Notes
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    1. Pharmacology
        1.2. Inhalation anaesthetic agents (AA)
1.2.3. CNS effects of AA

CNS effects of AA

[Ref: SH4:p47-50]

Effects of inhaled anaesthetics

EEG

All AA increase frequency and voltage on EEG at <0.4 MAC

Cerebral metabolic oxygen requirement starts to decrease abruptly at about 0.4 MAC

 

Seizure activity

ENF can produce fast frequency and high voltage on EEG and can lead to seizure-like EEG activity
* Especially when > 2 MAC or PaCO2 < 30
* Only AA to cause frank seizures

ISO causes burst suppression at 1.5 MAC, and electrical silence at 2.0 MAC
* Suppresses convulsion

DES and SEVO do not produce convulsive activity

SEVO can suppress convulsive activity induced with lidocaine

Nitrous oxide

N2O may increase motor activity with clonus and opisthotonus

N2O at high concentration (in hyperbaric chamber)
--> alternating periods of muscle activity and relaxation

Acute N2O dependency can lead to withdrawal seizure

 

Awareness

Volatile anaesthetic agents are not equally effective in preventing awareness

For example,

ISO at 0.4 MAC prevents recall and response to command

N2O requires greater than 0.5 to 0.6 MAC to produce similar effect

 

Cerebral blood flow (CBF)

Two opposing forces:

Overall,

Dose-dependent increase in CBF
* Despite decreased cerebral metabolic requirement

Intrinsic vasodilatory property

SEVO < ISO and DES < N2O

 

ICP and CSF

ICP tends to increase with anaesthetics due to increased CBF

ICP

Hyperventilation to reduce PaCO2 to 30mmHg opposes the tendency of inhaled anaesthetics to increase ICP

DES <0.8 MAC does not increase ICP

DES 1.1 MAC increases ICP by 7mmHg

CSF

ISO does not affect production, but decrease resistance to absorption
--> Minimal increase in ICP

ENF increase both rate of production and resistance to absorption
--> Increased ICP

N2O does not affect production or absorption
--> ICP increase with increased CBF

 



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