supply. In other words, if the organ demands less oxygen, then it will be supplied with less blood. The brain and its associated vasculature are a perfect example of autoregulation in action!

Cerebral perfusion pressure (CPP) is defined as the mean arterial pressure (MAP) minus the intracranial pressure (ICP), or CPP = MAP – ICP. If the central venous pressure (CVP) exceeds the ICP, then the CPP = MAP – CVP instead. Normally, the CPP generates a cerebral blood flow (CBF) of ~50 cc per 100 grams of brain tissue per minute (cc/100g/min). Therefore, high systemic MAPs can translate to high CPPs and vice versa. This can be catastrophic during hypo OR hypertensive episodes, but thanks to autoregulation, the brain does a remarkable job of maintaining constant CPP over a wide range of MAPs by the myogenic actions of vascular smooth muscle that constrict when MAPs are high (thereby “shielding” the brain from high blood pressure) and dilate when hypotensive (to send more blood to the brain). This autoregulation occurs primarily at MAPs of 60 – 160 mmHg, but in patients with chronic hypertension, may occur at an even higher range.

Additionally, the partial pressure of carbon dioxide (PaCO2) is incredibly important in cerebral autoregulation. Normally, our PaCO2 is ~ 40 mmHg. As this drops, the vasculature constricts dropping CBF by ~ 1-2 cc/100g/min for every 1 mmHg drop in PaCO2. By extrapolating this, you can see that during hyperventilation, a very low PaCO2 will significantly drop CBF. This can be useful in extenuating circumstances (ie, impending brain herniation), but also places the brain at a real risk fo ischemia-related damage. On the contrary, as PaCO2 increases (ie, CO2 retention from narcotics), the cerebral vasculature will dilate leading to increased CBF which can be detrimental in patients struggling with preexisting elevations in ICP.

Interestingly, the partial pressure of oxygen (PaO2) really doesn’t affect CBF in HYPER-oxia. As the patient becomes more hypoxemic, CBF will start to increase once the PaO2 drops below ~40-50 mmHg to deliver more blood (and therefore oxygen content) to the brain.

Hopefully this illustrates the importance of MAP, PaCO2, and PaO2 on cerebral blood flow! Drop me a comment below with questions! 🙂

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