Anaesthesia /prosthodontic courses

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INDIAN DENTAL ACADEMY
Leader in continuing Dental Education

CONTENTS
 INTRODUCTION
 GENERAL ANAESTHESIA
-HISTORY
-CLASSIFICATION
-IDEAL REQUIREMENTS
-MECHANISM OF ACTION
-STAGES OF ANAESTHESIA
- COMMONLY USED ANAESTHETICS

 LOCAL ANAESTHESIA
-HISTORY
-CLASSIFICATION
-MECHANISM OF ACTION
-COMPOSITION
-COMMONLY USED
ANAESTHETICS
-NERVE BLOCKS
-COMPLICATIONS
 NEWER ADVANCES
 CONCLUSION
 REFERENCES

Indian Dental academy
• www.indiandentalacademy.com
• Leader continuing dental education
• Offer both online and offline dental courses

ANAESTHESIA
(greek word)
An aesthesis
CLASSIFICATION
General Local

GENERAL ANAESTHESIA
A state of unconsciousness produced by an anesthetic
agent,with absence of pain sensation over the entire
body and a greater or lesser degree of muscle
relaxation

CARDINAL SIGNS -
Loss of all sensations
Unconsciousness (sleep)
Muscle relaxation
Abolition of reflexes

History-
Before 1846 -
- physical methods(packing the limb in ice)
- drugs like alcohol,opium
1776 - Priestley - 1st anesthetic nitrous oxide
1844 - Horace Wells - nitrous oxide - extraction
1846 - William Morton – ether
After 1846
1847 - James Simpson – chloroform
1868 - Edmond Andrews – N2O+ O2
1929 – Cyclopropane
1935 – Thiopentone
1956 - Halothane

CLASSIFICATION
INHALATIONAL
INTRAVENOUS
DISSOCIATIVE
ANESTHESIA INDUCING AGENTS
BENZODIAZEPINES
NITROUS OXIDE
ETHER
HALOTHANE
SEVOFLURANE
ENFLURANE
PROPOFOL
THIOPENTONE
KETAMINE
DIAZEPAM

IDEAL REQUIREMENTS :
 Smooth & rapid induction
 Produce unconsciousness
 Produce amnesia
 Maintain essential physiological functions while
blocking the reflexes
 Produce skeletal muscle relaxation
 Adequate analgesia
 Smooth,rapid & uneventful recovery

MECHANISM OF ACTION
 Inhibit reticular activating system
 OVERTON & MEYOR(1901)
 potency---------lipid solubility
 Ligand gated ion channels—target
 I.V. anesthetics – GABA receptors
 N2O & ketamine – NMDA receptors

STAGES OF
ANAESTHESIA :
Guedel (1920) –
i. Stage of analgesia
ii. Stage of delirium
iii. Stage of surgical
anesthesia
iv. Medullary paralysis

Pharmacokinetics of inhalalational anaesthetics
alveoli blood brain
Factors affecting the transfer of anesthetic agent :
 Solubility of the agent in blood
 Rate of blood flow through lungs & tissues
 Partial pressure of the agent
Elimination :
Halothane – 20% in liver

 Open drop method
 Through anesthetic machines
- open system
- closed system
METHODS OF ADMINISTRATION
Open systemClosed system

PREANESTHETIC MEDICATION
Need for :
 Rapid & smooth induction
 Sedation
 Counteract adverse effects
 Relieve pain
DRUGS USED:
 Chronic medication
 Anticholinergics – atropine
 H2 receptor antagonist – ranitidine
 Sedative – hypnotics – diazepam
 Opoids
 Anti-emetics – metachlopromide

INHALATIONAL ANESTHETICS
 NITROUS OXIDE –
colorless / odorless / non irritating /
non inflammable / sweet taste
good analgesic
poor anesthetic
70% N2O + 25- 30% O2+ 0.2 – 2% ether – anesthesia
(G- O –E Technique)
 METABOLISM :
rapidly eliminated unchanged – lungs

ADVANTAGES :
 rapid induction & recovery
 No deleterious effects on heart ,kidney ,liver
 Nausea, vomiting uncommon
DISADVANTAGES :
 Not a potent anesthetic
 Co2 accumulation or hypoxia – prolonged administration
 Special apparatus required
CONTRAINDICATION :
 Patients with collection of air in pericardial, pleural and
peritoneal cavities, COPD.

