Cerebral blood volume physiology and potential for therapeutic intervention

Most of the intracranial blood volume of about 200 ml is contained in these venous sinuses and pial veins, which constitute the capacitance vessels of the cerebral circulation; reduction in this volume can buffer rises in the volume of other intracranial contents (the brain and CSF). Conversely,

Intracranial Contents

Fig 7.2 Venous sinuses of the brain, showing drainage of the superior sagittal sinus into the right jugular vein via the transverse and sigmoid sinus. Note that the first extracranial tributary of the internal jugular vein (the common facial vein or CFV) enters it below the lower level of the body of the second cervical vertebra. Consequently, a retrograde jugular catheter with its tip above this level samples blood that drains exclusively from intracranial contents.

Fig 7.2 Venous sinuses of the brain, showing drainage of the superior sagittal sinus into the right jugular vein via the transverse and sigmoid sinus. Note that the first extracranial tributary of the internal jugular vein (the common facial vein or CFV) enters it below the lower level of the body of the second cervical vertebra. Consequently, a retrograde jugular catheter with its tip above this level samples blood that drains exclusively from intracranial contents.

when compensatory mechanisms to control intracranial pressure (ICP) have been exhausted, even small increases in cerebral blood volume (CBV) can result in steep rises in ICP (Fig. 7.3).

The position of the system on this curve can be expressed in terms of the pressure volume index (PVI), which is defined as the change in intracranial volume that produces a tenfold increase in ICP. This is normally about 26 ml,11 but may be markedly lower in patients with intracranial hypertension, who are on the steep part of the intracranial pressure-volume curve (see effects of arterial carbon dioxide tension, PaCÜ2 on CBV).

With the exception of oedema reduction by mannitol, the only intracranial constituent whose volume can be readily modified by the anaesthetist via physiological or pharmacological interventions is the CBV. Although the CBV forms only a small part of the intracranial volume, and such interventions only produce small absolute changes (typically about 10 ml or less), they may result in marked reductions in ICP in the presence of intracranial hypertension. Conversely, inappropriate anaesthetic management may cause the CBV to increase. Again, although the absolute

Pressure Volume Index

Fig 7.3 Intracranial pressure-volume curve. The pressure volume index (PVI), defined as the change in intracranial volume required to cause a tenfold increase in ICP, increases non-linearly, from approximately 25 ml in normals (A on the curve), to as little as 5 ml in patients with raised ICP (B on the curve).

Fig 7.3 Intracranial pressure-volume curve. The pressure volume index (PVI), defined as the change in intracranial volume required to cause a tenfold increase in ICP, increases non-linearly, from approximately 25 ml in normals (A on the curve), to as little as 5 ml in patients with raised ICP (B on the curve).

magnitude of such an increase may be small, it may result in steep rises in ICP in the presence of intracranial hypertension.

The appreciation that pharmacological and physiological modulators may have independent effects on CBV and CBF is an important one for two reasons. First, interventions aimed at reducing CBV in patients with intracranial hypertension may have prominent effects on CBF and result in cerebral ischaemia12 (Fig. 7.4). Conversely, drugs that produce divergent effects on CBF may have similar effects on CBV, and using CBF measurement to infer effects on CBV and hence ICP may result in erroneous conclusions.13

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Responses

  • Bernd
    What are the extracranial vessels?
    7 years ago

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