General Anaesthesia
General Anaesthesia
A- Intravenous:
B- Inhalation :
•Some anaesthetics are metabolized by the liver, and their metabolites are often toxic
•Produces analgesia.
•Inexpensive.
Effect of general anesthetics on CNS:
Mechanisms of Action :
•They alter the excitation of the neuronal membrane → Modify the impulse
conduction → ↓ sodium influx→ ↓ initiation of action potential.
1- Overton-Mayer theory:
GA are lipid soluble drugs. ↑↑Lipid solubility→↑↑ BBB →↑↑ GA effect
GA dissolves in the membrane lipids and results in membrane fluidization.
membrane fluidization.
These stages are due to ↑↑concentrations of the anesthetic agent in the brain.
Stage I: (Analgesia)
A- liquid agent :
Isoflurane
Sevoflurane Most commonly used
Desflurane
Enflurane
Halothane
B- gas agent :
Nitrous oxide - Mainly used for maintenance of anesthesia.
- Rapidly eliminated from the body.
Adjuvant (not used alone) - No post operative respiratory depression.
Pharmacokinetics of Inhaled anesthetics.
agents inspired with oxygen and absorbed from lung alveoli → blood →pass the
BBB → brain.
Diffusion from lung alveoli to blood depend on:
1- Partial pressure between alveolar air and blood
→↑ Partial pressure →↑ anesthetics in blood
2- Partition coefficient
Blood/gas (must be low)
Brain/ gas (must be high)
3- Cardiac output
side effects of Inhaled anesthetics.
N.B.
NO CVS depression
NO Resp.depression
No Hepatotoxicity
Strong analgesic effect.
Intravenous anethesics
Thiopental
S.E:
-Myocardium depress.
-Hypotension.
-respiratory depress.
Etomidate
S.E:
-nausea and vomiting
-suppression of adrenal cortex
Midazolam