General anesthesia is defined as a Reversible and controllable state of
Analgesia. (relief of pain)
amnesia. (memory disturbance or loss) نسيان
loss of coconsciousness. (the patient will be unaware of himself)
inhibition of sensory and autonomic reflexes.
Variable degree of skeletal muscle relaxation.
When we talked about neuromuscular blocker in the previous lecture we
said, before administration of GA we have to relax the skeletal muscle.
Because administration of GA need endotracheal intubation, and
endotracheal intubation is only possible when the skeletal muscles of the
larynx are completely paralyzed, so without complete paralysis we cant
introduce endotracheal intubation >> which is essential for GA
adminstartion. So before admin of GA we should give skeletal muscle
blocker or neuromuscular blocking agent.
For prolonged surgical operation we give curare like compound but for
short surgical procedures we use depolarizing agent called succynel
One of the uses of atropine is preanesthetic medication. so what is
Administration of drugs before general anesthesia in order to:
Produce sedation and decrease anxiety and apprehension . قلقwhich
are usual symptoms of a pt going to have surgical operation, and so
to relief these manifestations the pt should be sedated by sedative
drugs or anti-anxiety drugs such as diazepam , antihistamine,
To provide amnesia. The same group of drug used for sedation.
These groups of drugs when given before GA will relief the pt from
the fearful experience of surgical operation.
To produce analgesia when there is pain. we should not leave the pt
in his painful condition at least before 2 hours( im sorry I couldn’t
hear nor understand what the doctor was saying, his voice was low).
The groups of drug used to produce analgesia are opioids.
Potentiate weak GA as nitric oxide (N2O). Because its weak it cant
be used alone to produce GA, we should use other GA or by
Facilitate induction without prolonging recovery.
Reduce some undesirable S/Es of GA such as H2 blockers
(cimetidine) is used to reduce gastric acidity which is a common
effect of GA, and metochlopramide (anti-emetic) it will reduce the
incidence of vomiting after receiving GA. Most GA have emetic
effect and so to reduce this S/E the pt is medicated with anti-emetic
To produce vagolytic effects (or anti-cholinergic effect, anti
parasympathetic effect) such as atropine and hyocine.
Inhibiting vomiting and decreasing gastric acidity to reduce
Classification of GA:
GA are classified according to their route of admin. Either
Drugs which can produce GA. Their route of admin is by endotracheal
They are also sub classified into either:
o Volatile liquids
They are liquid in room temp but under pressure. When the
pressure is relieved the liquid starts to change from liquid state to
vapor and the vapor of this liquid will be inhaled through an
endotracheal tube. The evaporated liquid will be taken by a carrier
gas and admin to the pt.
They are compressed gases in gas cylinder. When the pressure is
relieved it will be administrated in its gas state. Its also taken by a
So now what's the difference between them?
Liquid evaporates into vapor and the gas is already in its gaseous
Intravenous (IV) GA
**he will discuss the drugs later on
Explanation of what's meant by induction and recovery. Look at this
diagram (refer to slide page 3) here we have 0 time or time of admin
(induction) where we start giving the pt GA, so the time taken from
admin of GA until the pt loses his consciousness is called induction. Of
course before admin of GA the pt is fully conscious. After loss of
consciousness surgical operation will be performed, the period during
which the pt is unconscious is called maintenance period or effective
surgical GA period or sustained GA. Then after finishing the surgical
operation the surgeon asks the anesthetist to stop giving the pt GA, so the
time needed from the time of stoppage of GA admin until the time of
regaining full consciousness is called recovery. Therefore we need a
good GA to produce a rapid induction (which is better than delayed
induction) and rapid recovery (better than prolonged recovery).
Properties of an ideal GA:
Should produce safe and pleasant anesthesia
Good muscle relaxation
Be potent, stable, non-irritant, and non-inflammable
Non-toxic and free of S/Es. (it could be non-toxic, BUT free of S/E
is not achievable)
Produce rapid and smooth induction and rapid recovery
*AN IDEAL GA IS STILL BEYOND OUR REACH*
Its impossible to provide all these requirements in a single GA.
What's ED50? It’s the dose which can produce an effect in 50% of tested
animals or pt or whatever. Here the potency GA is measured by what's
called MAC (median alveolar concentration) which is defined as:
End tidal conc. of GAs needed to prevent response in 50% of pts
challenged by standardized skin incision. Skin incision produces painful
sensation, so the dose of GA which can prevent this painful sensation in
50% of tested pts is called MAC >> usually expressed as % of GAs in the
mixture of carrier gas "air or oxygen". Here MAC is small for potent &
large for weak GAs.
Therefore MAC represents the dose of drug. So less potent drugs are
given in large doses , more potent GA have small MAC and GA carrying
very large MAC are less potent, for example nitric oxide is a weak GA
while halothane, flurane, isoflurane are more potent and so are effective
in smaller conc.
MOA of inhalational GAs:
They produce their effect by depression of the CNS neuron activity by
increasing their threshold and reducing the rise of action potential by
interfering with sodium influx.
Almost the same effect as the local anesthetic, they prevent sodium influx
but peripherally. The GA interferes with sodium influx not locally nor
peripherally but in CNS.
-They can increase transmission of inhibitory neurons such as GABA
chloride channel complex, & glycine receptors in spinal cord, both are
inhibitory neurotransmitters in the CNS, increasing the level of these
neurotransmitters the end result will be inhibition.
