Brain perfusion autoregulation

Brain perfusion autoregulation in general
The brain is supplied with blood through the right and left a. carotis communis (anterior circulation) and vertebral arteries (posterior circulation). Cerebral autoregulation is the ability to maintain a constant blood flow to the brain as systemic blood pressure changes. Autoregulation is determined by the relationship between cerebral perfusion (= cerebral blood flow, CBF) and cerebral perfusion pressure (= cerebral perfusion pressure, CPP):
 * CPP = MAP &minus; ICP

Mechanisms of cerebral perfusion autoregulation
The self-regulation itself consists in the fact that when the system pressure increases, vasoconstriction occurs compensatively  in the CNS, and when the system pressure decreases sufficient CNS flow is maintained by vasodilation of the cerebral flow. Brain perfusion drops sharply when the CPP falls below a critical value (usually 50 torr). Hypoperfusion, ischemia, and eventually brain death occur. The most stable CNS perfusion is in the range CPP 50–160 torr. At values >&thinsp;160 torr on the other hand, CNS flow rises rapidly, the blood-brain barrier fails with the subsequent development of cerebral edema  and bleeding during cerebral vascular rupture.
 * In newborns and infants MAP  alone is in the range of 40-50 torr. In this age group, therefore, the most stable CNS perfusion is achieved in the range of 40-80 torr.
 * CNS circulation is also characterized by minimal effects of vasomotor activity via catecholamines due to the presence of the blood-brain barrier.

Autoregulation disorder
When cerebral perfusion autoregulation is impaired, an increase in arterial pressure leads to an increase in intracranial pressure and, conversely, a decrease in arterial pressure leads to a decrease in intracranial pressure. The situation is evaluated by the so-called PRx index (pressure–reactivity index), which expresses the relationship between MAP (mean arterial pressure) and ICP (intracranial pressure):
 * PRx = MAP/ICP


 * We obtain the index by obtaining about 40 consecutive correlations from the MAP and ICP curve recordings over time (ie at the same time we determine the intersection of the MAP value from the X-axis and the ICP from the Y-axis). *Positive index values ​​indicate a loss of cerebral perfusion autoregulation . In practice, PRx results correlate well with transcranial Doppler sonography.

he increase in blood flow to the brain in the event of a disorder of autoregulation is accompanied by a decrease in perfusion brain pressure and is assessed by the Mx index:
 * Mx = Vic/CPP


 * Vic = blood flow rate in the a. carotis interna measured by a transcranial ultrasonograph.
 * CPP = perfusion brain pressure, which can be determined from mean arterial pressure, intracranial pressure and CVP.
 * CPP = MAP &minus; (ICP + CVP)

The CPP value should not fall below 50 torr (6,6 kPa), in newborns and infants <40 torr.

Intracranial pressure
The physiological value of ICP in spontaneous breathing is 5–20 torr (0,33–2,66 kPa), in children we tolerate values <&thinsp;15 torr, in newborns and infants <&thinsp;10 torr. In adult intensive care guidelines, intracranial hypertension is defined  as ICP >&thinsp;20 torr (>&thinsp;2,66 kPa). The CVP value is not reported in some samples. In relation to the MAP values, it is essentially negligible.

Intracranial pressure is determined by the pressure of brain tissue, MMM and blood on the cranial skeleton. The development of intracranial hypertension results from the fact that the brain, its vessels and MMM are stored in a relatively rigid calf. Enlargement of any intracranial compartment will cause both an increase in ICP and a decrease in other parts of the intracranium. The so-called Monro-Kellie doctrinespeaks about the connections of individual compartments to the influence of ICP : the sum of components involved in the resulting ICP (ie brain parenchyma, cerebrospinal fluid and blood) should be constant. However, the increase in ICP, However, the increase in ICP  is not linear!

ICP is affected in this order: venous blood&thinsp;<&thinsp;MMM&thinsp;<&thinsp;brain parenchyma.

Venous blood represents 5% of the volume of the intracranium, MMM also 5%, the brain parenchyma then 90% of the volume. When cerebral perfusion auroregulation is affected, pressure changes from the arterial circulation are adversely reflected in changes in intracranial pressure . When the CPP falls below 50 torr, the regulatory mechanisms decompensate. The increase in intracranial pressure is accompanied by a dramatic  decrease in CPP. Establishing normal conditions is very difficult, but can be achieved by inducing cerebral vasoconstriction and increasing MAP. The goal of treatment is to normalize both CPP and ICP. The above pressure and perfusion changes are accompanied by cerebral edema, which is a non-specific response of brain tissue to noxus.

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