General Anesthesia

dr. Imam Ghozali.,SpAn,.Mkes.

Content

Introduction
History
Theories of mechanism of action of general anesthesia
Pre operative evaluation & premedication of the patient
Stages of anesthesia
The anesthetic machine
Anesthetic agents
Other drugs administered during anesthesia
Muscle relaxants
Analgesics

Reversal of anesthesia
Tracheal intubation
Monitoring
Complications of general anesthesia
2

Introduction
General anaesthesia = Hypnosis + Analgesia + Relaxation

Hypnosis = suppression of consciousness

Analgesia = suppression of physiological responses to pain stimuli
Relaxation = suppression of muscle tone and relaxation

A controlled reversible state of:

Amnesia (with loss of consciousness)
Analgesia
Akinesia (skeletal muscle relaxation)
Autonomic and sensory reflex blockade
Called the 4 As of General Anaesthesia.

In practice these effects are produced with a combination of drugs

rather than with a single anaesthetic agent.

Introduction
Anesthesia- ( Greek) - Insensible/without any feeling
According to Bennet: Anesthesia means loss of all modalities of sensation,
particularly pain, along with reversible loss of consciousness
According to Goodman and Gillman: The anesthetic state is defined as a
collection of component changes in behavior or perception.
GENERAL ANAESTHESIA is a controlled state of unconsciousness,
accompanied by partial or complete loss of protective reflexes, including
the inability to maintain an airway independently and respond
purposefully to stimulation or verbal command.

Early painkilling techniques

Non-pharmacological methods:
Blood-letting
(undoubtedly relieved pain, though it was carried
out to dangerous and often fatal excess.)

Cooling with cold water, ice;

Distraction by counter irritation
with stinging nettles;
Carotid compression and
nerve clamping.
Concussion anaesthesia relied on
the
hammer stroke.
Acupuncture
Hypnosis
Cocaine
5

History
Original discoverer of general
anesthetics
Crawford Long: 1842, ether
anesthesia

Nitrous oxide
Horace Wells 1844

Chloroform introduced
James Simpson: 1847

19th Century physician

administering chloroform
6

History
William Morton
October 16, 1846
Gaseous ether

Public demonstration gained

world-wide attention
Public demonstration consisted
of an operating room, ether
dome, where Gilbert Abbot
underwent surgery in an
unconscious state at the
Massachusetts General
Hospital
7

Queen Victoria
(born 1819, reigned 1839 - 1901)

Chloroform (CHCl3)

The delivery in 1853 of

Victoria's eighth child and
youngest son, Prince
Leopold, was successful:
chloroform was
administered
by Dr John Snow, the
world's first
anaesthetist.

History
In. 1887 Frederic Hewitt invented a gas & oxygen machine.
In 1910 Mc Kesson introduced intermittent flow machine, which
provided control of O2 and N2O on demand.

In 1929 Cyclopropane was introduced,

In 1935 Thiopentone, the first intravenous anesthetic agent was
introduced.
In 1956 Halothane was introduced
9

Theories of mechanism of action of general

anesthesia
Still now exact mechanism not known.
Various theories have been proposed. They are:
Lipid/water partition theory
Surface tension theory
Theory of inhibition of energy production/ utilization
Clathrates formation theory
Membrane expansion theory
Membrane fluidization/ perturbation theory
10

1. LIPID/WATER PARTITION THEORY

Meyer and Overton in 1901
A direct parallelism exists between lipid water
partition co efficient of drugs and their anesthetic
potency. The minimum alveolar concentration (MAC)
shows excellent correlation with oil/gas partition
coefficient of inhalation anesthetics.
However this only reflects the capacity of anesthetics
to enter the CNS and attain a sufficient concentration
in neuronal membrane but not the mechanism by
which anesthesia is produced.
11

2. SURFACE TENSION THEORY.

General anesthetics reduce surface tension at
all cell membrane and thus affect its
permeability, electrical and /or enzymatic
properties.
This theory is generally not accepted.

12

3. THEORY OF INHIBITION OF ENERGY PRODUCTION /

UTILIZATION.

This theory states that general anesthetics

decreases the production of action potential
in the brain.
Decrease in energy production In the brain is
probably an effect rather than the cause of
general anesthesia.