-blocking the excitatory post-synaptic nicotinic receptors.
The net result of both is Generalized Loss of sensation
Pharmacokinetics of inhalational GAs:
Uptake and distribution
in the other drugs pharmacokineticly speaking we have absorption,
distribution, metabolism and excretion, here we have uptake instead of
You can see here the depth of GA is directly proportional with the
tension of GA in the brain, where as for the other drugs it's directly
proportional with blood conc.
(**there was a part I couldn’t hear what the Dr was talking about and I
hope it wasn't important)
(Refer to the slides page 5)
This is the alveolar space (AA), after admin, the GA will go to the
lung to the alveolar air, and from the AA to the blood, and from the
blood to target organ the brain. And always there is equilibrium
between tension of GA in the AA in the blood and in the brain.
- The rate of induction and recovery depends on the rate of change
of tension in the brain and again the tension of the GA in AA
approximately equals the tension in the blood which is also
approximately equal to the tension in the brain. Therefore after
admin of GA the tension of the GA will rise gradually in the brain
until it reaches complete loss of fxn > > induction, then the tension
will maintain at this level for the duration needed to perform the
surgical procedure, and then when we stop admin of GA, the
tension in the AA, in the blood, and in the brain starts to decline
until it reaches 0 while the pt is still conscious. the period between
stopping admin of GA until gaining full consciousness is called
Factors that determine brain GAs tension "GAs conc":
brain GA tension is directly proportional to the depth of GAs, in other
words GAs conc is directly proportional to the depth of GAs , so as
the conc or tension in the blood follow the conc or tension in the AA.
1. Blood solubility: referred as lambda.
It depends on blood /gas partition coefficient which means the conc
of GA level in the blood over conc of GA in the air or in the gas is
For example nitric oxide = 0.5 and halothane = 2.3 , which means
that nitric oxide has a low lambda or low blood/gas partition
coefficient and halothane has high lambda or high blood/gas
High lambda will give slow induction and vice versa. Because
halothane has high lambda it means its conc in the blood is higher
than its conc in AA so it needs a lot of time for the conc of
halothane to be increased in the blood (saturating the blood). 2.3
means that the conc of halothane is about double the conc in the
AA, so we need low …for the blood to be saturated with the
halogane. In contrast to that of nitric oxide which has a low lambda
its conc in the blood is much less than its conc in the air so we need
a very short period to saturate the blood, that’s why induction is
slow in high lambda while its very rapid or fast in low lambda, and
that's why nitric oxide Is mainly used as an inducing agent and
usually the anesthetist starts induction with N2O and maintenance
with the other general anesthetics.
2. We talked about this relationship GAs conc in the inspired air is
proportional to the alveolar air which is also directly
proportional to the blood and brain tension.
3. the other factor which can determine the brain GA tension is
pulmonary blood flow. Increased pulmonary blood flow will lead
to slow rate in the arterial tension and slow induction. incase of
heart failure the pulmonary blood flow is low and induction of
GA is faster (im not sure). Increase in pulmonary blood flow
means large blood volume to the lung, so we needs more time for
this blood volume to be saturated with the GAwhich means
4. pulmonary ventilation rate. Hyperventilation will hasten
induction. Hyperventilation means: increasing the air in the lungs
so the amount of administered GA will be more, therefore the
induction will be fast. in heart failure the induction will be fast
because pulmonary blood flow will drop and will be easily and
rapidly saturated that’s why patients with heart failure should
receive lower doses of GA.
Elimination of GA:
This will follow the opposite factors as in the admin of GA. The
main organ of elimination of GA is the lungs, while other drugs the
main organ for metabolism is the liver and elimination is the
kidney. Here few amount of GA could be metabolized by the liver
and eliminated by the kidney but the major amount of elimination
is by the lungs, so it's introduced by inspiration and eliminated by
There is something in common between these member of GA, all
of them are halogenated (having an atom of halogen) hydrocarbon.
Halogens are fluoride, bromide, chloride, and iron. Here most of
them are fluorinated hydrocarbons or halogenated hydrocarbon
Quick induction and recovery. If we give one plus + for the speed
of induction and recovery we will give 2 plus for enflurane, 3 plus
for isoflurane and so on. They are arranged according to their
speed of induction and recovery.
Best GA in pediatric pts simply because it has a good smell
(acetone or old apple smell).
Good for asthmatic pt. its relatively non-irritant.
It has the property of decreasing blood pressure producing
hypotension, thats why if we need less bleeding during surgery we
can use halothane. It also reduces hemorrhage
Unfortunately it’s a cardiac depressant and sensitize the heart for
Hepatotoxic after repeated use
Malignant hyperthermia (high and prolonged rise in body temp
probably a degree centigrade every 1/2hour, after 2 hours body
temp might reach 41, and after 3 hrs the pt might die)
good muscle relaxation
Safer on the heart and liver. It's not a cardiac depressant and not
As a S/E it might lead to epileptic fits and risk of convulsion
it has a very rapid induction and recovery
marked muscle relaxation
no convulsant effect
no serious S/E on liver and heart
it differs from halothane in being not a hepatotoxic nor cardiotoxic and
differs from enflurane in being less convulsive GA.
done by: afnan alduaij