Clinical application of local anesthetics

1. Neural blockade at terminal nerve endings and

receptors (surface and infiltration anesthesia)
2. Peripheral Nervous system (Nerve and plexus blocks)
. CN! (!pinal and epidural anesthesia)
!urface anesthetics
". Cyclomethycaine
#. #en$ocaine (ethylaminoben$oate)
C. #utamben (butylaminoben$oate)
%. Cocaine
&. 'idocaine ((ylocaine)
). *etracaine (Pontocaine)
+nfiltration , field block
". 'idocaine
#. -epivacaine
C. #upivacaine
%. &tidocaine
&. Chlorprocaine
Peripheral Nerve block , .egional "nesthesia
". 'idocaine
#. -epivacaine (Carbocaine)
C. #upivacaine
"dverse effects
1. CN!
i. &xcitation (due to blockade of
inhibitory path/ay on cerebral
cortex)
ii. %epression (blocking all neural
conduction)
iii. -uscle t/itching0 tremors0 tonic
clonic sei$ures0 %iplopia0 tinnitus0
dro/siness0 circumoral numbness0
respiratory depression0 apnea
2. C1
i. 2ypotension0 arrythmia0
bradycardia0 sinus arrest
ii. 'ocal anesthetics /ith greater
potency0 lipid solubility and protein
binding are more cardiotoxic
(#upivacaine0 &tidocaine)
. 2ypersensitivity , -ore /ith esters (P"#")
3. Neurotoxicity
i. Neurologic deficit
1. %irect trauma from
in4ection needle
2. +ntraneural in4ection or
neural +schemia produced
by pressure of in4ection
. &xcessive concentration of
local anesthetics or
contamination /ith foreign
thing.
5 !mall non myelinated fibers (nerve) /hich transmit pain and
autonomic impulses are more susceptible
5 +n spinal anesthesia0 the order of blockade /ith the
sympathetic outflo/ ff by6
1. Pain sensation
2. Cold
. 7armth
3. *ouch
8. %eep pressure
9. Proprioception
:. -otor activity .ecovery
%rug 'ipid
solubility
Protein
binding
%uration Potency
Esters
Procaine
*etracaine
'o/
-oderate
9;
:9;
!hort
'ong
1
19
Amides
#upivacaine
&tidocaine
-oderate
2igh
<8;
<3;
'ong
'ong
19
19
Chemistry of procaine
+ntermediate chain , determine the metabolism stability0
allergic potential0 toxicities of local anesthetics
!ubstitution on the aromatic ring of the amino group change
by6
1. 'ipid solubility
2. -olecular binding to protein
-ore lipid soluble , more potent
2ighly protein bound , 'onger duration of action
'o/ p=a > faster onset of effect
-echanism of action
1. +ncrease the threshold for electrical excitation in the
nerve
2. !lo/ propagation of depolari$ation
. .educing the rate of rise of the action potential
3. #locking conduction of cation potential
8. %ecrease Na conductance and blocks depolari$ation
Classification
1. &sters , -etaboli$ed in the plasma? hydroly$ed by
cholinesterase (pseudo) to P"#" (allergenic
response)
a. Cocaine
b. Procaine
c. *etracaine
d. Chlorprocaine
2. "mides , -etaboli$ed in the lover , not associated
(rarely) in allergic reactions
a. 'idocaine
b. -epivacaine
c. #upivacaine
d. &tidocaine
e. Prilocaine
!pinal anesthesia
a. 'idocaine
b. #upivacaine
c. *etracaine
&pidural anesthesia , Caudal anesthesia
a. 'idocaine
b. -epivacaine
c. #upivacaine
d. &tidocaine
e. Chlorprocaine