13

4. CLATHRATES FORMATION THEORY

Pauling & Millerin 1961
Water has a crystal like molecular arrangement.
General anesthetics are believed to fill up the spaces
between micro crystals (clathrates) and make water
structured. They plug the pores and impede ionic fluxes.
However this behavior is also dependant on
hydrophobicity.
But there is no evidence of clathrate formation at body
temperature.
14

5. MEMBRANE EXPANSION THEORY

The general anesthetics occupy the space in the
nerve membrane in the brain and expand it
disproportionately (about 10 times their molecular
volume).
This causes increased surface pressure in the
membrane, there by closing ionic channels.
This theory in much widely accepted.
15

6. MEMBRANE FLUIDIZATION / PERTURBATION

THEORY.
The anesthetics by dissolving in the membrane lipids,
increases the degree of disorder in their structures, favoring a
gel-liquid transition. (Fluidization).
Normally fluidization occurs at high temperatures.
General anesthetics make it possible to occur at low
temperatures.

This affects the state of membrane bound proteins which

regulates ionic fluxes.

16

Pre operative evaluation

Purpose:
1.
2.
3.

4.

5.

To obtain pertinent information about the patients medical history

and physical as well as mental condition.
To determine the need for a medical consultation and the kind of
investigations required.
To educate the patient about anesthesia, per operative care, pain
treatment, in the hope of reducing anxiety and thereby facilitating
recovery.
To choose the anesthesia plan to be followed, guided by the risk
factors, uncovered by the medical history.
To obtain an informed consent.

17

Contd..
History

Current problems.
Other known problems
Treatment/ medications for the problem.
Current drug use.
H/O use of tobacco, alcohol etc
H/O drug allergies.
Prior anesthetic exposure.
General health of the patient And
Review of systems.

Physical examination:

Vital signs
Airway.
Heart.
Lungs.

18

ASA PHYSICAL STATUS CLASSIFICATION SYSTEM:

In 1962 the American Society of
Anesthesiologists adopted the ASA physical
status classification system.
It is a method by which a doctor can estimate
the medical risk to a patient who is scheduled
to receive anesthesia for a surgical procedure.
The classification is as follows:

19

ASA Classification
Class 1
Class 2

Healthy
Mild systemic disease, no functional limitations

Class 3

Moderate to severe systemic disease, functional

limitations
Severe systemic disease, constantly life
threatening, functionally incapacitating
Not expected to survive with or without surgery
24h
Organ Donor
20
Emergency

Class 4

Class 5
Class 6
Class E

Review of systems

Neurologic evaluation of the patient

Cerebro vascular evaluation of the patient
Cardiovascular evaluation
Pulmonary evaluation.
Gastro intestinal evaluation
Endocrinal system evaluation.

21

PRE ANAESTHETIC PREPARATION AND PRE

MEDICATION
The objectives of pre medication.
Reduce anxiety and fear.
Reduce secretions
Enhance the hypnotic effect of GA agents.
Reduce post op nausea and vomiting
Produce amnesia.
Reduce the volume and pH of gastric contents
Attenuate vagal reflexes
Attenuate sympatho adrenal responses.
22

DRUGS USED FOR PREMEDICATION.

BENZODIAZEPINES:
E.g.: Diazepam, Midazolam, Oxazapam, Lorazepam.
Produces anxiolysis, sedation and amnesia

OPIOD ANALGESICS:
E.g.: Morphine, Fentanyl, Pethidine, Pentozocaine etc
It produces sedation and analgesia.

ANTICHOLINERGIC AGENTS:
E.g.: Atropine, Glycopyrolate, Scopolamine
Dosage
Atropine- 0.12 mg/kg
Glycopyrolate- 0.44mg/kg
23

Contd..
ANTICHOLINERGIC AGENTS:
Increases the heart rate by blocking the action of acetylcholine on
muscarinic receptors in SA node.
Very useful in preventing intraoperative bradycardias resulting from
stimulation of carotid sinus or vagal stimulation.
Antisialagouge action
Glycopyrolate is more potent and long acting drying agent and is likely to increase
the heart rate.
Scopolamine is more effective Antisialagouge than atropine.

Sedation and amnesia: Glycopyrolate doesn't cross blood brain barrier and hence doesn't cause sedation/
amnesia.
Scopolamine has good sedative and amnesic effect.
Atropine cause delirium in elderly individuals, so glycopyrolate is better than
atropine for elderly individuals

24

ASPIRATION PROPHYLAXIS,
Histamine receptor(H2 receptor blocking agents)
E.g.: Cimetidine, Ranitidine, and Famotidine.

Gastro kinetic drugs

E.g.: Metoclopramide

Antacids
E.g.: Sodium citrate solution

Antiemitic agents.
E.g.: Droperidol, Metoclopramide, Phenothiazines like
Ondasteron, Prochlorperazine

25

FASTING GUIDELINES FOR SURGERY.

CLEAR FLUIDS

NONCLEAR
FLUIDS \ OR
SOLIDS.