ETHER :
 Oldest anesthetic
 Not used – highly inflammable , pungent odor
post operational nausea & vomiting
HALOTHANE :
 Fluorinated ,volatile anesthetic
 non irritating / non inflammable / colorless liquid with sweet
odor
 potent anesthetic : 2 - 4% -induction
0.5 – 1% - maintenance
METABOLISM :
 60 – 80% -eliminated unchanged
 Rest – liver

ADVANTAGES :
 Quick & pleasant induction
 Quick recovery
 No post op nausea & vomiting
DISADVANTAGES :
 Inadequate muscle relaxation
 Hypotension
 Sensitizes heart to Adrenaline – arrhythmias
 Expensive & special apparatus

INDICATIONS :
 Bronchial asthma
 Plastic surgery – bloodless field
CONTRAINDICATIONS :
 Intracranial lesions
 Hepatic diseases

INTRAVENOUS ANESTHESIA
THIOPENTAL :
 Ultra short acting barbiturates
 Induction dose : neonates – 5 – 8 mg / kg
adults – 3-5 mg / kg
elderly – 1 - 3 mg / kg
METABOLISM :
 Metabolized in liver
USES :
 For induction of GA
 Anesthetic for short duration surgery
 As an anti convulsant

ADVANTAGES :
1. Ease of administration
2. Rapid & pleasant induction
3. Low incidence of nausea & vomiting
4. Quick recovery
DISADVANTAGES :
1. Depth of anesthesia cant be judged
2. Apnea , coughing , laryngospasm ( occasional )
3. Shivering & delirium during recovery
4. Depresses vasomotor centre & myocardium
5. Poor analgesic & muscle relaxant

PROPOFOL :
Oily liquid – 1% emulsion
Unconsciousness – 15 -45 sec
Rapidly metabolised in liver
USES :
 Induction
 Short duration surgeries
 Day care surgery

DISADVANTAGES :
 Induction apnea
 Respiratory depression – higher doses
 Bradycardia
 Pain during injection
ADVANTAGES :
 rapid induction & recovery
 no bronchospasm
 low post op nausea & vomiting
 safe during pregnancy

KETAMINE :
 Non – barbiturate anesthetic
 Induces dissociative anesthesia
 Primary site of action – cortex ( limbic system)
 Dose – 1-3 mg / kg / IV
- 5 – 10 mg /kg / IM
DISADVANTAGES :
 Delirium / hallucination
 Poor muscle relaxant
 Laryngospasm rare
USES :
 Children – induction & maintainence of anesthesia
 Adults – short surgical procedures

CONTRAINDICATIONS :
 Hypertensive patients
 Thyrotoxic patients
 Abdominal surgery
 Ocular surgery

COMPLICATIONS :
During Anaesthesia :
 Respiratory depression
 Salivation
 Hypotension
 Cardiac arrhythmias
 Aspiration of gastric contents
 Delirium , convulsions
After anesthesia :
 Nausea , vomiting
 Organ toxicity
 Emergence delirium

POST ANESTHETIC MEDICATION
Need for:
 Relief of pain
 Post op nausea & vomiting
DRUGS USED:
 Opioids
 Anti-emetics

LOCAL ANAESTHESIA
Reversible loss of sensation in a area of the body caused by a
depression of excitation in nerve endings or an inhibition of the
conduction process in peripheral nerves.
History :
1860 – Neimann isolated cocaine
1884 – Sigmond Frued – cocaine induced localised numbness
1884 – Koller introduced cocaine as LA
1884 – Nash used cocaine for extraction
1905 – Einhorn developed procaine
1943 – Lofgren synthesized lignocaine
1948 – Gordh used lignocainewww.indiandentalacademy.com

CLASIFICATION :
I. BASED ON APPLICATION :
INJECTABLE SURFACE ANAESTHETICS
Low potency/short duration Soluble
procaine, chloroprocaine cocaine, lignocaine
Intermediate potency/duration Insoluble
lignocaine, prilocaine benzocaine
High potency/long duration
tetracaine, bupivacaine

