Local anaesthetics

Regional Anaesthetics
Dr.Rakshitha
Pharmacology PG
HIMS, Hassan

CONTENTS
 Introduction- Definition
 History
 Classification
 Mechanism of action of local
anaesthetics
 Pharmacological action
 Therapeutic uses
 Conclusion

Regional anaesthesia
DEFINITION
• The word anaesthesia is coined from two Greek
words: "an" meaning "without" and "aesthesis"
meaning "sensation".
• There are various types of anaesthesia.

DEFINITION
• Anaesthesia of a segment of the body
• Selective interruption of nerve transmission (i.e.,
Peripheral or neuraxial)
• No loss of consciousness.

PRINCIPLES OF REGIONAL ANAESTHESIA
• Review physiology of nerve impulse conduction
• Identify equipment and preparation to provide
peripheral nerve blocks
• Identify types of local anaesthetic agents,
characteristics and risk factors
• Identify techniques and its risks.

History
• COCAINE -first local anaesthetic agent isolated by
NIEMAN -1860 from the leaves of the coca tree.
• Its anaesthetic action was
demonstrated by KARL
KOLLER in 1884.
Deepak V et.al.,The Historical Perspective of Local anaesthetics

Some highlights on local anesthesia
• 1850s - Invention of the syringe and hypodermic
hollow needle.

• 1884 -Halsted, an American surgeon, blocks the
brachial plexus with a solution of cocaine under direct
surgical exposure
• 1885 -Wood, in the United Kingdom, is credited with
the introduction of conduction anaesthesia through
hypodermic injection.
• 1897-- Epinephrine is isolated by John Abel at Johns
Hopkins Medical School.
• 1897-- Braun in Germany relates cocaine toxicity with
systemic absorption and advocates the use of
epinephrine.

• 1898- Bier is set to receive the
first planned spinal anaesthesia from
his assistant Hildebrandt.
• Bier then performs the first spinal
anaesthesia on Hildebrandt using
cocaine. They both experience the
first spinal headaches.

First effective and widely used synthetic local
anaesthetic -PROCAINE -produced by EINHORN in
1905 from benzoic acid & diethyl amino ethanol.

• 1908-- Bier introduces the intravenous
peripheral nerve block (Bier block) with
procaine.
• 1911-- Hirschel performs the first percutaneous
axillary block.
• 1911-- Kulenkampff performs the first
percutaneous supraclavicular block.

LIDOCAINE
• In 1940, the first modern local
anaesthetic agent was
lidocaine(Xylocaine®)
• It developed as a derivative of
xylidine
• Belongs to the amide class, cause
little allergenic reaction; it’s
hypoallergenic
• Sets on quickly and produces a
desired anaesthesia effect for
several hours

DEFINITION
• Local anaesthesia is defined as a loss of
sensation in a circumscribed area of the body
caused by depression of excitation in nerve
endings or an inhibition of the conduction
process in peripheral nerves. STANLEY
F.MALAMED (1980)

DESIRABLE PROPERTIES OF LOCALANAESTHETICS
• Non irritating .
• It should not cause any permanent alteration of nerve structure .
• Systemic toxicity should be low .
• Fast onset of action .
• It should be effective regardless of whether it is injected into the tissue
or applied locally to mucous membrane
• Long duration of action.

DESIRABLE PROPERTIES OF LOCAL
ANAESTHETICS
• It should have the potency sufficient to give complete
anaesthesia without the use of harmful concentration
solutions.
• It should be free from producing allergic reactions.
• It should be stable in solution and relatively undergo
biotransformation in the body.
• It should be either sterile or be capable of being
sterilized by heat with out deterioration.

