13. general anaesthesia.docx

7/30/2019 13. general anaesthesia.docx

1/23

Page 1 of23

( Maybe it is a long script .. but its very easy and enjoyable to study .. GOOD LUCK ^_^ Eman Nazzal )

General Anaesthesia (GA) Definition : General anaesthesia is defined as a condition in which

the patient has lost :

1-consciousness

2- analgesia : loss of pain sensation .

3- amnesia : loss of memory . Why amnesia ??

((Bcz in Any surgery the patient become in a fear situation so it is preferredthat the patient loss his memory, in order not to remember anything))

4-muscle relaxation. Why muscle relaxation ??

((In order to enhance surgery we need a good muscle relaxation ))

5- loss of autonomic reflexes .

General anaesthetic has . That are administered for induction tomake any general anaesthetic which is VERY important before anysurgery , in which once the patient go to surgery ( it is a must )

must have lost of consciousness , no pain sensation , amnesia in

which the patient cant remember anything .

So, general anaesthesia is a condition which characterized byanalgesia, amnesia, loss of consciousness, inhibition of sensory andautonomic reflexes, and, in many cases, skeletal muscle relaxation.

Local anaesthesia : we induce analgesia, without loss of

consciousness , and administered locally to certain area , in which the

atient cant sense the ain at the side o administration .


2/23

Page 2 of23

General anaesthesia Drugs:

So general anaesthesia Drugs it is a reversible loss of consciousness

( many of us think that anesthesiologists career is very easy , But it is Not bcz u

induce a consciousness , u induce a reversible comma , and in the case of over

dose this lead to death .But when the dose calculated carefully this will induce or

maintain general anesthesia to facilitate surgery.


3/23

Page 3 of23

4 Stages of General anaesthesia :

The anesthesia goes in 4 main stages , and also some sub stages :

1-Analgesia2-Excitement3-Surgical anaesthesia4-Medullary paralysis

stage 1 : Analgesia

Analgesic effect is the partial loss of pain sensation with impairment

loss of consciousness , ( start with impairment loss of consciousness. )

Analgesia is partial until stage II is about to be reached.

stage 2 : Excitement

It is stage of excitement or stage of dis-inhibition.

Here there are excitement , involuntary movement , irregular BP& irregular respiration .

## What did u think ! We now in this stage >> should we go to the

next stage rapidly ? or keep the patient in this stage ?? did u think

that this is the stage of surgical anaesthesia ??

No , We should go to the next stage as rapid as we canBcz this as the stage of excitation , there are undesirable effect on

the patient and we should go to the next stage rapidly


4/23

Page 4 of23

stage 3 : Surgical anaesthesia :

here we get the anesthetic purpose ( which we mentioned at the

beginning of Lecture. e.g : analgesia etc) ,

at the same time respiratory and the cardiovascular system are

maintained , and there is regular respiration , Blood pressure is

controlled at the same time I will get the anesthetic purpose >

Once we reach this stage the surgery is proceed.

stage 4 :Medullar paralysis:

Stage of medullary depressor that seen in the case of anestheticover-Dose and we will have respiratory and cardiovascular

depression center in the medulla , and without full control or

support : death will occur ( in the case of over-Dose ) .

Induction of anaesthesia

3 group of drugs can be administered :1-Drugs that administered as Pre-anesthetic medication ( prior to surgery)2-Drugs that administered to induce anaesthesia3-Drugs that administered to maintain anaesthesia

( the doctor say something but it is not clear at (10:10 min ) in the record )


5/23

Page 5 of23

1-Induction of anaesthesia :what did we mean by induction ? To reach or to start anaesthesia .

this is done by administration ofIntravenous Drugs anesthetic in which

the time from anesthetic administration until the patient reach stage 3(which is the stage of surgical anesthesia and here the doctor can proceed the surgery ) .

2-maintain anaesthesia :Now , how we can maintain anaesthesia ? How can we maintain the

loss the consciousness , analgesia , amnesia , loss of muscle relaxation

and autonomic reflexes . HOW TO KEEP THE PATIENT IN All THESE

CONDITIONS OR HOW TO KEEP HIM IN STAGE 3 ??

this is done by Inhaled anesthetics

3- Recovery period:is the time of discontinuation of GA until the patient regains to his

consciousness.