II. BASED ON CHEMICAL STRUCTURE :
Esters Amides
Benzioc acid esters lignocaine
cocaine prilocaine
Para-amino benzoic esters mepivacaine
procaine / tetracaine bupivacaine
benzocaine / chloroprocaine
III. BASED ON ORIGIN :
a. Natural : Cocaine
b. Synthetic: PABA derivatives – procaine / tetracaine
Acetanilide derivatives – lignocaine
Quinolone derivatives – cinchocaine
Acrinide derivatives – bucricaine

CHEMISTRY :
Amphiphilic in nature
LA consists of :
Hydrophobic
group
Aromatic
residue
Hydrophilic
group
Tertiary
amine
Intermediate
alkyl
Intermediate
alkyl

Ester:
Amide:
R —COO—R —N
R —NHCO—R —N
1 2
R
R3
4
21
R
R3
4
R — Lipophilic aromatic residue.
R — Aliphatic intermediate connector.
R , R — Alkyl groups, occasionally
H. Constitute with N the hydrophilic
terminus.
1
2
3 4

IDEAL REQUIREMENTS :
 Non irritating to tissues
 Not cause permanent alteration in the nerve
 Low systemic toxicity
 Highly effective
 Rapid onset of anesthesia
 Long duration of action
 No allergic reactions
 Readily undergo biotransformation
 Should be stable in solution
 Should be sterile

MECHANISM OF ACTION :
STRUCTURE OF A NERVE CELL –

Differential sensitivity of nerve fibre
CLASS MYLENATION DIAMETER CONDUCTION
VELOCITY
FUNCTIONS
Aα
heavy 12-20 70-120 Motor and propioception
Aβ
Moderate 5-12 30-70 Touch and pressure
Aχ
Moderately 3-6 15-30 Motor to muscle spindle
Aδ
lightly 2-5 12-30 Pain, temperature, touch
B lightly 1-3 3-15 Preganglionic autonomic
C None
none
0.4-1.2
0.3-1.3
0.7-1.3
0.7-1.3
Pain & reflex response
Postganglionic sympathetics

PHYSIOLOGY OF NERVE CONDUCTION :

MECHANISM OF ACTION :
THEORIES :
 Acetylcholine theory
 Calcium displacement theory
 Surface charge theory
 Membrane expansion theory
 Specific receptor theory – most accepted

HOW DOES LA WORK ?
 Displacement of Ca2+ from Na channel receptor site
which permits
 Binding of LA to the receptor site which produces
 Blockade of Na+ channel &
 Decrease in Na conductance which leads to
 Depression of rate of electrical depolarisation &
 Failure to achieve threshold potential , along with a
 Lack of development of propagated action potential
which is called conduction blockade

R-NHR-NH++
R-N +R-N +
HH++
acidacid basebase
pH = pKpH = pKaa + log+ log
basebase
acidacid

Factors Affecting the Reaction of Local Anesthetics
Lipid solubility
 Increase in the lipid solubility leads to faster nerve penetration,
block sodium channels, and speed up the onset of action..
 Local anesthetics have two forms, ionized and nonionized. The
nonionized form can cross the nerve membranes and block the
sodium channels.
 So, the more nonionized present, the faster the onset of action.
pH influence
 Usually at range 7.6 – 8.9
 Decrease in pH shifts equilibrium toward the ionized form,
delaying the onset action.

Vasodilation
 Affects the anesthetic potency & duration of action .
 Lower vasodilator activity of a local anesthetic leads to a slower
absorption and longer duration of action
Protein binding
 Protein binding regulate the duration of anaesthetic activity
 Highly protein bound LA will remain for a long time Procaine
 6% protein bound
 Ropi, bupi, etidocaine  94-96% protein bound

Local anesthetic metabolism
NHC
CH 3
O
CH N
R1
R2
R3
Hydroxylation
and conjugation
N-dealkylation
(and cyclization)
R4
Hydrolysis
Hydrolysis
AmideAmide
EsterEster

LIGNOCAINE
COMPOSITION:
 Lignocaine – Local anesthetic agent
 Adrenaline – Vasoconstrictor
 Sodium metabisulfite – Antioxidant
 Methyl paraben – Preservative
 Thymol – Fungicide
 Sodium chloride – Isotonicity of solution
 Water - Diluent

