Local Anaesthesia

LOCAL
ANAESTHETIC
DRUGS
NUR MEALIELLA OMAR,
OUTLIN
definition
ES
structural of LA
mechanism of action
types of LA
properties of LA
LA toxicity
Local anaesthesia produce a
transient and reversible loss of sensation
(analgesia) in a circumscribed region of
the body without loss of consciousness.
HISTORY
cocaine isolated 1860.
topical anaesthesia produced by Koller:
1884.
spinal anaesthesia by Corning: 1885; Bier:

1898.
procaine 1905

IV LA 1908
epidural anaesthesia 1921
lignocaine 1948
amino amides 1963

PROPERTIES
OF LA
Nonirritating to the tissues
Should not cause any permanent damage

to nerves
No systemic toxicity
Rapid onset of action
Duration of action should be sufficient to

allow contemplated surgical procedures,
however not so long as to require an
extended period of recovery
pKa
the pH at which the ratio of ionized to
non-ionized molecules is 1:1
ambient pH < ambient pH>
pKa pKa
more ionized more

weak base
(lipid insoluble) unionized
The higher the pKa, the slower the onset.
The higher the protein binding, the longer the duration.
The higher the lipid solubility, the more potent the drug is hence it has longer
duration of action and intense motor blockade.

***fibre size and fibre type are determinants of sensitivity to local anaesthetics (Nathan & Sears, 1961)

A drug that induces local anesthesia
by reversibly prevent both the
generation and conduction of nerve
action potential by blocking the
Na+ channel.
ESTHER AMIDE
PROCAINE BUPIVACAINE
COCAINE LEVOBUPIVACAINE
TETRACAINE LIGNOCAINE
CHLOROPROCAINE MEPIVACAINE
PRILOCAINE
of the following local
anesthetics , which is not an
ester ?
procaine
lidocaine
tetracaine
cocaine
all of the above
COCAINE PROCAINE
derived from leaves Erythroxylon coca
used for topical anesthesia and local
vasoconstriction eg Moffetts solution.
Usage in anesthesia mainly during
fibreoptic intubation via nasal route. short duration
cocaine blocks conduction when applied metabolism produces PABA, may cause
directly to nerve tissue & may therefore allergy reaction
be used in surface anaesthesia
may prolonged effect of succinylcholine
stimulates CNS + sympathetic nervous degradation reduced by atypical
system butrylcholinesterase
small dose: bradycardia
higher dose: convulsion, coma
larger dose: tachycardia, hypertension,
myocardial depression, death
LIGNOCAINE BUPIVACAINE
used as local anesthetic agent, anti-arrythmic racemixture containing 50% mixture of dextro
and levo isomers; levo-bupivacaine (chirocaine)
(Class Ib) solution.
solution (0.5-2 %), gel (2%), ointment (5%), or clear, colourless solution prepared as a 0.25 and
spray (10%). Can be combined with adrenaline 0.5% (with or without epinephrine 1:200,000).
(1in 80,000 - 200,000) for its vasoconstrictive and mixed with glucose (80mg/ml) aka heavy
properties bupivacaine.
fast in, fast out fast in, slow out, moderate tissue penetration
LEVOBUPIVACAINE ROPIVACAINE
S(-) isomer of bupivacaine. S(-) isomer of bupivacaine.
It is prepared as a sterile, colourless

solution, CONCENTRATION 2.5 three concentrations (2, 7.5 and 10
mg/ml, 5.0 mg/ml and 7.5 mg/mL of mg/ml
levobupivacaine.
HARMACOKINETIC PHYSIOCHEMICAL PROPERTIES
DOSAGE
ADSORPTION SITE OF INJECTION
+VASOCONSTRICTOR
PHYSIOCHEMICAL PROPERTIES
DISTRIBUTION REGIONAL BLOOD FLOW
ESTHERS: PLASMA pseudoCHOLINESTERASE, LIVER

