Abstract
Hypocapnic hyperventilation is used in neuroanesthesia and in neurointensive care for the treatment of raised intracranial pressure (ICP) in the context of traumatic brain injury (TBI) [1, 2]. The careful and targeted use of hypocapnia for the shortterm control of raised ICP remains a useful therapeutic tool [1, 3]. Hypocapnia lowers ICP by the induction of cerebral vasoconstriction with a subsequent decrease in cerebral blood volume. Over the past decade, relatively more attention has been paid to the adverse effects of hyperventilation than to the beneficial and concern seems to exceed enthusiasm because of the potential downside of hyperventilation, i. e., decreasing cerebral blood flow (CBF) to ischemic levels [2]. There is no evidence in the literature unequivocally demonstrating that hyperventilation for the treatment of raised ICP in patients with TBI is related to poorer outcome, and there is also no evidence showing beneficial effects on overall outcome [3, 4].
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Froio, S., Conte, V., Stocchetti, N. (2013). Extracerebral Effects of Hyperventilation: What are the Mechanisms?. In: Vincent, JL. (eds) Annual Update in Intensive Care and Emergency Medicine 2013. Annual Update in Intensive Care and Emergency Medicine. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-35109-9_45
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