2 hours prior

4-6 hours prior

2. Child 6-36 months

2-3 hours prior

6 hours prior

3. Child> 36 months

2-3 hours prior

6-8 hours prior

2-3 hours prior

6-8 hours prior

or after the
previous midnight

AGE

1. Child <6 months

4. Adults

26

STAGES OF ANAESTHESIA [Guedel l920 with ether]

STAGE OF ANALGESIA.
Starts from the beginning of anesthetic inhalation
and lasts up to loss of consciousness. Pain is
progressively abolished at this stage

STAGE OF DELIRIUM
Starts from the loss of consciousness to beginning
of irregular respiration. Apparent excitement is
seen. Heart rate and BP may rise and pupils dilate
due to sympathetic stimulation.
27

 SURGICAL ANAESTHESIA.
Extends from the onset of regular respiration to
cessation of spontaneous breathing
Plane 1- Roving eye balls. This plane ends when eyes become
fixed.
Plane 2- Loss of corneal and laryngeal reflexes.
Plane 3- Pupil starts dilating and light reflex is lost.
Plane 4- Intercostal paralysis, shallow abdominal respiration,
dilated Pupil

As anesthesia passes to deeper planes progressively, the

muscle tone decreases, BP falls, HR increases with weak
pulse, and respiration decreases in depth and later in
frequency also.
28

 MEDULLARY PARALYSIS.
Cessation of breathing to failure of circulation and
death. Pupil is widely dilated,
Muscles are totally flabby, BP very low.

29

Stages
smooth m.

abdomen

reflexes

limb

vomiting

swallowing

light

secretion

Resp.

coughing

cornea

conjunctiva

eye closing

pupil size

eye motion

thorax

diaphragm

consciousness

Planes

Stages of anaesthesia (ether administration)

Muscle tone

Analgesia

Excitation

Tolerance

Asfixia

30

THE ANESTHETIC MACHINE.

Comprises of
A means of supplying gasses either from attached
cylinders or from piped medical supplies.
Methods of measuring flow rate of gasses.
Apparatus for vaporizing volatile anesthetic agents.
Breathing system and ventilators for delivery of the
gasses and vapors from the machine to the patient.
Apparatus for scavenging anesthetic gasses in order to
minimize environmental pollution.
31

Pipeline supply
Primary gas source for the
anesthesia machine
Supplies oxygen, nitrous oxide, and
air
"normal working pressure" 50 psi

32

Cylinder supply
Reserve E cylinders
Color-coded
Pressure regulator
Oxygen 2200 psi/g to 45 psi/g
Nitrous oxide 745 psi/g to 45 psi/g

33

Flow meter
Delivers the mixture of oxygen, N2O and air.
Minimum O2 concentration at the common gas outlet is
between 23% and 25%

They are of two types

Quantiflex
Oxygen flow is fixed.
N2O flow can be controlled independently

Linked flow meter

Oxygen flow meter and the N2O flow meter are connected
mechanically which will cause reduction of the oxygen flow
when N20 flow will be increased and vice versa.
34

The flow meter sequence is a

potential cause of hypoxia
A and B, In the event of a flow meter leak, a potentially dangerous arrangement exists
when nitrous oxide is located in the downstream position.
C and D, The safest configuration exists when oxygen is located in the downstream
position

35

An oxygen leak from the flow tube can produce a hypoxic mixture, regardless
of the arrangement of the flow tubes

36

Vaporizer
They results in the increase
of the temperature
The liquid form of the
anesthetic agent vaporizes to
its gaseous form.
The vaporization can be with
Dry heat or
With Ultraviolet light

37

Circle Breathing System

A circle system can be semiopen, semiclosed,
or closed, depending on the amount of fresh
gas inflow
Semiopen system has no rebreathing and requires
a very high flow of fresh gas
Semiclosed system is associated with rebreathing
of gases
Closed system is one in which the inflow gas
exactly matches that being consumed by the
patient
38

Circle Breathing System

Advantages
Stability of inspired gas concentrations,
Conservation of respiratory moisture and
heat,
Prevention of operating room pollution

Disadvantage
Complex design
39

ABSORPTION
Lack of toxicity with common anesthetics, low
resistance to airflow, low cost, ease of
handling, and efficiency
3 formulations
Soda lime
Baralyme
Calcium hydroxide lime (Amsorb)

40

ABSORPTION

Soda lime (most commonly used )

80% calcium hydroxide, 15% water, 4% sodium

hydroxide, and 1% potassium hydroxide (an activator)

Baralyme
20% barium hydroxide and 80% calcium hydroxide

Calcium hydroxide lime

Lack of sodium and potassium hydroxides
Advantage:
Carbon monoxide and the nephrotoxic substance known as
compound A not produced

