CONTROLLED ARTERIAL-HYPERTENSION AND CERE BRAL PROTECTION

Citation
G. Boulard et al., CONTROLLED ARTERIAL-HYPERTENSION AND CERE BRAL PROTECTION, Annales francaises d'anesthesie et de reanimation, 14(1), 1995, pp. 83-89
Citations number
NO
Categorie Soggetti
Anesthesiology
ISSN journal
07507658
Volume
14
Issue
1
Year of publication
1995
Pages
83 - 89
Database
ISI
SICI code
0750-7658(1995)14:1<83:CAACBP>2.0.ZU;2-M
Abstract
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.