Although lidocaine is not typically used as a general anesthetic, it is frequently administered during the induction of anesthesia to blunt the pain associated with propofol injection and mitigate hemodynamic alterations during procedures like laryngoscopy. An intravenous dose of 1.5 mg/kg given 60 to 90 seconds before laryngoscopy, suctioning or head pinning also blunts the ICP rise these stimuli provoke, which is its usual role in neuroanesthesia. Lidocaine’s effects on cerebral perfusion are dose-dependent. Moderate doses (0.5 mg/kg) tend to increase regional CBF, while higher doses (5 mg/kg) result in modest reductions in both CBF and CMRO₂.
In the app: Calculators > Local Anesthetic Dose Calculator takes the patient's weight and the agent and returns the maximum dose in mg and mL. The 5 mg/kg figure above is a research dose that already exceeds the 4.5 mg/kg plain-lidocaine ceiling the calculator applies, which is why 1 to 1.5 mg/kg is the clinical intravenous dose.
Lidocaine has also been associated with reductions in intracranial pressure (ICP), making it a useful adjunct in neurosurgical procedures where controlling ICP is critical. In animal studies, lidocaine has shown potential neuroprotective properties during states of threatened CBF. However, in humans, studies investigating the role of lidocaine in preventing post-operative cognitive dysfunction have produced conflicting results, and no definitive conclusions can be drawn regarding its neuroprotective utility in clinical practice.
| Agent | Effect on CBF and CMRO2 | Mechanism and clinical note |
|---|---|---|
| Propofol | Marked reduction in CBF with a corresponding decrease in CMRO2 | Flow-metabolism coupling stays intact, so the fall in flow reflects reduced demand rather than vasoconstriction — applied directly to cerebral vessels it dilates them; autoregulation preserved to 200 µg/kg/min |
| Ketamine | Increases CBF; recent work suggests any rise in CMRO2 is minimal and likely reflects enhanced metabolite supply | The CBF rise comes from direct vasodilation of medium-sized cerebral vessels; recent human studies with modern practice do not show increased ICP |
| Etomidate | Reduces CBF, CMRO2, and ICP | Thought to be secondary to the fall in CMRO2, plus possible direct vasoconstriction, likely through inhibition of nitric oxide signaling; reduced cerebral oxygenation has been reported after induction doses even with intact cerebral vasculature |
| Dexmedetomidine | Reduces CBF and lowers CMRO2 | Likely direct vasoconstriction of cortical vasculature via postsynaptic α2-adrenergic receptors; cerebral oxygenation is preserved only while the patient remains hemodynamically stable |
| Opioids | Broadly neutral for global CBF and CMRO2, but regional flow changes on MRI and PET | Fentanyl raises CBF in the prefrontal cortex and caudate nucleus; sufentanil and remifentanil are biphasic, low doses raising CBF and higher doses lowering both CBF and CMRO2; vasomotor reactivity stays intact |
| Benzodiazepines | Dose-dependent, well-matched reductions in both CBF and CMRO2 | Largest regional reductions in the hippocampus and prefrontal cortex; chronic use may bring tolerance to the CBF-reducing effect |
| Barbiturates (thiopental) | Reduce CBF and CMRO2, lowering metabolic demand | Autoregulation and CO2 reactivity preserved; CMRO2 falls to about half of baseline at an isoelectric EEG, with no further reduction beyond it |
| Lidocaine | Dose-dependent — 0.5 mg/kg increases regional CBF, while 5 mg/kg modestly reduces both CBF and CMRO2 | Also lowers ICP, making it a useful adjunct where pressure control matters |