At the end of the surgery ( this is important ) , the dose of inhaled

anesthetic is gradually reduced until it stop , during this time the

patient return to his/her consciousness ( this is the Recovery period)

So Recovery period it is the time from which the general anesthetic

administration is stopped, until the patient regain back to his

consciousness .

This is the phases :


6/23

Page 6 of23

Summary

Administration of GA the period in which from the time of GA

administration until the patient go to stage 3 ( loss of consciousness

and other effects ) this is known as induction period

Then sustained GA is important for maintenance of anaesthesia to

keep the patient in stage 3 .

Then from the time of discontinuation of GA until return back the full

consciousness this is known as recovery period

Over-Dose comma or death , this is mean that no recovery period the

patient cant return back to his consciousness , this is mean the

paitient go to stage 4 the stage of medullary depression .

A student ask a Qs but i cant hear it ..The doctor answer :

((Ok >> analgesic drug , it is drugs that are administered in which we

have loss of pain without loss of consciousness , in local anesthetic

they produce the same effect , they produce the same wide the

analgesic but the term name as an anesthetic. we will talk about it

Insha-Allah in next lecture , local anesthetic although there are noloss of consciousness but they are named as anesthetic))


7/23

Page 7 of23

Pre-anesthetic medications

From their name , pre- : mean before

So it is a group of drugs that are administered before GA to get multiplepurposes .

1) Sedation and amnesia. ex: Benzodiazepaines derivatives like Diazepam2) Analgesic . ex: Drugs opioids and its derivatives for example morphine .3) inhibition of parasympathetic reflexes . ex: Atropine or hyoscine4) H1 receptor antagonist. ex: diphenhydramine5) H2 receptor antagonist. ex: cimetidine or ratitidine6) Antiemetics drugs. ex: Metochlopramide

1)Sedation and amnesia.First of all we are looking to sedate the patient and relief anxiety , it is

normal that anyone know that he will go to a surgery procedure he will

become anxious , in order to relief an anxiety and induce sedation we

will give him pre-anesthetic medication .

Benzodiazepaines derivatives like Diazepam is administered as apre-anesthetic medication to relief anxiety , apprehension , to reduce

fear . Benzodiazepaines administration

2)analgesic Drugsanalgesic agent or pain killer are administered . we should not wait

until patient will complain from pain , the post-operative pain , in

which an analgesic agent is administered before and at the end of

surgery in order to reduce pain . The best analgesic drug is opioidsDerivatives as Morphine and Pethidine , and specially they are used

with the anesthetic if the anesthetic has a low analgesic effect we

should use another analgesic like for example opioids and its

derivatives for example morphine .


8/23

Page 8 of23

3) inhibition of parasympathetic reflexesBy using ofantimuscarinic drugs in order to:

The lungs in order to reduce the bronchial secretion as a way as we looking toreduce the salivary secretion once we have ??? the salivary secretion will

induce laryngospasm that may enter the larynx to will induce laryngospasm.

Antimuscarinic agent are also administered with other aim to reduce the riskofcardiac arrhythmia , example ofantimuscarinic agent are either Atropine

or hyoscine .

Which one did you think is preferred ? Atropine or hyoscine ?The best is hyoscine . Ok why hyoscine ? Bcz hyoscine is responsible to cause

more CNS depression that is required in anaesthesia ( hyoscine is more

preferred for CNS depression , loss of memory which is amnesia ) so it is

preferred due to its CNS effect and also peripheral affect .

4)H1 receptor antagonist:

They are used to prevent allergic reaction ex: diphenhydramine5)H2 receptor antagonist:

They decrease acid secretion ( I am looking to suppress gastric acidsecretion In order to prevent the retention of gastric content back to the

lungs that may induce a aspiration pneumonia .

