General anesthetics are drugs that produce reversible loss of sensation and consciousness. They are administered by anesthesiologists to facilitate surgery. The key effects are loss of sensation including pain, unconsciousness and amnesia, loss of reflexes, immobility, and muscle relaxation. Anesthetics have stages including analgesia, delirium, and surgical anesthesia. Common general anesthetics are inhalational gases like nitrous oxide and volatile liquids like sevoflurane and intravenous drugs like propofol and thiopentone sodium. They work by potentiating GABA receptors or inhibiting NMDA receptors. Inhalational anesthetics are delivered via gases or vapors and include nitrous oxide, halothane, sevoflurane and isoflurane.

1. GENERAL
ANAESTHETICS

2. WHAT ARE GENERAL ANAESTHETICS?
 Definition : Anesthesia (an =without, aisthesis = sensation )
The drugs which produce reversible loss of all sensations and
consciousness
Generally administered by an anaesthesiologist in order to
induce or maintain general anaesthesia to facilitate surgery.

3. THE CARDINAL FEATURES OF GENERAL
ANAESTHETICS
Loss of all sensation, especially pain
Sleep (unconsciousness) and amnesia
Abolition of somatic and autonomic reflexes
Immobility and muscle relaxation

4. STAGES OF GENERALANAESTHESIA
Stage-1
• Analgesia : Start from beginning of anaesthesia
administration and last upto loss of consciousness,
feels a dream like state, reflexes and respiration
remains normal
Stage-2
• Stage of delirium : From loss of consciousness
to beginning of irregular respiration. Apparent
excitement is seen. Muscle tone increases. Jaws are
tightly closed. Heart rate and blood pressure may
rise.

5. Stage-3
• Surgical anaesthesia : Extends from onset of irregular
•
•
•
•
•
respiration to cessation of spontaneous breathing. This has been
divided into 4 planes
Plane1:This plane ends when eyes become fixed
Plane 2: Loss of corneal and laryngeal reflexes
Plane 3:Pupil start dilating and light reflexe
Plane 4: Dilated pupil, decrease muscle tone ,BP
falls
Stage-4
• Medullary paralysis : Respiratory and vasomotor control
ceases

6. DIFFERENCE BETWEEN GENERAL AND
LOCALANAESTHETICS

7. CLASSIFICATION OF GENERAL
ANAESTHETICS
General
anaesthetics
Inhalational
Gas:
Nitrous oxide
V
olatile
liquids:
Halothane
Desflurane
Sevoflurane
Isoflurane
Enflurane
Intravenous
Thiopentone
sod.
Etomidate
Ketamine
Propofol
Methohexiton
e sod.

8. MECHANISM OF ACTION OFGENERAL
ANAESTHETICS
 GABA –A receptor : Potentiated byHalothane,
Propofol, Etomidate ,Enflurane,
isoflurane, Desflurane,
sevoflurane
 NMDA receptors:
 Glycine receptors :
Inhibited by Ketamine,
nitrous oxide and xenon
Potentiated by Halothane,
Propofol, ,Enflurane,
isoflurane, Desflurane,
sevoflurane
Also has effect on neuronal nicotinic receptors and
5-HT3 receptors

9. INHALATIONALANAESTHETICS
Inhalational anaesthesia refers to the delivery of gases or
vapours to the respiratory system to produce anaesthesia
Ether
It is explosive
Irritant to respiratory tract
High incidence of nausea and vomiting during
induction and post-surgical emergence

10. Colourless, odourless gas at room temperature.
Very insoluble in blood and other tissues (quick recovery)
Rapid induction of anaesthesia and rapid emergence
following discontinuation of administration.
Completely eliminated by the lungs.
It is weak anaesthetic and powerful analgesic.
The mac value is 105%.
Causes megaloblastic anaemia.
Used as adjunct to supplement other inhalationals.
Nitrous oxide

11. Volatile liquid at room temperature.
Light sensitive
High fat solubility => slow induction & recovery
Eliminated unchange via lungs
Commonly used in children, where preoperative
placement of an iv catheter can be difficult
It is marketed in amber bottles with thymol added as a
preservative
Metabolised in liver by Cyt-P450
Halothane