41

ABSORPTION
Absorptive Capacity
Soda lime is 26 L of carbon dioxide per 100 g of
absorbent
Calcium hydroxide lime has been reported at 10.2
L per 100 g of absorbent

Absorption depends on:

Size of the absorptive granules
Surface area
Air flow resistance
42

SCAVENGING SYSTEM
The collection and the subsequent removal of vented gases
from the operating room
Attached to the exhaust valve
Consists of tubings that collects gases and directs them
outside the building or to a charcoal canister

Components
(1) the gas-collecting assembly
(2) the transfer means
(3) the scavenging interface
(4) the gas-disposal assembly tubing
(5) an active or passive gas-disposal assembly
43

Scheme of anaesthetic circuit

44

Gas supply

45

Rebreathing
circuit

46

CLASSIFICATION OF GENERAL ANESTHETICS

A. INHALATIONAL.
Gases:
- Nitrous oxide,
- Cyclopropane.

Liquids.

- Ether
- Halothane
- Enflurane- Isoflurane
- Trichloroethylene
- Methoxyflurane
47

Contd..
B. INTRA VENOUS.
1. Inducing agents:

- Thiopentone sodium
- Methohexitone sodium
- Propofol
- Etomidate

2. Slower acting drugs.

Benzodiazepines: Diazapam, Lorazapam, Midazolam
Dissociate anesthesia: Ketamine
Neuroleptanalgesia: Fentanyl + Droperidol.
48

Properties of an ideal anesthetic

A. For the patient: It should be
Non irritating
Should not cause nausea or vomiting

B. For the surgeon: It should:

Provide adequate analgesia
Immobility
Muscle relaxation
Non inflammable
Non explosive
49

Contd..
C. For the anesthetist: Its administration should
be easy, controllable and versatile.

Wide safety margin

Heart, lever or other organs should not be affected
Should be potent in low concentration
Rapid adjustment of depth of anesthesia should be
possible
Cheap, stable and easily stored
Should not react with rubber tubing or soda lime.
50

MINIMUM ALVEOLAR CONCENTRATION

[MAC]
The amount of drug used to produce lack of reflex response
to skin incision in 50% of patients.
Factors which decreases the MAC.

Sedative drugs such as pre medication agents, analgesics

N20.
Increasing age
Drug which affect the neurotransmitter release such as
methyldopa, pancuronium, clonidine
Higher atmospheric pressure.
Hypocapnia
51

 Factors which increases the MAC.

Decreasing age
Pyrexia
Induced sympathoadrenal stimulation E.g.:
hypercapnia.
Thyrotoxicosis
Chronic alcohol ingestion

52

HALOTHANE [fluothane]

MAC 0.75%
Colorless volatile liquid with sweet odour.
Non irritant and non inflammable.
This is 4 to 5 times more potent anesthetic
agent than ether.

53

Contd..
Actions:
BP falls in proportion to the concentration of the vapors inhaled.
Hypotension
Respiratory depression in proportion to the concentration of
halothane inhaled.
Breathing: shallow and depressed.
Increases the CSF pressure.
Causes moderate relaxation of skeletal muscles.
Post op nausea and vomiting not severe as in ether.
Shivering.

54

ETHER
Highly volatile and colorless liquid.
It is inflammable in air and explosive with oxygen,
Should not be used when cautery is being used for surgery.

About 85 to 90% of the drug will get excreted

through the lungs.
Stimulates the sympathetic system yielding to
increase in heart rate and to depress the vagus
nerve.
BP falls in the deeper planes of anesthesia
55

Contd..
Respiratory movements first increase due to stimulation of
respiratory centre and later on it decreases as the anesthesia
deepens.
Stimulates salivation, so atropine pre medication is advised.
Irritant to respiratory tract and produces cough and laryngeal
spasm.
On induction it induces analgesia followed by-excitement and
then anesthesia.
Increases CSF pressure and blood glucose levels.
Produces post operative nausea and vomiting in 50 % of
patients
56

ENFLURANE

MAC 1.68%
Non inflammable
Non irritant
Strong anesthetic agent with pungent odour

57

Contd..
ACTIONS
Depresses the cardiovascular system.
Heart rate remains relatively stable.
Increases the BP
As the depth of the anesthesia increases,
respiratory system will be depressed.
Induction and recovery slower compared to
Halothane. Produces brief clonic seizures at
deeper levels if respiration is not assisted.
Contraindicated in Epileptics .
58

ISOFLURANE

MAC 1.15%
Non inflammable,
Mild pungent smell.
Actions:

Rapid onset and reversal.