ESTERASES
METABOLISM AMIDES: HEPATIC ENDOPLASMIC RETICULUM
EXCRETION RENAL
The higher the pKa, the slower the onset.
The higher the protein binding, the longer the duration.
The higher the lipid solubility, the more potent the drug is hence it has longer duration of action
and intense motor blockade.
Cocaine Lignocaine Bupivacaine Levobupivacaine Ropivacaine
pKa 8.7 7.9 8.1 8.1 8.1
Lipid solubility - 3 20 20 6
Plasma protein 98 64 96 96 94
binding (%)
Relative - 2 8 8 8
potency
Duration (hr) 0.5 - 2 2 3 3 3
Max dose 2 3-4 (over 3 hr) 2 (over 4 hr) 2 (over 4 hr) 3

(mg/kg) 7 (with
adrenaline)
the adjustment of lidocaine dose is
necessary in the patient with which
one of the following
hepatic insufficiency
renal insufficiency
patient with CHF
respiratory insufficiency
patient on propanolol
Regional anesthesia that is associated with the
greatest degree of systemic vascular absorption of
LA agents :
Intercostal nerve block > caudal > epidural >
brachial plexus > sciatic-femoral > subcutaneous :-
related to the degree of local vascular supply.
CONTRAINDICATION OF LA
allergy / hypersensitivity to local anaesthetics
allergy / hypersensitivity to solution additives
adrenaline is contraindicated for,

i. conditions where tachycardia is detrimental (thyrotoxicosis, CCF, IHD)
ii. anaesthesia around end-arteries
patient refusal
LA TOXICITY
TOXICITY
ALLERGIC REACTION
METHAEMOGLOBINAEMI
A
LOCAL TISSUE TOXICITY
SYSTEMIC TOXICITY
Allergies
true allergic reactions to local anesthetics are rare
and usually involve type 1 or Type IV reactions
anaphylaxis to amides is rare

increased allergic reactions to esters most likely
the result of derivatives of PABA
may also be the result of additives methylparaben

and metabisulfite
Methemoglobinemia
prilocaine is metabolized to O-toluidine
result is a hemoglobin that is less able to bind
oxygen
fetal hemoglobin is much more sensitive to the
metabolite
appear cyanotic and cause interference with the
pulse oxymetry
cking transmission in nerve axons, local anaesthetics affect all tissues where conduction
s of muscle fibre, especially cardiac

CNS TOXICITY
1. relatively fatal
2. PaCO2 inversely related to the convulsive threshold

decrease plasma protein binding
3. pH pH convulsive threshold decrease

diffusion into the cell.
cardiovascular
toxicity
decrease in the rate of depolarization in the fast
conduction tissues f the purkinjie fibers and
ventricular muscle
high concentration of dose dependent negative

inotropic action on cardiac muscle
comparative
cardiovascular toxicity
ratio of the dosage of bupivicaine to lidocaine
fatal ventricular arrythmias may occur more often
with bupivicaine than with lidocaine
pregnant patients may be more sensitive to

cardiotoxic effects of bupivicaine
acidosis and hypoxia enhance the cardiotoxic

effects
INTRALIPID
MOA:
lipid sink theory
metabolic theory
RISK: anaphylaxis
WHY INTRALIPIDS: 100%
longchain fatty acids

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LOCAL

spinal anaesthesia by Corning: 1885; Bier:

epidural anaesthesia 1921

amino amides 1963

Should not cause any permanent damage

Rapid onset of action

Duration of action should be sufficient to

more ionized more

The higher the pKa, the slower the onset.

The higher the protein binding, the longer the duration.

duration of action and intense motor blockade.

S(-) isomer of bupivacaine. S(-) isomer of bupivacaine.

It is prepared as a sterile, colourless

ESTHERS: PLASMA pseudoCHOLINESTERASE, LIVER

pKa 8.7 7.9 8.1 8.1 8.1

Max dose 2 3-4 (over 3 hr) 2 (over 4 hr) 2 (over 4 hr) 3

allergy / hypersensitivity to local anaesthetics

allergy / hypersensitivity to solution additives

adrenaline is contraindicated for,

ii. anaesthesia around end-arteries

anaphylaxis to amides is rare

may also be the result of additives methylparaben

s of muscle fibre, especially cardiac

2. PaCO2 inversely related to the convulsive threshold

3. pH pH convulsive threshold decrease

high concentration of dose dependent negative

pregnant patients may be more sensitive to

acidosis and hypoxia enhance the cardiotoxic

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