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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

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

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


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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
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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, 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
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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

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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/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.
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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 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.

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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.

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.

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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 Class 2
Class 3 Class 4

Healthy Mild systemic disease, no functional limitations


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 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.

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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.

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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. E.g.: Atropine, Glycopyrolate, Scopolamine Dosage

ANTICHOLINERGIC AGENTS:

Atropine- 0.12 mg/kg Glycopyrolate- 0.44mg/kg

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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. E.g.: Metoclopramide E.g.: Sodium citrate solution

Gastro kinetic drugs

Antacids

Antiemitic agents.

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


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FASTING GUIDELINES FOR SURGERY.


AGE CLEAR FLUIDS NONCLEAR FLUIDS \ OR SOLIDS. 4-6 hours prior 6 hours prior 6-8 hours prior 6-8 hours prior or after the previous midnight 26

1. Child <6 months 2. Child 6-36 months 3. Child> 36 months 4. Adults

2 hours prior
2-3 hours prior 2-3 hours prior 2-3 hours prior

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.

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Stages

Excitation

Tolerance

Asfixia Analgesia Planes thorax cornea light limb

consciousness
diaphragm Resp. eye motion pupil size eye closing conjunctiva

reflexes

coughing

secretion

swallowing vomiting

abdomen smooth m.

Muscle tone

Stages of anaesthesia (ether administration)

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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.
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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

Oxygen 2200 psi/g to 45 psi/g Nitrous oxide 745 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 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.
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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

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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 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

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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 patient

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Circle Breathing System


Advantages
Stability

of inspired gas concentrations, Conservation of respiratory moisture and heat, Prevention of operating room pollution
Disadvantage
Complex

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 (an activator)

Baralyme

20% barium hydroxide and 80% calcium hydroxide


Lack of sodium and potassium hydroxides Advantage:

Calcium hydroxide lime


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 (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
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Components

Scheme of anaesthetic circuit

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Gas supply

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Rebreathing circuit

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CLASSIFICATION OF GENERAL ANESTHETICS

A. INHALATIONAL.

Gases:
-

Nitrous oxide, - Cyclopropane.

Liquids.
-

Ether - Halothane - Enflurane- Isoflurane - Trichloroethylene - Methoxyflurane


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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.


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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 explosive

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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 should be possible Cheap, stable and easily stored 50 Should not react with rubber tubing or soda lime.

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. 51 Hypocapnia

Factors

which increases the MAC.


age

Decreasing 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 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.
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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 anesthesia
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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 to Halothane. Produces brief clonic seizures at deeper levels if respiration is not assisted. Contraindicated in Epileptics .

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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

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 60 system in the brain stem.

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%

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Concentration of Nitrous oxide oxygen during various stages :


Induction Slow 0.5-1 lit/min Rapid 24 lit/min 40% nitrous oxide 60% oxygen 20-30% nitrous oxide 100% oxygen

and

Maintenance Reversal

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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 of thiopentone and opiates.

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FOUR ZONES OF N20 ANESTHESIA.


MODERATE ANALGESIA [6 to 25%]


25%

N2O is more potent than 10 mg morphine. symptoms and lack of ability to

DISSOCIATIVE ANALGESIA [26 to 45%]


Psychological

concentrate

ANALGESIC ANAESTHESIA [46 to 65%]


Near

complete analgesia. Patient may respond to commands analgesia and amnesia.

LIGHT ANESTHESIA [66 to 80%]


Complete
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Properties of inhalation anaesthetics


Nitrous oxide Induction Recovery Analgesic effect Respiratory track irritation Blood pressure MAC Induction dose Maintaining dose fast fast + 105 % Halothane Enfluran Isofluran Sevofluran Desfluran

medium medium Decrease 0.75 % 3% 2.05 %

medium medium Decreases 1.6 % 1-10 % 0.6-3 %

medium medium decreases 1.2 % 1-4 % 0.5-3 %

fast fast decreases 2.05 % 5-8 % 0.5-3 %

fast fast + decreases 6% 4-11 % 2-6 %

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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.

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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.

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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 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.

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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.

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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 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

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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.

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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 dreams


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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 minutes intervals.

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


Drug Induction Recovery Main unwanted effects
Cardiovascul ar and respiratory depression

Notes

Thiopentone
(barbiturate)

fast

accumula tion occurs giving slow recovery slower than others

Widely used agent for routine purposes

Midazolam
(benzodiazepine)

slow

Little cardiovascular and respiratory depression

Ketamine

slow

Psychotomimetic effect
very fast Cardiovascul ar and respiratory depression

Produces good analgesia and amnesia


Rapidly metabolized. Possible to use as continuous infusion
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Propofol

fast

The advantages and disadvantages


Inhalation anaesthesia Intravenous anaesthesia
- fast induction

Advantages

- controllable reversibility
(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)

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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

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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

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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.


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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..
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 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 dosage: 0.1 to 1mg IV.

Flumazenil

Neostigmine

dosage: 0.05 to 0.07 mg/kg IV


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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.

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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
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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 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

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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

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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

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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

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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 a suction catheter through the lumen of the endotracheal tube Ensure that the patient is not in a semiconscious state

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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

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

COMPLICATIONS AT EXTUBATION

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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 The placement of this device (usually on one of the fingers) allows for early detection of a fall in a patient's 99 haemoglobin saturation with oxygen (hypoxemia).

2. Continuous pulse oximetry (SpO2):

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
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Monitoring

4.Urine outputA

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%).
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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

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

105 Stop surgery! 100% oxygen; Dantrolene Sodium and ice to cool

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:Drug Pethidine Clonidine Tramadol Ondansetron Suggested Dose And Route 0.35 mg/kg may repeat 4 at 5 min. intervals iv 0.15 mg iv 1mg/kg iv 8mg iv Role Treatment Treatment Treatment or Prophylaxis Prophylaxis
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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

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Thank you!