17
BASED ON DURATION OF ACTION
• Procaine
• Chloroprocaine
Short duration
20- 45min
• Lignocaine
• Articaine
• Mepivacaine
• Prilocaine
• Cocaine
Intermediate
duration
60 -120min
• Bupivacaine
• Levo-bupivacaine
• Ropivacaine
• Etidocaine
Long duration
6-7 hours

18
1.BASED ON SITE
Cocaine, Prilocaine, LignocaineTopical
Lignocaine,Bupivacaine
Mepivacaine, Prilocaine,Injectable

DIFFERENCES
E S T E R S A M I D E
Short duration of action Longer lasting analgesia
Less intense analgesia Produce more intense analgesia
Hydrolyzed by Plasma Cholinesterase
in blood
liver microsomal enzymes
Not plasma protein bound Bind to alpha1 acid glycoprotein in plasma
Higher risk of hypersensitivity
reactions
(free aromatic compound released
during hydrolysis )
Rarely cause hypersensitivity reactions
Useful for topical and on mucous
membranes
Used for Infiltration anesthesia, spinal
anaesthesia

Chemistry
1. Lipophilic group- an
aromatic group, usually an
unsaturated benzene ring.
2. Intermediate bond- a
hydrocarbon connecting
chain, either an ester (-CO-)
or amide (-HNC-) linkage.
3. Hydrophilic group- a
tertiary amine and proton
acceptor

Esters Am”i”des
•Cocaine
•Chloroprocaine
•Procaine
•Tetracaine
•Bupivacaine
•Lidocaine
•Ropivacaine
•Etidocaine
•Mepivacaine

Physicochemical properties-activity relationship
1. Lipid solubility:
Determines intrinsic local anaesthetic activity.
↑ Lipid solubility
↑ Penetration into neuronal membrane
↑uptake
Hence, Lipid solubility parallels LA Potency

2. Protein binding: The most important binding proteins
in plasma are albumins and alpha-1-acid glycoprotein
(AAG).
• Protein binding affects the duration of action of local
anaesthetics: Bupivacaine (95%) , Ropivacaine (94%),
Tetracaine (85%) , Mepivacaine (75%) , Lidocaine (65%)
Procaine (5%) and 2-chloroprocaine (negligible).
• Drugs as Lidocaine, Tetracaine, Bupivacaine have been
incorporated into liposomes to prolong their duration of
action.

3.Pka and pH: determines the ratio between the ionized
(cationic) and the uncharged (base) forms of the drug.
• pKa is the pH at which the ionized and non-ionized
forms of the local anaesthetic are equal
The pka of local anaesthetics ranges from 7.6 to 9.2.

Drug Lipid
Solubilit
y
Protein
Binding
(%)
pKa
(Unionized
Fraction
pH
7.4)
%
Nonioniz
ed
at pH 7.4
Onset
Of
Action
(Min)
Duration
after
Infiltrati
on
(min)
Procaine 0.02 6 8.9 3 14-15 45-60
Chloro
procaine
0.14 0 8.7 5 6-12 30-60
Lidocaine 2.9 64 7.9 24 2-4 60-120
Mepivacai
ne
0.8 78 7.6 39 2-4 90-180
Bupivacain
e
8.2 96 8.1 17 5-8 240-480
Ropivacain
e
8.0 92–94 8.1 17 5-8 240-480

Mechanism of action
ELETROPHYSIOLOGY OF NERVE
CONDUCTION
• There is an electrical charge across the membrane- membrane
potential
• Resting potential is negative electrical potential of -70 to -90mv

GENERATION OF THE ACTION POTENTIAL:
• Voltage-gated sodium channels are responsible for action
potential initiation and propagation.
• Sodium channels consist of a highly processed α subunit, which is
approximately 260 kDa, associated with auxiliary β subunits of 33-
39 kDa .
• The α subunits are organised in four homologous domains (I–IV),
which each contain six transmembrane alpha helices (S1–S6) and
an additional pore loop located between the S5 and S6 segments

• Gate m (the activation gate) is normally
closed, and opens when the cell starts to get
more positive.
• Gate h (the deactivation gate) is normally
open, and swings shut when the cells gets too
positive.

