[Cerebral hemodynamics and intracranial hypertension].
Various cerebral aggressions, either primary or secondary, can lead to the development of raised intracranial pressure. The presence of an elevated intracranial pressure often results in cerebral ischaemia/hypoxia and, eventually, neuronal death. In face of this cascade of events, several therapeutic approaches have been suggested. Two management concepts for patients with raised intracranial pressure have retained the most attention in recent years: the first suggests a therapeutic increase in cerebral perfusion pressure with the objectives to improve perilesional collateral perfusion and decreased cerebral blood volume, and consequently intracranial pressure in areas where autoregulation is preserved. The second concept supports the diminution in perilesional capillary pressure with the aim of decreasing vasogenic oedema. Although these two concepts are antagonistic and cannot be used simultaneously, they are probably complementary in the sequence of therapeutic events of patients experiencing severe head injury. This article reviews these therapeutic concepts and their clinical applications.
Bracco
D
D
Département d'anesthésiologie, hôpital de Sion, Suisse.
Bissonnette
B
B
Favre
J B
JB
Moeschler
O
O
Boulard
G
G
Ravussin
P
P
D018686:Anesthetics, Intravenous / Q000494:pharmacology / Q000627:therapeutic use; D001929:Brain Edema / Q000209:etiology; D002545:Brain Ischemia / Q000209:etiology; D016923:Cell Death; D002560:Cerebrovascular Circulation; D006259:Craniocerebral Trauma / Q000150:complications; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D002534:Hypoxia, Brain / Q000209:etiology; D019586:Intracranial Hypertension / Q000209:etiology / Q000503:physiopathology*; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology / Q000627:therapeutic use
D018686:Anesthetics, Intravenous; D014662:Vasoconstrictor Agents