Cerebral blood flow (CBF) is the blood supply to the brain in a given period of time.
In an adult, CBF is typically 750 millilitres per minute or 15% of the cardiac output.
CBF is a function of the pressure drop across the cerebral circulation divided by the cerebrovascular resistance (CVR).
CBF = (CAP - JVP) ÷ CVR
Where CAP is carotid arterial pressure, JVP is jugular venous pressure, and CVR is cerebrovascular resistance. CVR is derived from the pial arteriolar resistance.1
Autoregulation of Cerebral Blood Flow
Autoregulation
Cerebral blood flow is maintained at a relatively constant rate by intrinsic cerebral mechanisms referred to as autoregulation.
In addition to this global phenomenon, a region of brain tissue can also bring about an acute regional change in CBF. This coupling of local blood flow to local changes in metabolic activity is determined by a number of "neuro-energetic" signals.
A clinical illustration of this phenomenon is by the blood oxygen level-dependent ("BOLD") time series used in functional magnetic resonance imaging (fMRI) that can show "activated" regions with mental tasks.
The brain normally tolerates a wide range of blood pressure, with little change in blood flow. The cerebral vasculature rapidly (10-60 s) adapts to changes in CPP. Decreases in CPP result in cerebral vasodilation, whereas elevations induce vasoconstriction. In normal individuals, CBF remains nearly constant between MAPs of about 60 and 160 mm Hg (Figure 26-2). Beyond these limits, blood flow becomes pressure dependent. Pressures above 150-160 mm Hg can disrupt the blood-brain barrier (see below) and may result in cerebral edema and hemorrhage.
Normal cerebral autoregulation curve.
The cerebral autoregulation curve (Figure 26-2) is shifted to the right in patients with chronic arterial hypertension. Both upper and lower limits are shifted. Flow becomes more pressure dependent at low “normal” arterial pressures in return for cerebral protection at higher arterial pressures. Studies suggest that long-term antihypertensive therapy can restore cerebral autoregulation limits toward normal.
Both myogenic and metabolic mechanisms may explain cerebral autoregulation. Myogenic mechanisms involve an intrinsic response of smooth muscle cells in cerebral arterioles to changes in MAP. Metabolic mechanisms indicate that cerebral metabolic demands determine arteriolar tone. Thus, when tissue demand exceeds blood flow, the release of tissue metabolites causes vasodilation and increases flow. Whereas hydrogen ions were once thought to mediate this response, other metabolites are likely involved.
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