PHARMACOLOGICALACTIONS
LOCAL ACTIONS
- Block sensory nerve endings , nerve trunks, ganglionic synapse.
- Receptors level: Reduce release of Ach from motor nerve endings
- Myelinated fibres more susceptible
• Small fibres > larger fibres
• Type C and B fibres> small A delta fibres> type A alpha/beta/
gamma fibres
• ORDER OF BLOCK
Pain – temperature- touch- deep pressure- motor
Fibres more susceptible to LA first to be blocked and last to recover

Fibers Diameter
(µm)
Myelin Conductio
n velocity
(m/s)
Innervation Function
A-alpha 12-20 +++ 75-120 Afferent from muscle
spindle
Propioceptors
Efferent to skeletal muscle
Motor and
reflex activity
A-beta 5-12 +++ 30-75 Afferent from cutaneous
mechanoreceptors
Touch &
pressure
A-gamma 3-6 ++ 12-35 Efferent to muscle spindle Muscle tone
A-delta 1-5 ++ 5-30 Afferent pain and temp,
Nociceptors
Fast pain,
touch and
temp
B <3 + 3-15 Preganglionic sympathetic
efferents
Autonomic
C 0.2-1.5 - 0.5-2 Afferent pain and
temperature
Slow pain ,
temp

COCAINE
• It stimulates the CNS and in low doses produces
euphoria and "well being"
• Higher doses cause convulsions, coma, medullary
depression & death
• Cocaine stimulates the vomiting centre
• Blocks the uptake of catecholamines into peripheral
nerve terminals.

COCAINE
• Vasoconstriction and mydriasis
• Small doses – bradycardia(central vagal stimulation)
• Larger doses - tachycardia, increased TPR and
hypertension,direct myocardial depression, VF &
death
• Cocaine itself constricts blood vessels and the use of
adrenaline is contraindicated as it sensitises the
myocardium

PROCAINE(NOVOCAINE)
• Synthesised by Einhorn in 1905
• Procaine has a short duration of action and a high pKA,
therefore it spreads poorly through tissues
Procaine
hydrolysed butyrylcholinesterase
Para-aminobenzoic acid
inhibits the action of the Sulphonamides
• Procaine may prolong the action of Succinylcholine(
anticholinesterase )

PROCAINE(NOVOCAINE)
• Currently, Procaine is seldom used for peripheral
nerve or epidural blocks because of its low potency,
slow onset,
short duration of action, and
limited ability to penetrate tissue.

Chloroprocaine
• Chlorine substitution on the aromatic ring of procaine
gave chloroprocaine, which has a rapid onset and a
short duration of action
• Its use declined rapidly after 1980 following reports
of prolonged sensory and motor block.
• severe back pain developed after large epidural doses
of 3% chloroprocaine

TETRACAINE
• In 1930, Tetracaine was the last ester type local
anaesthetic developed.
• This is a useful agent when the amide agents are
contraindicated.
• It is available as a 1% -4% solution

Lidocaine
• Lidocaine, prepared in 1944, is the first amide local
anaesthetic to be used clinically, by Lofgren in 1948.
• Lidocaine -widely employed because of its potency,
rapid onset, and effectiveness for infiltration,
peripheral nerve block, and both epidural and spinal
anaesthesia.