( : Aspiration pneumonia isbronchopneumoniathat develops due to the entranceof foreign materials into the bronchial tree, usually oral or gastric contents including

food, saliva, or nasal secretions. ) . ex: cimetidine or ranitidine

6)Antiemetic drugs : it is the drugs that prevent emesis ,in which

emesis can be a verse effect of GA

ex: Metochlopramide

H is related To histamine

H1 receptor responsible for allergic manifestation

H2 rece tor if the are stimulated the induce astric acid secretion
http://en.wikipedia.org/wiki/Antimuscarinichttp://en.wikipedia.org/wiki/Antimuscarinichttp://en.wikipedia.org/wiki/Antimuscarinichttp://en.wikipedia.org/wiki/Bronchopneumoniahttp://en.wikipedia.org/wiki/Bronchopneumoniahttp://en.wikipedia.org/wiki/Antimuscarinichttp://en.wikipedia.org/wiki/Antimuscarinichttp://en.wikipedia.org/wiki/Antimuscarinic


9/23

Page 9 of23

general anesthetic are represent in 2 main groups :1)inhaled anesthetic

They are given through the respiratory track and they are used

for maintenance of anaesthesia . either they are volatile liquids ,

or Gases like Nitrous oxide .

a)Volatile liquids : in which they are liquids under pressure once the pressure isreleased they are evaporated.

Example of the volatile liquid is the halogenated compounds . what did we mean by halogen ? halogens which are in group 7 .So halogenated compound they are the groups of drugs that contain

(Cl , Br ,I , F ) .

These are examples of halogenated general anesthetic :Halothane/ Isoflurane / Methoxyflurane / Sevoflurane

b)Gases : example is : Nitrous oxide . I think you know about nitrous oxide , commonly used by Dentistas an analgesic and it has a powerful analgesic effect , which is N2O

and known as a laughing gas bcz it induce laughing.

2)intravenous anesthetic drugs They are given intravenously To induce GA. They are different groups :

a)Barbiturate derivatives like : Thiopentalb)Benzodiazepaines derivatives like :Midazolamc)Opioid derivitives like : Fentanyld)Ketaminee)Propofol


10/23

Page 10 of23

Ideal Characteristics of Inhalational Anesthetics:

Rapid & pleasant induction & recovery . Be potent, stable, non irritant and non inflammable

(( Now Ether , you know either? it is a general anesthetic drug by inhalation

but one of the most important problem of Ether that it is Flammable . and

this is the most thing that make us afraid and carefull in surgery rooms ,

that the anesthetic drug may become flammable and induce fire.))

Adequate relaxation of smooth muscle Wide margin of safety Absence of toxic effect ( or adverse drug reaction ) (( keep in your mind that during anaesthesia in some cases , if the

general anesthetic drug has inadequate relaxation of smooth

muscle effect , we will use a neuromuscular blocking agent like

Tubocurarine . Also neuromuscular blocking agent are useful in

Tracheal intubation for general anesthetic administration .


11/23

Page 11 of23

Mechanism of Action of inhaled anesthetics

Now the mechanism is little difficult , but the general mechanism(?)

they produce CNS depression , they will inhibit neuronal excitation in

the CNS by different mechanism

First mechanism :With the increase in threshold, there is a decrease in neuronal activity.

(they will rise the neuronal firing threshold , this is mean they make

the neuron difficult for excitation )

Second mechanism :- At the cellular level, anesthetic agents affect synaptic transmission

rather than axonal conduction. The release of excitatory transmitters

and the response of the postsynaptic receptors are both inhibited.

- (They will inhibit the release of excitatory neurotransmitter in theCNS)

Third mechanism :- In general the previous 2 mechanisms will induce the CNS

depression . BUT the third mechanism will enhance the GABA

effect

- ( as u remember GABA is a inhibitory neurotransmitter that willcause opening the chloride channels so induce neuronal

hyperpolarization this is mean inducing neuronal excitation


12/23

Page 12 of23

The pre-synapticneuron for example will inhibit calciumentrance , by that I will inhibit the release of excitatory

neurotransmitter .

The Post-synaptic neuron they either increase chlorideinflux , or they will increase potassium efflux , ya3ni they willinduce hyper-polarization or re-polarization ( respectively ) ,

and by that will inhibit neuronal excitation.