PROPERTIES:
 Amide type of anesthetic
 Potency = 2
 Toxicity = 2
 Metabolism: in liver (microsomal enzymes)
 Excretion: via kidney
 Vasodilating property less than procaine
 pH = 6.5 (plain solution)
5.0 – 5.5 (with vasoconstrictor)
 8.Onset of action – rapid (2 –3 mins)
 9.Effective dental concentration is 2%
 10.Maximum recommended dose (with vasoconstrictor)
- 7.0 mg/kg; not to exceed a dose of 500 mg
- 4.4 mg/kg; not to exceed a dose of 300 mg
(without vasoconstrictor)

ARTICAINE :
 Classification : Amide
 Potency : 1.5 times lignocaine , 1.9 times
procaine
 Toxicity :same as lignocaine
 Metabolism :partially in liver &plasma
 Half-life :shorter than lignocaine (30
min)
 Excretion :via kidneys
 Onset of action : 2-3 min (nerve block)
1-2 min (infiltration)
 Effective dental conc. :4%
 Maximum recommended dose :7.0mg/kg
body wt
lignocaine
articaine

NERVE BLOCKS

INFRA-ORBITAL NERVE BLOCK

NASOPALATINE NERVE BLOCK

GREATER PALATINE NERVE BLOCK

POSTERIOR SUPERIOR NERVE BLOCK

INFERIOR ALVEOLAR NERVE BLOCK

MENTAL NERVE BLOCK

LONG BUCCAL NERVE BLOCK

COMPLICATIONS
LOCAL COMPLICATIONS :
 Paresthesia
 Facial nerve paralysis
 Trismus
 Hematoma
 Pain on injection
 Infection
 Edema
 Soft tissue injury
 Sloughing of tissues

Systemic Complications :
 Overdose reactions
 Allergy
 Syncope

CLINICAL MANIFESTATIONS :
CNS ACTIONS :
Concentration(µg/ml) Effect
0.5 – 4.0 Anticonvulsant action
4.5 – 7.0 Excitation, agitation, talkativeness
7.5 – 10.0 Tonic-clonic seizures
Above 10 Generalized CNS depression
OVERDOSE REACTIONS :
 Slow biotransformation
 Slow elimination
 Too large a total dose
 Rapid injection

Basic Emergency Management
 P – position
unconscious – supine with feet elevated slightly
conscious – based upon patients comfort
 A – airway
unconscious – assess and maintain the airway
conscious – assess the airway
 B – breathing
unconscious – assess and ventilate if necessary
conscious – assess breathing
 C – circulation
unconscious – assess and provide external cardiac
compression if necessary
conscious – assess circulation
 D – Definitive care
Diagnosis
Management: Emergency drugs and/or assistancewww.indiandentalacademy.com

CVS actions
Concentration(µg/ml) Effect
1.8-5.0 Antidysrhythmic actions
5.0-10.0 ECG alterations,
Myocardial depression,
Peripheral vasodilation.
Above 10.0 Massive peripheral
vasodilation,
Intensive myocardial
depression,
Cardiac arrest.

ALLERGY
Hypersensitive state due to exposure to a particular allergen, re-
exposure to which produces a heightened capacity to react.
• Causes –
 Methyl paraben
 Sodium bisulfite
 Epinephrine
• Signs and symptoms –
 Skin reactions
Urticaria, Angioedema
 Respiratory reactions
Respiratory distress, Wheezing, Dyspnea, Cyanosis
 Generalized anaphylaxis

MANAGEMENT
 ELECTIVE DENTAL CARE
-treatment postponed
 EMERGENCY DENTAL CARE
-no treatment of invasive nature
-use GA
-histamine blockers as local anesthetics
-electronic dental anesthesia

Newer advances
Wand Comfort control syringe

REFERENCES :
 The pharmacological basis of therapeutics : Goodman &
Gillman 10th
ed.
 Pharmacology & pharmacotherapeutics : Satoskar – 18th
ed.
 Essentials of medical pharmacology : Tripathi – 5th
ed.
 Local anesthesia & pain control in dental practice :
Monheim’s – 7th
ed.
 Handbook of LA : Malamed – 5th
ed.
 Dental update 2005, (32) , 8 – 14
 Dental update 2005 , 32 , 66 - 72 .

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