Lidocaine
DOSAGE & ADMINISTRATION:
• 1% Lignocaine = 10mg/mL
• 2% Lignocaine = 20mg/mL
INDICATION:
• Treatment or prophylaxis of VF, VT, Tosarde’s de pointes
• Local or regional anaesthesia for nerve block, infiltration
injection, caudal or other epidural blocks

Lidocaine
LOCAL ANAESTHETIC
Maximum dose:
• Lignocaine without adrenaline - 3mg/kg
• Lignocaine with adrenaline -7mg/kg
ARRHYTHMIAS
Bolus dose
• Bolus of 1 to 1.5 mg/kg (usually 75 to 100 mg) IV, over 1
to 2 minutes
• Duration of action of single bolus dose is 10-20minutes

Lidocaine
Other constituents with Lignocaine:
Sodium hydroxide /HCl- To acidify weak base
Methylparaben- Antiseptic
Sodium Metabisulphite-Antioxidant

Lidocaine
Adverse/effects:
• CVS: hypotension, bradycardia, decreased cardiac
output, heart block, arrhythmia and cardiac arrest
• CNS: circumoral paraesthesia, numbness of the tongue,
light headedness and tinnitus.
• Tremors.
• Unconsciousness
• Malignant hyperthermia

Lidocaine

Lidocaine
Contraindication:
• Hypersensitivity
• Inflammation or sepsis
• Myasthenia gravis,
• Severe shock or impaired cardiac conduction
• Supraventricular arrhythmia
• Severe degrees of sinoatrial, atrioventricular or
intraventricular block

Prilocaine
• Prilocaine, also related to lidocaine, was introduced
in 1960.
• It is used for infiltration, peripheral nerve block, and
peridural anesthesia.
• It produces less vasodilatation than lidocaine and has
a lesser potential for systemic toxicity at similar
doses

Prilocaine
Prilocaine (10 mg/kg)
hydrolysis
o-toluidine
Methaemoglobinaemia
(limiting factor to the use of prilocaine)
EMLA Cream: equal portions of Lidocaine + Prilocaine

Bupivacaine Hydrochloride
• High concentrations of Lidocaine for spinal
anaesthesia have been associated with transient
neurologic symptoms and cauda equina syndrome.
• It was first introduced into clinical use in 1963.
• The apparition of Bupivacaine in 1963 is a very
important step in the evolution of regional
anaesthesia.

Bupivacaine Hydrochloride
• On the cyclic amino group, an aliphatic
Chain is appended in form of a butyl group
instead a methyl one (C4 instead C1)
• Long-acting local anaesthetic
•Indication: Infiltration,
Peripheral nerve block,
Epidural, and spinal anesthesia.
• Concentration of the drug varies from
0.0625% to 0.5%.

Peripheral block-0.25%-0.5%
Spinal anaesthesia-0.5%(Hyperbaric)
Epidural anaesthesia-0.25%-0.5%

Bupivacaine Adverse/Effects: {0.5-5µg/ml}
• Prolong QT interval
• Ventricular tachycardia
• Cardiac depression
• Cardiac arrest
• Hypotension,
• Bradycardia
Cox B, Durieux ME, Marcus MA. Toxicity of local anaesthetics. Best practice &
research Clinical anaesthesiology. 2003 Mar 1;17(1):111-36

CONTRAINDICATIONS
• Allergy/hypersensitivity
• Obstetrical paracervical block
• Intravenous regional anaesthesia (bier's block)
• Coagulopathy
• Sepsis

Indication in
adults
Concentration
(%)
Volume Dose
Lumbar Epidural 0.75 15-20 mL 113-150 mg
Peripheral nerve
block
0.75 10-40 mL 75-300 mg
Intrathecal
administration
0.5 3-4 mL 15-20 mg
Postoperative
pain
Lumbar epidural
0.2 6-10 mL/h 12-20 mg/h
BUPIVACAINE

LEVOBUPIVACAINE
• Interest in Levobupivacaine arose after several cases of severe
cardiotoxicity (including death) were reported where it was
shown that the D isomer of Bupivacaine had a higher
potential for toxicity.
• Protein binding of Levobupivacaine is more than 97%, mainly
to acid alpha1-glycoprotein, rather than to albumin.
• Levobupivacaine demonstrated less affinity and strength of
inhibitory effect onto the inactivated state of cardiac sodium
channels than the racemic parent or dextroBupivacaine
Burlacu CL, Buggy DJ. Update on local anaesthetics: focus on levobupivacaine.
Therapeutics and clinical risk management. 2008 Apr;4(2):381