Profound respiratory depression with decreased tidal volume
Depresses the cardiovascular system.
Decreases the BP as the dosage increases.
Produces good muscle relaxation.
Increases the intra cranial pressure secondary to increased
cerebral blood flow (vasodilatation).
59

NITROUS OXIDE [N20]

MAC 105%
This is a non inflammable anesthetic agent but
supports combustion.
Heavier than air.
Insoluble in blood.
Can produce gastric distress- nausea, vomiting.
Acts in the ascending reticular activating system
in the brain stem.
60

Contd..
Actions:
Moderate increase in pain threshold
Slight amnesia effect
Euphoria is frequent
Decreased sense of smell
Improved hearing
Slight myocardial depression
Minimal effect on respiration
Reduces MAC of other gaseous agents by 50%
61

Concentration of Nitrous oxide and oxygen

during various stages :
Induction

Slow 0.5-1 lit/min

Rapid 24 lit/min
40% nitrous oxide
60% oxygen

Maintenance
Reversal

20-30% nitrous oxide

100% oxygen

62

 Side effects of N20

Post op nausea and vomiting
Chronic use causes bone marrow depression, vit B
12 and folate metabolic disturbances
Teratogenic effects in the first trimester of
pregnancy.
Augments the respiratory depressant effect of
thiopentone and opiates.

63

FOUR ZONES OF N20 ANESTHESIA.

MODERATE ANALGESIA [6 to 25%]
25% N2O is more potent than 10 mg morphine.

DISSOCIATIVE ANALGESIA [26 to 45%]

Psychological symptoms and lack of ability to
concentrate

ANALGESIC ANAESTHESIA [46 to 65%]

Near complete analgesia. Patient may respond to
commands

LIGHT ANESTHESIA [66 to 80%]

Complete analgesia and amnesia.
64

Properties of inhalation anaesthetics

Nitrous
oxide

Halothane

Enfluran

Isofluran

Sevofluran

Desfluran

Induction

fast

medium

medium

medium

fast

fast

Recovery

fast

medium

medium

medium

fast

fast

Analgesic
effect

Decrease

Decreases

decreases

decreases

decreases

105 %

0.75 %

1.6 %

1.2 %

2.05 %

6%

3%

1-10 %

1-4 %

5-8 %

4-11 %

2.05 %

0.6-3 %

0.5-3 %

0.5-3 %

2-6 %

Respiratory
track
irritation
Blood
pressure
MAC
Induction
dose
Maintaining
dose

65

INTRAVENOUS ANAESTHETIC AGENTS.

THIOPENTONE SODIUM.

Dosage: 3-5mg/kg
Ultra short acting barbiturate
Highly soluble in water
Produces unconsciousness in 15-20 seconds
Produces CNS depression which persists for> 12 hours.
Poor analgesic and weak muscle relaxant
Respiratory depression with inducing doses of
thiopentone is generally transient, but with large dose
it will be severe.
66

Contd..
Bp falls immediately after injection but recovers
rapidly.
Cardiovascular collapse may occur if hypovolemia,
shock or sepsis are present.
Adverse effects: Laryngospasm
Shivering and delirium during recovery.
Pain in the post operative period.

67

METHOHEXITAL SODIUM
Dosage:
1-1.5mg/kg.

3 times more potent than thiopentone.

Quicker and brief actions.
Unconsciousness is usually induced in 15-30 seconds.
Consciousness will regain within 2-3 minutes.
Actions:

Less hypotensive compared to thiopentone.

Causes slight increase in heart rate.
Moderate hypoventilation
Short period of apnea may be seen after iv injection.
This drug is contraindicated in epileptic patients.
68

PROPOFOL

Phenol derivative.
Oil in water emulsion
pH between 7.0 and 8.5.
Dosage:
G.A Induction: 2 to 2.5 mg/kg titrated over 20 to
3.0 seconds.
Maintenance: 25% of the induction dose.
Sedation: 3mg/kg/hr in an infusion pump.
69

Contd..
Action
Rapid onset: 45 seconds.
Average duration of anesthesia: 10 minutes.
Antiemetic property is present. So post op nausea
and vomiting less.
Decreases arterial pressure by 30%.
No heart rate change.
Cardiac output decreases minimally.
Incidence of phlebitis is 0.6%.
Pain at the injection site.
70

DIAZEPAM BENZODIAZEPINE GROUP

Dosage:
0.2 to O.5 mg/kg.

Site of action: Thalamus, hypothalamus at gammaaminobutyric acid (GABA) receptors

Action:
Mild decrease in BP by decreasing anxiety and causing muscle
relaxation.
Antiemetic property is present.
Produces amnesia which increases as the dose increases .
Produces emotional responses in adolescent females.
71

MIDAZOLAM [1-5mg/ml]

Onset of action: 1 minute.