Rout of admimistration :

1) Inhaled anesthetic :-the anesthetic drug is given by inhalation , the site ofaction is in the CNS , this is mean given by inhalation theyshould be absorbed through the alveoli , reaching the

blood , distributed through the body , until it reach the

site of action which is CNS or the brain .

-Keep in your mind that the site of action is the CNS THEY

SHOULD REACH THE BRAIN ( CNS )

2) IV anesthetic

They go directly to the blood , reach the CNS in order to produce theanesthetic effect

So, regardless to their route of administration(inhaled or IV anesthetic )

BOTH of them , their site of action is the CNS to cause CNS depression


13/23

Page 13 of23

Inhaled anesthetic-How they are taken ? they are taken by inhalation , usually they are mixture

with Gas , with oxygen , carrier gas , ok ? with air or with oxygen .

- Ok , these anesthetic as we said they should be transferred from thealveolar space to the blood and from the blood they should reach the brain .

How fast ? this is the pathway

So, inspired Gas to the alveoli arterial blood other tissue andfinally it should reach the brain and in the brain to produce their site

of action

Vice versa , or the opposite way , or redistribution process is the way of their

elimination .

How they are eliminated ? what will be the pathway for their elimination ?

From , the brain blood vessels other tissues the major way fromthe blood return back to the lungs to the alveoli finally by expiration

. This is known as ( redistribution process ) for the ( elimination ).


14/23

Page 14 of23

To get a therapeutic effect the drug should reach the brain

from the alveolar space to the blood and from the blood to the brain

and this depends on many factors :

First factor : Drug solubility :

Something that u have to know ( blood : gas partition coefficient)which will determine the solubility of the drug in the blood .

What did u think , if the drug has a high drug solubility does this

mean that its induction will be faster or slower ?? SLOW .

As we increase (blood : gas partition coefficient) and increase in gas

solubility in the blood increase the onset of induction will be slower

bcz as the solubility increase the drug will need more time to reach the

partial pressure in the blood .

So there are reverse relationship between drug lipid solubility andits onset of induction ,as it is more the induction onset will be slow.

The more soluble the anesthetic in the blood , the more it shouldbe dissolved in order to reach the desired partial pressure

( bcz we r talking about Gases , the gases is measured with partial pressure Not in mg ) .


15/23

Page 15 of23

In the figure : Different anesthetic drugs , you will see the ratio of

partial pressure of the anesthetic in the blood compared to the alveoli ,

we find that

1)Nitrous oxide :has low blood solubility / halothane is medium /

methoxyflurane is high , this is the type of induction.

- This is mean bcz of low blood solubility of Nitrous oxide itsonset of induction will be FAST .

- At the same time the onset of the speed of recovery will beFAST , this is ,mean the drug will leave the brain and returned

back to the blood , from the blood to the alveoli to get a

recovery phase Also will be fast .

2)Halothane:It has a high blood gas partial coefficient in which the solubility in

the blood higher than Nitrous oxide , so it will induce a slow speed

of induction or for anaesthesia comparing with nitrous oxide .

- These is the differences . There is a reverse relationshipcomparing between nitrous oxide and Halothane . ok? Lowsolubility in the blood fast induction . comparing with

halothane

- usually nitrous oxide is mixed with halothane to fasten its onsetof action , So are given in combination .


16/23

Page 16 of23

Second Factor : Anesthetic Concentration in the inspired air

This factor That depend or that can control or that affect onset of drug

effect is its concentration in the inspired Air

What did you think the relationship ? direct ? or reverse ? DIRECT**this is mean as its concentration of the inspired air increase

this is mean it will reach the blood very fast , this is mean it will

reach the brain in very fast onset , the speed of induction or onset

of action will be FAST .

SO , increase the concentration of the anesthetic in the inspired air willincrease the speed of induction on anaesthesia , by increasing the rate

of transfer to the blood ( DIRECT RELATIONSHIP )

Thirs Factor : Pulmonary Ventilation

What did u think ? direct or indirect ? DIRECT .