LEVOBUPIVACAINE
• As a result of its lower cardiac and neurotoxicity compared to
racemic Bupivacaine, anaesthetists feel safer working with
Levobupivacaine, than with Bupivacaine.
Adverse Effects
• Hypotension,
• Bradycardia,
• Nausea, vomiting,
• Headache, dizziness, constipation,
• vomiting and convulsion
Burlacu CL, Buggy DJ. Update on local anaesthetics: focus on levobupivacaine.
Therapeutics and clinical risk management. 2008 Apr;4(2):381

Ropivacaine
• Ropivacaine is a long-acting regional anaesthetic that is
structurally related to Bupivacaine.
• It is a pure S(-)enantiomer,developed for the purpose of
reducing potential toxicity and improving relative sensory and
motor block profile.
• Ropivacaine is less lipophilic than Bupivacaine and is less
likely to penetrate large myelinated motor fibres
Kuthiala G, Chaudhary G. Ropivacaine: A review of its pharmacology and clinical use. Indian journal
of anaesthesia. 2011 Mar;55(2):104

Ropivacaine
Adverse effects:
• Hypotension ,
• Nausea , Vomiting , Bradycardia ,
• Fever , Pain ,
• Headache ,
• Pruritus , and
• Back pain
Kuthiala G, Chaudhary G. Ropivacaine: A review of its pharmacology and clinical use. Indian journal
of anaesthesia. 2011 Mar;55(2):104

Pharmacokinetics:
Absorption (injected or topical)
-Affected by vascularity.
-Presence of additional vasoconstrictor

2. Presence of vasoconstrictors
Addition of Epinephrine{5 mcg/ml (1:200,000)}
vasoconstriction at the site of administration
↓ absorption , ↓ the Drug concentration in blood,
facilitates neuronal uptake,
•Enhances the quality of analgesia,
•Prolongs the duration of action,
•limits toxic side eff ects.
• Vasoconstrictors have More pronounced effects on shorter-acting than
Longer-acting

II Distribution
•Alpha phase –rapidly
redistributed to well-
perfused tissues
•Beta phase –distribution to
less perfused or slowly
equiliibrating tissues
•Gamma phase –clearance
representing metabolism
and excretion

Metabolism
Esters (rapid) –Metabolized by
plasma cholinesterases
• Rapid plasma degradation
• Produce PABA, important in
allergy
Amides (slower) –Hepatic
metabolism (N-dealkylation and
hydroxylation)
• Allergy very rare
• Longer plasma half-life

DRUG TERMINAL
HALF
LIFE(min)
CLEARANCE
(ml/mim/kg)
Vd
(L/kg)
metabolites
Cocaine 48 31 2.0 Norcaine,Ecgonine
Procaine 8 60 0.7 Diethylethanolamino
P-aminobenzoate
Tetracaine 15 47 1.0 Butyl-aminobenzoate
Dimethyl-aminoethanol
Lidocaine 100 15 1.3 Monoethylglycine-xylidine
Ethylglycine,2,6-xylidine
Prilocaine 100 34 2.7 N-propylamine
O-toludine
Bupivacaine 200 9 1.1 Pipecolic acid,Pipecolyl-xylidine
Levobupivacaine 200 9 1.1 Pipecolic acid,Pipecolyl-xylidine
Ropivacaine 110 7 0.7 3-hydroxy-Ropivacaine
3-hydroxy-Ropivacaine glucuronide
4-hydroxy-Ropivacaine

