CLASSIFICATION OF

GENERAL ANAESTHETICS

1.INHALATIONAL

Gases: N2O,Cyclopropane,Xenon
Liquids: Ether, Halothane,
Enflurane, Desflurane,
Isoflurane, Sevoflurane,
Methoxyflurane

2.INTRAVENOUS
Inducing Agents: Thiopentone sodium,
Methohexitone sodium,
Propofol, Etomidate
Dissociative Anaesthesia:Ketamine
Neuroleptanalgesia:
Fentanyl+Droperidol
(Analgesic)(Neuroleptic)
BZDs: Diazepam,Lorazepam,Midazolam

Pharmacokinetics
Rapidly diffuse across the alveoli
Alveoli
blood
brain
Depth of anaesthesia-potency & pp
Induction & Recovery-rate of change
of pp

Minimum Alveolar Concentration

Conc of the inhalational GA that
renders 50% of the subjects immobile
when exposed to a strong noxious
stimulus
Halothane
0.75%
Ether
Enflurane
Isoflurane
Desflurane
Sevoflurane
Nitrous oxide

1.9%
1.68%
1.2%
6%
2%
105%

 0.3 MACmild analgesia

0.5 MACamnesia
1.0 MAC50% patients immobile even
after stimulation
1.3 MACsympathetically mediated
response blunted
2.0 MACpotentially lethal
MAC

1/Potency

1.

Minimum Alveolar
Concentration
limitations
Leaves 50% subjects

2. At 1.3MAC awareness & recall may still exist

3. Large no. of patients receive muscle relaxants
4. Other indicators of awareness-highly
suggestive when present but not definitive
when absent
5. A patient who moves with incision is not
necessarily awake &one who does not move is
not necessarily unconscious

Factors affecting pp of anaesthetic

in brain
PP of anaesthetic in inspired air
Pulmonary ventilation rate
Alveolar exchange
Solubility of anaesthetic in blood
Solubility of anaesthetic in tissues
Cerebral blood flow

1.PP of the anaesthetic in

inspired air

PP of the anaesthetic in inspired

air
Increase in inspired anaesthetic conc
increases the rate of induction of
anaesthesia by increasing the rate of
transfer into blood according to Ficks
Law
Used for mod soluble-halothane3-4% 1-2%

Ficks Law of Diffusion

Flux=diff in conc x A x Permeability

Thickness of the path

2.PULMONARY
VENTILATION

lung animation.gif

2.Pulmonary Ventilation Rate

The rate of rise of anaesthetic gas
conc in the arterial blood is directly
dependent on both rate & depth of
ventilation
Effects- solubility
4x In VR 2x T of halothane bt only
15% in T of nitrous oxide

3.ALVEOLAR EXCHANGE

ALVEOLAR EXCHANGE
GAs diffuse freely across alveoli
Ventilation Perfusion mismatch delays
the attainment of equilibrium between
blood and alveoli

4.SOLUBILITY IN BLOOD

SOLUBILITY IN BLOOD
One of the most important factor
Blood:Gas Partition co efficient index
of solubility
When an anaesthetic with low solubility
diffuses from alveoli into arterial blood,
relatively few molecules are required to
raise its partial pressure and therefore
its arterial tension rises rapidly

5.SOLUBILITY IN TISSUES

SOLUBILITY IN TISSUES
Relative solubility of the anaesthetic in
blood and tissue determines its conc in
the tissue at equilibrium
expressed as tissue : blood pc
=ly soluble in lean tissue & blood.
More soluble in fat
Conc in white than in grey matter

6.CEREBRAL BLOOD FLOW

CEREBRAL BLOOD FLOW

Brain is highly perfused
GAs are quickly delivered
CO2 inhalation

Second gas effect

When certain gases like nitrous oxide
are administered in high conc, the
other anaesthetic gases are also
pulled in and their alveolar tension
rises more rapidly
Eg: halothane when given with N2O,
delivered at same rate

Concentration effect
When an anaesthetic is administered
in high conc, its alveolar tension rises
more rapidly than when the same gas
is inhaled in lower conc.

eElimination
gradients reversed
Through lungs- unchanged,
Metabolism-halothane>20% in liver
Lipid soluble anaesthetic-delayed
recovery