Hyperventilation , this is mean the amount of anesthetic drug thatgo to the lungs will be more , so it will reach the blood very fast ,

and also the amount that reach the CNS also will be very FAST .

So , increasing Pulmonary Ventilation will increase in arterial tension

( Tension here mean concentration but bcz we are talking about gases we

substitute concentration with tension )

The more Pulmonary Ventilation the more the drug that go to the blood so its

tension will be more ( its conc. Will be more ) and this will induce( NOT Clear) effect.


17/23

Page 17 of23

Fourth Factor : Pulmonary Blood Flow

What did u think ? direct or reverse ? REVERSE / INDIRECT As there is an increase in the blood flow to the lungs this is mean

the volume of the blood will be more , this is mean the amount of

anesthetic that should be dissolved also should be more ( high

anesthetic concentration ) , so the onset of speed of induction will

be slow . So ..

As pulmonary blood flow increase the Onset of induction will decrease

SUMMARY

So they are 4 factors 2 of them Direct and 2 of them Indirect L

2 factors with DIRECT relationship

2 factors with INDIRECT relationship

another factor : blood capacity

Increasing in blood capacity this is mean more anesthetic concentration

, more tension will rises very slowly .

concentration of anesthetic inspired air

pulmonary ventilation

pulmonary blood flow .

solubility of the drug in the blood.


18/23

Page 18 of23

Elimination

The ways of elimination as we said they are eliminated mainly by the lungs by expiration

Other way of clearance is done by other tissue like liver liver play an important rule in drug metabolism

like in case of halothane and methoxyflurane in which these

metabolize are excreted by kidney , but the major process of their

elimination is by the lungs

- This is seen specially in Nitrous oxide bcz it is inorganic , No

need for metabolism and mainly eliminated by the lungs .

Duration is very important :Duration of the exposure of the inhaled anesthetic will affect the

time of recovery , as the duration of exposure will be more the

recovery ( returning back of consciousness) will be slow .

AGAIN as we said , If the drug has low blood gas partition coefficient this is meanits onset of action will be fast on the same time its recovery also will be fast .

So , it is very important , KEEP this in your mind .

NOW Comparing between Nitrous oxide and halothane

which one has the fastonset of action ? Nitrous oxide . why?- Bcz it has low blood gas partition coefficient and low blood

solubility , it has fast induction or fast onset of action .

Which one will produce a fast recovery ? Nitrous oxide .


19/23

Page 19 of23

compare between them in the case ofpotency- potency is how much of drug is required to produce an effect , for drugs the potency

it is expressed by mg / units , in case of inhaled drugs partial pressure)

- drug potency is depend on drug lipid solubility as there is an increase in solubilitythe potency will be more this is mean that the amount of drug that needed to

produce an effect will be small .

So

Onset of action depend on the blood solubility , Potency of the drug depends on its lipid solubility

( as it is more the potency will be more )

Minimum Alveolar concentration (MAC)

The potency is measured by Minimum Alveolar concentration (MAC) which is :

The minimum concentration of the inhaled anesthetic that is looking to induce

immobility or prevent movement in response to surgical incision in 50% of patient

Comparing with other drug , the potency of other drug is expressed byED50 ( effective dose in 50% of population ) .

While in the inhaled anesthetic its potency is expressed by or dependson MAC 50 . it is defined as how much is the anesthetic is needed to

produce immobility or prevent movement or response to such

stimulus like surgical incision in 50% of population .

- As it Is small the potency of the drug will be more , and as it is high ,the potency of the drug will be low .

The MAC depends on the drug lipid solubility- high lipid solubility Low MAC the drug will be highly potent


20/23

Page 20 of23

Now we finish from the introduction and we will talk about examples :

** INHALED ANESTHETIC

1) Halothane

- It is one of the inhaled anesthetic- it is halogenated- not irritant- Colorless- High blood solubility slow induction and recovery .- High fat solubility low MAC highly potent .- Mainly this drug can be metabolized by liver enzymes Cyt-P450- One of its adverse effect Sensitize the myocardium to the effect of catecholamine

and it will induce cardiac arrhythmia.