Given slowly, 1 mg over 2 minutes.
Soluble in water.
Less chance of thrombophlebitis.
Respiratory depression may occur at higher
dose.
Faster acting.
Short clinical action than diazepam.
Half life 2.5 hours.
72

KETAMINE {100mg and 500mg/10ml

injection }
Produces 'dissociative' anesthesia
Profound analgesia, immobility, amnesia with
light sleep and feeling dissociation from ones
own body and surroundings.
Primary site of action:
cortex and sub cortical area.

Muscle tone increases.

Heart rate, cardiac output and BP are elevated
due to sympathetic stimulation
73

Contd..
Dosage:
1 to 4 mg/kg IV or 6.5 to 15 mg/kg IM

Onset of action: within 1 to 3 minutes

Recovery starts after 10 - 15 minutes, but the
patient remains amnesic for 1 to 2
hours. Delirium, hallucinations and
involuntary movements occurs in 50%
patients.
Children tolerate the drug well.
74

Contd..
Recommended for
Surgeries on the head and neck
Asthmatic patients (relieves bronchospasm)
Hypovolemic patients.

Contraindicated in:
Hypertensive patients
Ischemic heart diseases.
Unmarried females
As it causes lucid dreams
75

FENTANYL- DROPERIDOL
COMBINATION.
Fentanyl is a short acting (30 to 50 minutes)
potent opioid analgesic.
Droperidol is a rapidly potent neuroleptic.
When this combination is given IV a state of
'neuroleptanalgesia' is produced.
This state lasts for 30 to 40 minutes

76

Contd..
Dosage:
Fentanyl 0.5 mg+ Droperidol 2.5mg/ml
4 to 6 ml is diluted in 5% dextrose sol and infused over 10 minutes
.
Supplemental doses of Fentanyl can be given at 30 minutes
intervals.

Patient remains drowsy but conscious.

Respiratory depression present.
Slight fall in BP.
Heart rate increases.
Recovery is slow,
77

Contd..
Abnormal movements can be seen.
Psychomotor function remains depressed
for many hours.
Can be converted to 'neuroleptanesthesia'
by administering 65% N20 and 35% 02.

78

Properties of intravenous anaesthetics

Drug

Thiopentone

Induction

Recovery

Main
unwanted
effects

Notes

fast

accumula
tion
occurs
giving
slow
recovery

Cardiovascul
ar and
respiratory
depression

Widely used agent

for routine purposes

slow

slower
than
others

(barbiturate)

Midazolam
(benzodiazepine)

Ketamine

slow

Propofol

fast

very fast

Little cardiovascular
and respiratory
depression

Psychotomimetic
effect

Produces good
analgesia and
amnesia

Cardiovascul
ar and
respiratory
depression

Rapidly
metabolized.
Possible to use as
continuous infusion
79

The advantages and disadvantages

Advantages

Inhalation anaesthesia

Intravenous
anaesthesia

- controllable reversibility

- fast induction

(duration of action can be

controlled)

Disadvantages - relatively slow induction

- irritation of airways
- claustrophobic feeling

- duration of action can

not be controlled
(termination of action require
biotransformation or excretion
processes over which the
anesthetist has no control)

80

Muscle relaxants
Facilitate tracheal intubation at the start of
anesthesia.
During maintenance of anesthesia muscle
relaxation may be required to facilitate
surgery and intermittent positive pressure
ventilation

81

Muscle relaxants
Muscle relaxants are either depolarising or non-depolarising agents

Depolarising agents
For example - suxamethonium
Act rapidly within seconds and last for approximately 5 minutes
Used during induction of anaesthesia
Gets metabolized with pseudocholinestrase enzyme and its effect wears off.
Has a short duration of action.

Non-depolarising agents
For example Vecuronium, Pancuronium, Atracurium, Rocuronium
Act over 2-3 minutes and effects last for 30 minutes to one hour
Competitive antagonism of acetylcholine receptor
Used for muscle relaxation
82

Intraoperative Analgesic Agents

In boluses at induction and before incision, then
maintenance as needed.
Additional doses based upon sympathetic response
to pain, like increased HR, BP.
Fentanyl, a synthetic narcotic,
Onset 2min, peak 5min.
Metabolized by liver.

Gag is blunted, minimal cardiac depression, can

induce respiratory arrest.

83

Contd..

Morphine- 5min onset, peak at 20min.

Metabolites cleared by kidney
Histamine release with hypotension possible.
Ketamine-Intense analgesia, amnesia,
dissociative anesthesia.

