kuliah 7-8 general_anesthesia_semester genap.ppt

7/28/2019 kuliah 7-8 General_Anesthesia_semester Genap.ppt

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General Anesthesiadr. Imam Ghozali.,SpAn,.Mkes.

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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


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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.

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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.

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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 irritationwith stinging nettles;

Carotid compression and

nerve clamping.

Concussion anaesthesia relied on

thehammer stroke.

Acupuncture

Hypnosis

Cocaine5


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History

Original discoverer of

general anesthetics

Crawford Long: 1842, etheranesthesia

Nitrous oxide

Horace Wells 1844

Chloroform introduced

James Simpson: 184719th Century physician

administering chloroform

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History

William Morton

October 16, 1846

Gaseous ether

Public demonstration gainedworld-wide attention

Public demonstration

consisted of an operatingroom, ether dome, whereGilbert Abbot underwentsurgery in an unconsciousstate at the MassachusettsGeneral Hospital

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Queen Victoria(born 1819, reigned 1839 - 1901)

Chloroform (CHCl3)

The delivery in 1853 of

Victoria's eighth child and

youngest son, PrinceLeopold, was successful:

chloroform was

administered

by Dr John Snow, the

world's first

anaesthetist.

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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 agentwas introduced.

In 1956 Halothane was introduced

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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


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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/gaspartition coefficient of inhalation anesthetics.

However this only reflects the capacity ofanesthetics to enter the CNS and attain a sufficient

concentration in neuronal membrane but not the

mechanism by which anesthesia is produced.

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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.

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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.

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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 waterstructured. 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


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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.

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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.

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Pre operative evaluation

Purpose:

1. To obtain pertinent information about the patients medical history

and physical as well as mental condition.

2. To determine the need for a medical consultation and the kind of

investigations required.

3. To educate the patient about anesthesia, per operative care, pain

treatment, in the hope of reducing anxiety and thereby facilitating

recovery.

4. To choose the anesthesia plan to be followed, guided by the risk

factors, uncovered by the medical history.

5. To obtain an informed consent.

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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.

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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:

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ASA Classification

Class 1 Healthy

Class 2 Mild systemic disease, no functional limitations

Class 3 Moderate to severe systemic disease, functionallimitations

Class 4 Severe systemic disease, constantly life

threatening, functionally incapacitating

Class 5 Not expected to survive with or without surgery

24h

Class 6 Organ Donor

Class E Emergency 20


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Review of systems

Neurologic evaluation of the patient

Cerebro vascular evaluation of the patient

Cardiovascular evaluation Pulmonary evaluation.

Gastro intestinal evaluation

Endocrinal system evaluation.

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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


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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


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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

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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

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FASTING GUIDELINES

FOR SURGERY.

AGE CLEAR FLUIDS NONCLEARFLUIDS \ OR

SOLIDS.

1. Child 36 months 2-3 hours prior 6-8 hours prior

4. Adults 2-3 hours prior6-8 hours prior

or after the

previous midnight26


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STAGES OFANAESTHESIA

[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


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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 PupilAs 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


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MEDULLARY PARALYSIS.

Cessation of breathing to failure of circulation

and death. Pupil is widely dilated,

Muscles are totally flabby, BP very low.

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Stages of anaesthesia (ether administration)

Stages

Muscle tone

thorax

diaphragm

Resp.

Planes

consciousness

eyem

otion

pupils

ize

reflexes

eyeclo

sing

conjunc

tiva

cornea

vomitin

g

swallowing

coughin

g

secretion

light

smoothm.

abdomen

limb

Tolerance

Excitation

Analgesia

Asfixia

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THE ANESTHETIC


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THE ANESTHETIC

MACHINE.

Comprises ofA 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 thegasses and vapors from the machine to the patient.

Apparatus for scavenging anesthetic gasses in order

to minimize environmental pollution.

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Pipeline supply

Primary gas source for the

anesthesia machine

Supplies oxygen, nitrous oxide,

and air

"normal working pressure" 50 psi

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Cylinder supply

Reserve E cylinders

Color-coded

Pressure regulator

Oxygen2200 psi/g to 45 psi/g

Nitrous oxide745 psi/g to 45 psi/g

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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 typesQuantiflex

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.