- Repeated administration over a short period of time has been implicated toproduce halothane hepatitis , and induce the liver damage .

why?They said that halothane metabolism will induce reactive metabolites , and

these reactive metabolites either cause direct damage to the liver cells or they will

induce immune-mediated response ( all of this due to the reactive metabolites ) .

2)Nitrous Oxide (N2O) laughing gas -

It is a good analgesic drug- Low blood solubility rapid induction and recovery- Most rapid induction- Most rapid rate of recovery- least potent, highest MAC value bcz of low lipid solubility- Not metabolized, totally eliminated by lungs- Bcz of its good analgesic effect it can be used in dental procedure and

obstetrics.

- Given by inhalation and mixed with oxygen 50 to 50 percent bcz of itspowerful analgesic effect .

- One of its problems is its short duration of action , you put the mask and ifthere is pain you must return the mask ( y3ni it needs repetitive

administration bcz of its short duration of action )

- Multiple adverse effect ( bcz of rapid recovering it may cause washout ofoxygen from the alveoli and this will induce hypoxia , it is very important to

prevent hypoxia development by administration of significant amount of pure

oxygen.


21/23

Page 21 of23

** INTRAVENOUS ANESTHETIC :

1) Barbiturates : thiopental it is ultra short acting barbiturates in which its onset of

action within seconds , can be induce unconsciousness very rapid .

rapid onset induction and recoverygood anesthetic with poor analgesic effect

( in opposite to Nitrous oxide in which nitrous oxide is a poor

anesthetic with good analgesic effect ).

Dissociative Anesthesia

This term is defined in which we have analgesic effect as well as we have

amnesia , minimal effect of the respiratory function .

The patient is conscious , analgesic ,amnesic But he can open his eyes and

can swallow , but doesnt process any information ( decrees of awareness

of external environment )

Howwe get Dissociative Anesthesia ?

This is seen by the administration ofKetamine HCl . and its effects are :

1)muscular relaxation is poor2) this drug can increase Stimulates central sympathetic outflow

increasing HR, BP and CO.

3)Not used in hypertensive patients2)Propofol

It is a dug that produces anesthesia at a rate similar to that ofbarbiturates ( in compared with thiopental) in which it has a fast onset

of action .

post operative vomiting is less common and may have anti-emeticproperty

hypersensitivity is less common


22/23

Page 22 of23

3)BENZODIAZEPINES

Benzodiazepine derivatives (Diazepam, midazolam, lorazepam )

Not complete GA produces amnesia , muscle relaxation , sedation , no analgesia . Used for:

1) Premedication To relieve anxiety & prevent sympathetic activity.

2) Conscious sedation along with Opioids (for short surgical & diagnostic

procedures e.g : Endoscopy and Bronchoscopy

Neuroleptanalgesia:

It is a state in which there is an analgesia , amnesia , sedation

BUT he is consciousness and cooperative that mean he is able to respond to

commands or external orders .

Anxiety, motor activity, and sensitivity to painful stimuli are reduced;

the person is quiet and indifferent to surroundings

How we get Neuroleptanalgesia?

by administration of 2 drugs :

1)narcotic analgesics (Opioids derivatives) like Fantanyl2) Neuroleptic drugs (antipsychoticdrugs) like Droperidol

Droperidol+ Fantanyl Neuroleptanalgesia

If we add Nitrous Oxide to Droperidol and Fantanyl we will have

Neurolept anaesthesia ( NOT Neurolept analgesia)

Droperidol+ Fantanyl + Nitrous Oxide Neurolept anaesthesia
http://en.wikipedia.org/wiki/Antipsychotichttp://en.wikipedia.org/wiki/Antipsychotichttp://en.wikipedia.org/wiki/Antipsychotichttp://en.wikipedia.org/wiki/Antipsychotic


23/23

Page 23 of 23

THE END

GOOD LUCK

Im sorry for any mistake ..

Done By : Eman Nazzal

13. general anaesthesia.docx

Documents

Transcript of 13. general anaesthesia.docx