Cerebral autoregulation: static vs. dynamic

Today, I would just like to add some details regarding differences between static and dynamic cerebral autoregulation. In a previous post about cerebral blood flow, I stated that the mechanism known as static cerebral autoregulation considers the net change in cerebral blood flow following the manipulation of cerebral perfusion pressure under steady state. Static cerebral autoregulation is often studied with drugs that increase (phenylephrine) or decrease (sodium nitroprusside) arterial pressure. As demonstrated by the figure below (from Tiecks et al.), it represents the long-term steady-state control of brain blood flow. In that example, steady-state cerebral blood flow (LMCA/RMCA in the figure) stays relatively constant following an elevation in arterial pressure when static cerebral autoregulation is intact (top panel). However, cerebral blood flow increases with arterial pressure when static cerebral autoregulation is affected (down panel).

Still, the relationship between arterial pressure and brain blood flow is not completely flat and some investigators recently challenged the concept of static cerebral autoregulation.  Indeed, Lucas et al. didn’t observe constant cerebral blood flow (and oxygenation) when decreasing (with sodium nitroprusside) and increasing (with phenylephrine) arterial pressure in healty subjects with intact cerebral autoregulation. The figure below shows cortical oxygenation (measured by near-infrared spectroscopy;A) and cerebral blood flow velocity (measured by transcranial Doppler; B) changes with the modulation of mean arterial pressure.

These observations suggest that cerebral blood flow and oxygenation are not independent of changes in arterial pressure. However, further studies are needed to support this data since, as stated by Immink et al. in a letter to editor regarding this work by Lucas et al.

New data of the last 2 decennia made us aware that determination of the blood pressure-CBF relationship in humans continues to remain difficult, because deliberately induced changes in blood pressure are inevitably accompanied by changes in flow and resistance that each independently have the potential to modify CBF and oxygenation.

This being acknowledged, sudden changes (elevation/reduction) in arterial pressure are transmitted directly to the brain circulation under usual circumstances, but brain blood flow tends to return to its baseline value within a brief period of time. The fast mechanisms that permit the restoration of brain blood flow after acute changes (elevation/reduction) in arterial pressure are referred to as dynamic cerebral autoregulation. The latter is often evaluated from spontaneous fluctuations in arterial pressure and cerebral blood flow velocity at baseline and during different interventions (such as head-up tilt, the Valsalva maneuver, or standing up). It can also be assessed using a sudden drop in arterial pressure with the thigh cuff method.  Some evidence suggests that dynamic cerebral autoregulation is better at responding to an augmentation vs. a reduction in mean arterial pressure.

In upcoming posts, I will discuss the parameters (such as PaCO2, temperature, etc.) and diseases (such as hypertension, diabetes, etc.) influencing cerebral autoregulation.

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