84

Contd..
Ketamine increases HR, BP, bronchodilator,
Increased Cerebral Blood Flow.
Illusions, dysphoria.
Not a respiratory depressant,
Can be sole anesthetic agent.
One of several induction agents, good for
children, contraindicated in head injury.

85

REVERSAL OF ANESTHESIA.
The timing of the last dose of muscle relaxant is important, and
if it is too near to the conclusion of surgery, adequate time must
be allowed before reversal is attempted.
Non depolarizing muscle relaxants are reversed by
anticholinestrase drugs.
E.g.: Neostigmine Sulphate [0.05 to 0.07 mg/kg]
Atropine Sulphate (Anticholinergic) is administered along with
this to prevent muscarinic effects of neostigmine like
bradycardia, profuse salivation and bronchospasam
86

 Reversal agents:
Physostigmine.
dosage: 0.5 to 2 mg slow IV

Flumazenil
dosage: 0.1 to 1mg IV.

Neostigmine
dosage: 0.05 to 0.07 mg/kg IV

87

Tracheal intubation
Advantages of tracheal intubations:
Airway patency
Protects the airway
Maintains patency during positioning

Control of ventilation
ventilation over a long period of time without intubation
can lead to gastric distention and regurgitation

Route for inhalation anesthesia and emergency

medications

Narcan, Atropine, Lidocaine, Epinephrine.

88

Nasotracheal intubation
technique
Topical lidocaine or phenylephrine should be
applied to the nasal passages
0.5-1.0% phenylephrine and 4% Lidocaine, mixed
1:1 should also give satisfactory results
Generously lubricate the nares and endotracheal
tube
ET tube should be advanced through the nose
directly backward toward the nasopharynx

89

With Curved Blade (Macintosh)

Insert from right to left
Ensure the lower lip is
not being pinched by the
lower incisors and
laryngoscope blade
Visualize anatomy
Blade in vallecula
Lift up and away
Lift epiglottis indirectly

With Straight Blade (Miller)

Insert from right to left
Ensure the lower lip is not
being pinched by the lower
incisors and laryngoscope
blade
Visualize anatomy
Blade past vallecula and over
epiglottis
Lift up and away
Lift epiglottis directly

Nasotracheal intubation technique

loss of resistance to the ET marks the entrance
into the oropharynx
laryngoscope and Magill forceps can be used
to guide the endotracheal tube into the
trachea under direct vision
Inflate the cuff

92

Confirmation of tracheal intubation:

Direct visualization of the ET tube passing
through the vocal cords
CO2 in exhaled gases
Bilateral breath sounds
Absence of air movement during epigastric
auscultation

93

Confirmation of tracheal intubation:

Condensation (fogging) of water vapor in the tube on
exhalation
Refilling of reservoir bag during exhalation
Maintenance of arterial oxygenation
Chest X-ray: the tip of the ET tube should be
between the carina and thoracic arc or
approximately at the level of the aortic arch

94

Extubation
Ensure that the patient is recovering is
breathing spontaneously with adequate
volumes
Evaluate the patient's ability to protect his
airway by observing whether the patient
responds appropriately to verbal commands

95

Extubation steps:
Oxygenate patient with 100 percent high flow
O2 for 2 to 3 minutes
If secretions are suspected in the
tracheobronchial tree, remove them with a
suction catheter through the lumen of the
endotracheal tube
Ensure that the patient is not in a
semiconscious state
96

Extubation steps:
Turn the patient onto his side if he is still unconscious
Unsecure the endotracheal tube from the patient's
face
Deflate the cuff and remove the endotracheal tube
quickly and smoothly during inspiration
Continue to give the patient O2 as required

97

Complications of tracheal intubations:

COMPLICATIONS ASSOCIATED WITH INTUBATION.

Direct trauma to teeth, luxation of teeth

Fracture and or subluxation of cervical spine
Nasal hemorrhage
Surgical emphysema of the neck and mediastinum
Aspiration of gastric contents.
Accidental intubation of esophagus.
Obstruction of the airway
Rupture of the trachea and bronchus.

COMPLICATIONS AT EXTUBATION

Difficult extubation
Tracheal collapse.
Airway obstruction.
Aspiration of stomach contents.
98

Monitoring
1. Continuous Electrocardiography (ECG):
Placement of electrodes which monitor heart rate and rhythm.
Help the anaesthetist to identify early signs of dysrhythmias,
myocardial ischemia, electrolyte abnormalities.
Detect 95% of intraoperative ischemia, allowing for early
intervention

2. Continuous pulse oximetry (SpO2):

The placement of this device (usually on one of the fingers)
allows for early detection of a fall in a patient's haemoglobin
saturation with oxygen (hypoxemia).