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The flow meter sequence is a

potential cause of hypoxiaA 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

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An oxygen leak from the flow tube can produce a hypoxic mixture,

regardless of the arrangement of the flow tubes

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Vaporizer

They results in theincrease of the

temperature

The liquid form of theanesthetic agent vaporizes

to its gaseous form.

The vaporization can bewith

Dry heat or

With Ultraviolet light37


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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

patient38


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Circle Breathing System

Advantages

Stability of inspired gas concentrations,

Conservation of respiratory moisture andheat,

Prevention of operating room pollution

DisadvantageComplex design

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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)

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ABSORPTION

Soda lime (most commonly used ) 80% calcium hydroxide, 15% water, 4% sodium

hydroxide, and 1% potassium hydroxide (anactivator)

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

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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

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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 assembly43


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Scheme of anaesthetic circuit

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Gas supply

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R b thi


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Rebreathing

circuit

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CLASSIFICATION OF


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CLASSIFICATION OF

GENERAL ANESTHETICS

A. INHALATIONAL.

Gases:

- Nitrous oxide,

- Cyclopropane.

Liquids.

- Ether

- Halothane - Enflurane- Isoflurane

- Trichloroethylene

- Methoxyflurane47


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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


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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 explosive49


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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 shouldbe possible

Cheap, stable and easily stored

Should not react with rubber tubing or soda lime.50

MINIMUM ALVEOLAR


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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.

Hypocapnia51


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Factors which increases the MAC.

Decreasing age

Pyrexia

Induced sympathoadrenal stimulation E.g.:

hypercapnia.

Thyrotoxicosis

Chronic alcohol ingestion

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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.

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Contd..

Actions: BP falls in proportion to the concentration of the vapors

inhaled.

Hypotension

Respiratory depression in proportion to the concentration ofhalothane 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.

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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 anesthesia55


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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

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ENFLURANE

MAC 1.68%

Non inflammable

Non irritant Strong anesthetic agent with pungent odour

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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 toHalothane. Produces brief clonic seizures at

deeper levels if respiration is not assisted.

Contraindicated in Epileptics .58


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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


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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


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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

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Concentration of Nitrous oxide andoxygen 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

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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 ofthiopentone and opiates.

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FOUR ZONES OF N20


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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 tocommands

LIGHT ANESTHESIA [66 to 80%]Complete analgesia and amnesia. 64

P i f i h l i h i


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Properties of inhalation anaesthetics

Nitrousoxide Halothane Enfluran Isofluran Sevofluran Desfluran

Induction fast medium medium medium fast fast

Recovery fast medium medium medium fast fast

Analgesic

effect + - - - - -Respiratory

track

irritation

- - - - - +

Blood

pressure- Decrease Decreases decreases decreases decreases

MAC 105 % 0.75 % 1.6 % 1.2 % 2.05 % 6 %

Induction

dose3 % 1-10 % 1-4 % 5-8 % 4-11 %

Maintaining

dose

2.05 % 0.6-3 % 0.5-3 % 0.5-3 % 2-6 %

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INTRAVENOUS


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INTRAVENOUS

ANAESTHETIC AGENTS.

THIOPENTONE SODIUM.Dosage: 3-5mg/kg

Ultra short acting barbiturate

Highly soluble in waterProduces 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


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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.

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O SO


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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


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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.

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Contd..

Action

Rapid onset: 45 seconds.

Average duration of anesthesia: 10 minutes.

Antiemetic property is present. So post opnausea 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


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DIAZEPAM BENZODIAZEPINE

GROUP

Dosage: 0.2 to O.5 mg/kg.

Site of action: Thalamus, hypothalamus at gamma-

aminobutyric 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 5 / l]


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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


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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

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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

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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 dreams75

FENTANYL- DROPERIDOL


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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

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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 minutesintervals.

Patient remains drowsy but conscious.

Respiratory depression present.

Slight fall in BP. Heart rate increases.

