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Posted by / 04-Jan-2020 01:07

Sedating a patient

All intravenous sedative agents cause a dose-dependent decrease in CBF [6–9], although CBF reductions with benzodiazepines tend to be more variable than those with propofol, probably because benzodiazepines do not easily produce burst suppression or an isoelectric EEG.

Infusions of remifentanil may produce reduction in CBF similar to that seen with intravenous anaesthetics [10].

For all of these reasons, sedation and analgesia protect the brain against intracranial hypertension and brain hypoperfusion.

Seizures produce an increase in cerebral metabolism and possibly a mismatch between oxygen delivery and metabolism.

Sedatives and analgesics may reduce ICP by different mechanisms [3].

High bolus doses of opioids trigger cerebral vasodilatation in response to reductions in MAP and have been associated with increases in ICP and decrease of CPP [12].

These negative effects can be largely prevented if MAP is maintained.

Titration and withdrawal of sedation in the NICU setting has to be balanced between the risk that interrupting sedation might exacerbate brain injury (e.g.

intracranial pressure elevation) and the potential benefits of enhanced neurological function and reduced complications.

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In this review, we provide a concise summary of the main cerebral physiologic effects of sedatives and analgesics, the advantages/disadvantages of each agent, the comparative effects of standard sedatives (mainly propofol and midazolam) in patients with ABI, and the emerging role of alternative sedatives, particularly ketamine.

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