12.  Side effects of halothane :
CVS : Cardiac arrhythmia, depression of myocardial contraction.
Respiratory system : Depression of respiration
Muscles : Malignant hyperthermia
Kidney : Decrease renal blood flow and g.f.r
Liver and GIT: Cause halothane induced hepatitis & nausia and
vomitting
 DRUG INTERACTION : Halothane + adrenaline, theophylline => arrhythmia
may be precipitated.
 CONTRAINDICATION : Hepatic dysfunction and/or jaundice.

13.  Pleasant smell , non irritant and bronchodilation makes it agent of choice
for paediatric anaesthesia.
 2nd agent of choice for
Neuro anaesthesia.
Cardiac anaesthesia .
Asthmatics.
 Sevoflurane reacts with soda lime used in anaesthetic circuit to form
“compound A” which acts as renal toxin(nephrotoxic).
 Agents that should not be given with soda lime.
1) Trielene.(trichloro ethylene)
2) Sevoflurane.
3) Desflurane
Sevoflurane

14.  Isomer of enflurane. More potent and volatile than enflurane.
 More stable and non-inflammable
 Muscle relaxation is good.
 Hepatotoxicity is rare.
 Avoid in patients with coronary artery disease (CAD) because it
produces coronary steal phenomenaon.
Isoflurane

15. MEASURMENT OF INHALATIONAL
ANAESTHETIC POTENCY
MAC
 Minimum alveolar concentration
 MAC is the Concentration at which 50% of subjects have no
response (movement) to surgical stimulus (skin incision).
 Different for each inhaled agent
 Increase MAC
i. Hyperthermia
ii. Hypernatraemia
iii. Drug induced elevation of CNS catecholamine stores
iv. Chronic alcohol abuse
v. Increases in ambient pressure (experimental)

16.  Decrease MAC
i. hypothermia
ii. hyponatraemia
iii. increasing age
iv.hypotension
v . anaemia
vi. CNS depressant drugs
 No Change in MAC
i. sex
ii. weight,
iii. type of stimulus
iv. duration of anaesthesia
v. hypo/hyperkalaemia

17. INTRAVENOUS ANAESTHETICS
THIOPENTAL
 Ultrashort acting barbiturate
 High lipid solubility rapid entry into the brain
 Rapid onset (20 sec) , short duration
 Effect terminated not by metabolism but by redistribution
 Risk of sever vasospasm if accidently injected into artery
 Depress cerebral blood flow
 Decrease intracranial pressure
 Tissue necrosis—gangrene, Tissue stores, hypotension, apnea
 Build-up in adipose tissue = very long emergence from anaesthesia

18.  Rapid onset and have a short duration of action
 Highly protein bound in vivo and is metabolised by conjugation
in the liver
 Very good anesthetic for induction and maintaince of anesthesia
with no accumulation effect
 Side-effects are pain on injection, hypotension and transient
apnea following induction
 Used for the induction, maintenance of GA andsedation
 Useful for day-case surgery
Propofol

19.  Dissociative anaesthetic
 NMDA ReceptorAntagonist
 Cardiovascular stimulant
 Catatonia, analgesia, and amnesia without loss of consciousness
 Useful for anesthetizing patients at risk for hypotension and
bronchospasm and for certain paediatric procedures
Ketamine

20.  Rapid induction
 Minimal change in cardiac function and respiratory rate
 Not analgesic
 Cause pain on injection and nausea postoperatively
 Prolonged administration may cause adrenal suppression
Etomidate

21.  Pre-anaesthetic medication, induction, maintenance and
supplementation of anaesthesia.
 Don’t depress respiration heart or blood pressure.
 Don’t produce post operative nausea and vomiting.
 Have central muscle relaxant effect.
 Diazepam (0.2-0.5 mg/kg, i.v) and Midazolam (faster
acting) used for anaesthesia.
Benzodiazepines

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