G. Boulard et al., CONTROLLED ARTERIAL-HYPERTENSION AND CERE BRAL PROTECTION, Annales francaises d'anesthesie et de reanimation, 14(1), 1995, pp. 83-89
Among the techniques of cerebral protection, the use of controlled art
erial hypertension is based on the following arguments: 1) Cerebral is
chaemia is the final common pathway of any insult to the brain, partic
ularly through secondary lesions. Causes of secondary cerebral lesions
include pressure under the brain retractors, temporary clipping, arte
rial hypotension, hypoxaemia, anaemia and hypercapnia. 2)In the brain,
the critical lower value for cerebral blood flow is around 25 mL . 10
0 g(-1) . min(-1) under which two types of ischaemic areas can de defi
ned: the penlucida type where cerebral function is abolished, without
permanent cerebral lesion and the penumbra type where cerebral tissue
recovers only if Bow is rapidly restored. In the latter case the durat
ion of ischaemia is very important. 3) Cerebral blood flow is maintain
ed stable within a large range of variations of mean arterial pressure
through the autoregulation mechanisms, which is based on vasomotricit
y of the cerebral circulation, which implies major variations in cereb
ral blood volume. However, autoregulation needs several dozens of seco
nds to be achieved. Therefore, sudden variations in mean arterial pres
sure are associated with short lasting but major variations in cerebra
l blood volume. 4) In case of increased intracranial pressure, a decre
ase in cerebral perfusion pressure causes cerebral vasodilation throug
h the autoregulation mechanism, with an increase in cerebral blood vol
ume which will, in turn, increase intracranial pressure and thus decre
ase cerebral perfusion pressure, and so on. This is the vasodilatory c
ascade. The therapeutical increase in mean arterial pressure will corr
ect this phenomenon and decrease intracranial pressure. This is called
the vasoconstrictive cascade. 5) In case of vascular occlusion by vas
ospasm, extrinsic compression or during temporary clipping, cerebral p
rotection may be based on the collateral vessels near the ischaemic ar
ea and also on vascular anastomoses inside the circle of Willis. Follo
wing Poiseuille's law, as vasodilation is already maximal distally to
the stenosis, the major factor of vascular resistance is no longer the
radius of the vessel, but its length. Accordingly, the increase in pe
rfusion pressure will improve the local flow and participate in preven
tion or treatment of an ischaemic event. Indeed, the increase, althoug
h modest, of the local flow may be sufficient to switch from an ischae
mia of penumbra type to a penlucida type. Finally, controlled arterial
hypertension 1) implies to achieve the optimal cerebral perfusion pre
ssure in order to create the vasoconstrictive cascade under cover of i
ntracranial pressure monitoring and 2) helps to decrease the ischaemic
risk secondary to vasospasm, for example by achieving a mean arterial
pressure between 70 and 100 mmHg before clipping and between 100 and
120 mmHg after clipping. To obtain this level of pressure, phenylephri
ne, noradrenaline and dopamine are the agents of choice, as they are f
ree of harmful effects on the cerebral circulation.