Recovery is slow,

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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.

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Properties of intravenous anaesthetics


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Properties of intravenous anaesthetics

Drug Induction Recovery Main

unwantedeffects

Notes

Thiopentone(barbiturate)

fast accumula

tion

occurs

giving

slow

recovery

Cardiovascul

ar and

respiratorydepression

Widely used agent

for routine purposes

Midazolam(benzodiazepine)

slow slower

than

others

Little cardiovascular

and respiratory

depression

Ketamine slow Psychoto-

mimeticeffect

Produces good

analgesia andamnesia

Propofol fast very fast Cardiovascul

ar and

respiratory

depression

Rapidly

metabolized.

Possible to use as

continuous infusion79

Th d t d di d t


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The advantages and disadvantages

Inhalation anaesthesiaIntravenous

anaesthesia

Advantages - controllable reversibility

(duration of action can becontrolled)

- fast induction

Disadvantages - relatively slow induction

- irritation of airways- claustrophobic feeling

- duration of action can

not be controlled(termination of action requirebiotransformation or excretion

processes over which the

anesthetist has no control)

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M l l t


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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

Muscle relaxants

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Muscle relaxants


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Muscle relaxants

Muscle relaxants are either depolarising or non-depolarising agents

Depolarising agentsFor 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 agentsFor 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 relaxation82

Intraoperative Analgesic


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p g

Agents

In boluses at induction and before incision, thenmaintenance as needed.

Additional doses based upon sympatheticresponse to pain, like increased HR, BP.

Fentanyl, a synthetic narcotic, Onset 2min, peak 5min.

Metabolized by liver.

Gag is blunted, minimal cardiac depression, caninduce respiratory arrest.

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Contd


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Contd..

Morphine- 5min onset, peak at 20min.

Metabolites cleared by kidney

Histamine release with hypotension

possible.

Ketamine-Intense analgesia, amnesia,

dissociative anesthesia.

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Contd


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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.

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REVERSAL OF


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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 byanticholinestrase 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 bronchospasam86


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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


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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


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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)


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With Curved Blade (Macintosh)

Insert from right to left

Ensure the lower lip is

not being pinched by

the lower incisors andlaryngoscope blade

Visualize anatomy

Blade in vallecula

Lift up and away

Lift epiglottis indirectly

With Straight Blade (Miller)


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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



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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 thetrachea under direct vision

Inflate the cuff

92

Confirmation of tracheal


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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


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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


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Extubation

Ensure that the patient is recovering is

breathing spontaneously with adequate

volumes

Evaluate the patient's ability to protect hisairway by observing whether the patient

responds appropriately to verbal commands

95

Extubation steps:


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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 asuction catheter through the lumen of the

endotracheal tube

Ensure that the patient is not in asemiconscious state

96

Extubation steps:


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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


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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


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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


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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 transplantsurgery, 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

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Monitoring


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Monitoring

4.Urine output-A measure of end-organ perfusion;

Foley for all cases over 2 hrs,

Decompress bladder.

5. Agent concentration measurementMeasure the percent of inhalational anaesthetic agent

used

6. Low oxygen alarmThis warns if the fraction of inspired oxygen drops

lower than room air (21%).101

Monitoring


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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


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Monitoring

9. Temperature measurementTo diagnose hypothermia and fever, and to aid early

detection of malignant hyperthermia.

10. EEG or other systemTo 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


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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.

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Contd


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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 cool105


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Contd..


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Contd..

Prevention

Increasing the ambient temperature in theatre,

Using conventional or forced warm air blankets

Using warmed intravenous fluids.

107

Contd..


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Contd..

Drug treatment:-

Drug Suggested DoseAnd Route

Role

Pethidine 0.35 mg/kg mayrepeat 4 at 5 min.intervals iv

Treatment

Clonidine 0.15 mg iv Treatment

Tramadol 1mg/kg iv Treatment orProphylaxis

Ondansetron 8mg iv Prophylaxis

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Conclusion


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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 insome 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


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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!


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Thank you!

kuliah 7-8 general_anesthesia_semester genap.ppt

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