HEART:
Decrease cardiac excitability and
contractility
Decrease conduction rate
Exception: cocaine......it stimulates
heart
BLOOD VESSELS: Arteriolar
dilation
Cocaine is exception: produces
vasoconstriction
Neurotoxicity:
concentration-dependent
nerve damage to central and
peripheral NS
- transient neurological
symptoms
Smooth muscle:
-depress contractions in bowel
-Relaxation of vascular and
bronchial smooth muscle
-Increased GI tone
Neuromuscular junction :
-Block response of skeletal
muscle to Ach at concentration
at which muscle responds
normally to direct electrical
stimulation
-Block nicotinic Ach receptors

New drugs
Articaine
• thiophene ring + ester
group
• Lipid soluble,PPB-94%
• Pka-7.4,t1/2-27 minutes
• Onset of action: 1-2 min
• dental concentration: 4%
• A/E: methemoglobinemia,
paresthesia
Centbucridine
• Drug Research of India(1983)
• quinolone derivative with
intrinsic vasoconstricting and
anti-histaminic properties.
• Concentration of 0.5% can be
used effectively for infiltration,
nerve blocks and spinal
anaesthesia
• Can be used in patient
hypersensitive to lignocaine.

Types of local anaesthetia
Surface
anaesthesia
Infitration
anaesthesia
Conduction
block
anaesthesia
Central nerve
block anaesthesia
Intravenous regional
anaesthesia

Drug Delivery:
Topical application
• Mucous
membrane
• Sensory nerve
endings
• Superficial layer
Form: solution, ointments, cream ,
sprayed
Drug :
• Tetracaine (2%)
• Lidocaine(2-5%)
• Eutectic mixture: lidocaine
• Benzocaine(5%)
Uses:
• endoscopic procedures
• hemorroids/ anal sphincter.
On eyes:
 For tonometry,
 surgery
 To remove foreign bodies from corneal & conjunctiva
 For preoperative preparation.
Adavantage- Easy to do
Disadvantage- Systemic
toxicity.
Surface
anaesthesia

• Aims: to block sensory
nerve terminals.
• Onset of action: immediate
Uses:
 minor surgical procedures ( incision
& excision)
 Hydrocele
 Hernia
• Advantages - simple, faster, low cost,
very useful for small surgical
procedures.
• Disadvantages -limited efficacy, short
duration of action, potential for
adverse local toxic effects.
Drugs :
• Lidocaine (1%),
• Bupivacaine(0.25%),
• Ropivacaine(0.2%)
• Prilocaine(1%)
Infiltration anaesthesia

Field block
• Injected s.c
• All other nerve coming to a particular
field are blocked
Uses:
• Applied to scalp & anterior abdominal
wall where nerve travel superficially to
supply the area.
Nerve block
• Injected around appropriate nerve
trunks or plexuses.
• Muscle supplied by injected nerve/
plexus are paralysed.
 Lingual,Intercostal,Ulnar ,Sciatic
Drugs :
Lidocaine,(1%)
Bupivacaine(0.25),
Levobupivacaine(0.25%)
Prilocaine(1%)
Advantage: small dose of
drug provided for larger
area
Disadvantage: Technical
complexicity, Neuropathy
Conduction block anaesthesia

Central nerve block anaesthesia
Spinal block anaesthesia
• Injected LA in the spinal
subarachnoid space between L2
and L3, or L3 and L4
Drug used: Bupivacaine(0.5%),
Levobupivacaine(0.5%)
Uses:
• Surgical procedure on Lower
limb, pelvis, Lower Abdomen,
obstetrics & C-section
procedures.
Advantages
Safe, affords good analgesia , muscle
relaxation & no loss of consciousness
Preferred to be used in cardiac,
pulmonary & renal disease
Disadvantage:
A/E- Headache

Spinal Anaesthesia
Advantages of Spinal/Epidural Anesthesia
•Avoids Hazards of General Anesthesia
•Patient is Alert earlier postoperative
•Lower incidence of Nausea/Vomiting
•Better Pain Control/Less Narcotics