99

Monitoring
3. Blood Pressure Monitoring (NIBP or IBP):
Non-invasive blood pressure (NIBP) monitoring.
Placing a blood pressure cuff around the patient's arm,
forearm or leg.
A blood pressure machine takes blood pressure readings at
regular, preset intervals throughout the surgery.

Invasive blood pressure (IBP) monitoring.

For patients with significant heart or lung disease, the
critically ill, major surgery such as cardiac or transplant
surgery, or when large blood losses are expected.
Technique involves placing a special type of plastic cannula in
the patient's artery usually the femoral and radial sites
100

Monitoring
4.Urine output A measure of end-organ perfusion;
Foley for all cases over 2 hrs,
Decompress bladder.

5. Agent concentration measurement

Measure the percent of inhalational anaesthetic agent
used

6. Low oxygen alarm

This warns if the fraction of inspired oxygen drops
lower than room air (21%).
101

Monitoring
7. Circuit disconnect alarm
Indicates failure of circuit to achieve a given pressure
during mechanical ventilation.

8. Carbon dioxide measurement

(capnography) Measures the amount of carbon dioxide expired by the
patient's lungs.
Allows the anaesthetist to assess the adequacy of
ventilation.
Unexpected rise in CO2:
Malignant hyperthermia should be suspected
102

Monitoring
9. Temperature measurement
To diagnose hypothermia and fever, and to aid early
detection of malignant hyperthermia.

10. EEG or other system

To verify depth of anaesthesia may also be used.
Reduces the likelihood that a patient will be mentally
awake, although unable to move because of the
paralytic agents.
Also reduces the likelihood of a patient receiving
significantly more amnesic drugs than actually
necessary to do the job.
103

COMPLICATIONS OF GENERAL
ANESTHESIA.
DURING ANESTHESIA
Respiratory depression and hypercarbia.
Increased salivation, respiratory secretions.
Cardiac arrhythmias, asystole
Fall in BP.
Aspiration of gastric contents, acid pneumonitis.
Laryngospasm, asphyxia
Delirium, convulsions.
104

Contd..
AFTER ANESTHESIA.

Nausea, vomiting
Persisting sedation; impaired psychomotor function
Pneumonia
Liver / kidney damage
Nerve palsies- due to the faulty positioning
Delirium
Malignant hyperthermia
Stop surgery! 100% oxygen; Dantrolene Sodium and ice to cool

105

Post-operative shivering, causes, prevention and

treatment.
Causes
Is per- operative hypothermia secondary to
anaesthetic induced inhibition of
thermoregulation.
Causes both cutaneous vasodilation and reduction
in the thresholds for activation of vasoconstriction
and shivering.
In turn this results in redistribution of body heat
from core to periphery with subsequent rapid
hypothermia during anaesthesia.
106

Contd..
Prevention
Increasing the ambient temperature in theatre,
Using conventional or forced warm air blankets
Using warmed intravenous fluids.

107

Contd..
Drug treatment:-

Clonidine

Suggested Dose
And Route
0.35 mg/kg may
repeat 4 at 5 min.
intervals iv
0.15 mg iv

Tramadol

1mg/kg iv

Ondansetron

8mg iv

Drug
Pethidine

Role
Treatment
Treatment
Treatment or
Prophylaxis
Prophylaxis
108

Conclusion
Individual variation of patients response to general
anaesthetics are so great that
reliable dose/response relationship do not exist.
General anaesthetics can not be administered in a
predetermined dosage based on mg/kg body weight
without running the risk of serious over dosage in
some patients and inadequate depth of anaesthesia in
others.
Evaluation of depth of anaesthesia is neither easy nor
precise but instead highly subjective,
clinical signs varying not only with each general
anaesthetic but also with each patient.
109

Bibliography

ORAL AND MAXILLOFACIAL SURGERY Vol 1- Daniel Laskin

ORAL AND MAXILLOFACIAL SURGERY Vol 1 - ANESTHESIA. Fonseca
MANUAL OF ORAL AND MAXILLOFACIAL SURGERY- Paul Laskin
PHARMACOLOGY AND THERAPEUTICS FOR DENTISTRY- Enid A Neid 3rd
edition
A TEXT BOOK OF ANESTHESIA- Ailkenhead 4th edition
CLINICAL PHARMACOLOGY- K. D. Tripati
A PRACTICE OF ANESTHESIA . Thomas EJ Healy& Paul R Knight 3rd edition
CLINICAL PHARMACOLOGY. P. N. Bennette

110

Thank you!