Anaesthesia /certified fixed orthodontic courses by Indian dental academy

INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com

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

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


HistoryBefore 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

INTRAVENOUS
INHALATIONAL
NITROUS OXIDE
ETHER
HALOTHANE
SEVOFLURANE
ENFLURANE

DISSOCIATIVE
ANESTHESIA

INDUCING AGENTS

KETAMINE

BENZODIAZEPINES

PROPOFOL
THIOPENTONE

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


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

Closed system

Open 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

ADVANTAGES :
 rapid induction & recovery
 no bronchospasm
 low post op nausea & vomiting
 safe during pregnancy

DISADVANTAGES :
 Induction apnea
 Respiratory depression – higher doses
 Bradycardia
 Pain during injection

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 usedwww.indiandentalacademy.com
lignocaine

CLASIFICATION :
I.

BASED ON APPLICATION :

INJECTABLE
Low potency/short duration
procaine, chloroprocaine

SURFACE ANAESTHETICS
Soluble
cocaine, lignocaine

Intermediate potency/duration
lignocaine, prilocaine
High potency/long duration
tetracaine, bupivacaine

Insoluble
benzocaine

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

Intermediate
alkyl

Intermediate
alkyl


Hydrophilic
group

Tertiary
amine

R3
Ester:

R 1—COO—R2 —N

R 1 — Lipophilic aromatic residue.
R4
R3

Amide:

R 1—NHCO—R 2—N
R4

R 2 — Aliphatic intermediate connector.
R 3, R 4 — Alkyl groups, occasionally
H. Constitute with N the hydrophilic
terminus.


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-NH+
R-N +
+
H
acid
base
base
pH = pKa + log
acid


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

Ester

Hydrolysis
Hydrolysis
CH 3

Amide
Hydroxylation
and conjugation

O

NHC CH

R2

R3
N

R1

R4

N-dealkylation
(and cyclization)

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)

articaine

 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

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


OVERDOSE REACTIONS :
 Slow biotransformation
 Slow elimination
 Too large a total dose
 Rapid injection
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


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:www.indiandentalacademy.com and/or assistance
Emergency drugs

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, reexposure 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 .

Thank you
Leader in continuing dental education


Anaesthesia /certified fixed orthodontic courses by Indian dental academy

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