Intravenous regional anaesthesia
• Also reffered to Bier’s block
• Useful for rapid
anaesthetization of an
extremety.
• Uses: For the upper limb and
for orthopaedic procedures
Procedure :
1. The limb first is elevated
to ensure venous drainage
and then tightly wrapped
by an elastic bandage for
maximal exsanguination.
2. Tourniquet then applied
proximally and inflated
just above systolic BP.
3. Then elastic bandage
removed, lidocaine is
injected IV.
• Normally the cuff is
inflated for at least 20min
to minimise systemic
toxicity.
Drug:
Lidocaine (0.5%)
Prilocaine(0.5%)

NewerDrug delivery system
Transcutaneous Electrical Nerve Stimulation (TENS)
Indication
• Patient having needle phobia,Ineffective LA
• TMJ(chronic pain),Nonsurgical periodontal pain, Restorative dentistry
• Fixed prosthodontic procedure

DENTIPATCH
• A patch that contains 10-20% lidocaine is placed on the dried
mucosa for 15 minutes.
• Topical anaesthesia for both maxilla and mandible.

JET INJECTION
• It is based on the principle of using a mechanical energy source
to create a release of pressure sufficient to push a dose of liquid
medication through a very small orifice
• This technique is particularly effective for palatal injections
• Drug: Lignocaine(2%)
Peedikayil FC, Vijayan A. An update on local anesthesia for pediatric dental patients. Anesthesia, essays and researches. 2013 Jan;7(1):4

Local Anaesthetics
IONTOPHORESIS
• Non-invasive transdermal drug delivery
• This technique is a suitable alternative for application of drug in
achieving surface anaesthesia.
• Xylocaine(2% lidocaine) has a positive charge, so connect the anode
(red clamp) to the drug delivery electrode
Comeau M, Brummett R, Vernon J. Local anesthesia of the ear by iontophoresis. Archives of Otolaryngology. 1973 Aug 1;98(2):114-20.

Local Anaesthetics
VIBRAJET
• It is a small battery-operated attachment that snaps on to the
standard dental syringe.
• It delivers a high-frequency vibration to the needle.
• Uses vibrations to block pain sensation during local anaesthetic
injections(2% Lignocaine)
• It also lights the injection area and has an attachment to retract the
lip or cheek.

Local Anaesthetics
Conclusion
• LA never intentionally injected into nerve: painful
and cause nerve damage
• LA agent is deposited as close to nerve as possible.
• Careful attention to detail and a thorough
understanding of the limitations and potential
complications of the technique are essential to
achieve the optimal outcome.

References
• R J Litz et.al.,Successful resuscitation of a patient with
Ropivacaine-induced asystole after axillary plexus block
using lipid infusion Anaesthesia, 2006, 61, pages 800–
801
• Acute management of anaphylaxis ASCIA guidelines
• National Essential Anaesthesia Drug List (NEADL) 2015
•Tripati K.D “Essentials of medical Pharmacology” ,7 th
edition.
•Guidelines for the Provision of Anaesthesia Services
(GPAS)
• K eith J .Anesthesia Emergencies .Oxford University
press.
•Wolters K. “The Washington Manual of medical
Therapeutics”.32nd edition:p-241
• P.E. Marik, Handbook of Evidence-Based Critical Care,
• Miller’s Anaesthesia, 7th Edition, Vol 1:pP1378 -80

References
• Leone et al., Pharmacology,toxicology,and
clinical use of new long acting local
anaesthetics,ropivacaine and levobupivacaine.
ACTA BIOMED 2008; 79: 92-105
• Newer Local Anaesthetic Drugs and Delivery
Systems in Dentistry – An Update .2012:1; 10-16
• Peedikayil FC, Vijayan A. An update on local
anesthesia for pediatric dental patients.
Anesthesia, essays and researches. 2013
Jan;7(1):4
• Comeau M, Brummett R, Vernon J. Local
anesthesia of the ear by iontophoresis. Archives
of Otolaryngology. 1973 Aug 1;98(2):114-20.

Local anaesthetics

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