REGIONAL ANESTHESIA

FACULTY OF MEDICINE LAMPUNG UNIVERSITY

ANESTHETIC DRUGS

DRUGS THAT CAUSED ANESTESIA

NO PAIN
SENSATION

1. GENERAL ANESTHETICS
2. LOCAL ANESTHETICS
General sensory
Anesthesia cortex
• All sensation loss cerebral
• Unconscious

Subarachnoid
Local/Regional
Anesthesia
• Partial sensation loss
• Conscious
Nerve Ending
Epidural Medulla Spinalis
Local Anesthetics
 LA all include a lipophilic group joined by an
amide or ester linkage to a carbon chain,
which, in turn, is joined to a hydrophilic
group.
 AKA Regional anesthetics
 Block nerve conduction in specific area of body
 Prevents pain sensation
 2 Forms
 Topical
 Parenteral (injected)
 Local Anaesthesia

Topical Parenteral
Cream Infiltration
Lotion Epidural
Patch Spinal
Spray Nerve Block
Plexus Block
IV
MOA Local Anesthesi
Mechanism of Action LOCAL ANESTHESIA :

 MOA : block Na+ ion channels  prevent increase in

permeability of the nerve membrane to Na+  inhibit
action potential  block nerve conduction of sensory
impulses  sensation can’t be transmitted from the
source of stimulation to the brain
 In higher concentrations  block motor impulses from
the periphery to the CNS.
 Small, unmyelinated nerve fibers for pain,
temperature, and autonomic activity are most
sensitive.
 ADVANTAGES :

 Simple, Cheap
 No pollution
 Post op care relative easy
 Conscious  aspiration risk (-)
 maintain his own airway
 Blood loss 
 Autonomic & endocrine response 
 DISADVANTAGES :
 Patient prefer unconscious
 Not practical if several injection are needed
 some blocks require up to 30 minutes or more to
be fully effective
 Fear that the effect of drug vanished the surgery
not finished
 toxicity may occur if the LA is given IV or if an
overdose is injected
 Side effect so severe  death
Local Anesthetic Agent
1. Ester Compound
 Cocaine
 Procaine / Novocaine
 Tetracaine / Pontocaine
2. Amide Compound
 Xylocaine / Lidocaine
 Prilocaine / Citanest
 Bupivacaine / Marcaine
 Etidocaine / Duranest
 Ropivacaine
 Levo Bupivacaine
 Agent Concent: Clinical use Onset & Duration Potency

Cocaine 4-10% Topical •Rapid OOA -

•DOA : 30’ (short)

Procaine Infiltration 0,25-1% • OOA : 2’-5’ Low

Epidural 2% • DOA : 15’-60’
Plexus block 2% (short)
Spinal 10%
Chloro Infiltration 1% •OOA : 6’ Low-
procaine Epidural 2% • DOA : 30’ Intermediate
Plexus block 2%

Tetracaine Topical 0,5-1% •OOA : 15’ High

Infiltr 0,1-0,2% • DOA : 2h-3h
Epidrl 0,4-0,5%
Spinal 1%
 Agent Concent: Clinical use Onset & Duration Potency

Lidocaine Infiltr 0,5-2% •OOA : <2’ Low-

Epidural 1-2% • DOA : 60’-120’ Intermediate
N.block 1-1,5% (Intermediate)
Topical 4%
Spinal 0,2- 5%
Prilocaine sda •OOA : <2’ Intermediate
• DOA : ≥1h
Bupivacaine Infilt 0,25-0,5% •OOA : >5’ High
N.blok 0,375-0,75% • DOA : 2h-4h
Spinal 0,5-0,75%
Epidural 0,5-0,75%
Etidocaine Infiltr 0,5% •OOA : 3’-5’ High
N.blok 0,5-1% • DOA : 5h – 10h
Epidrl 1-1,5%
 Anesthetic Profile of Local Anesthetic is
depend on :
 Lipid solubility  intrinsic potency
 The Higher lipid sol  Higher potency
 Procaine L.S. = 1
 Bupivacaine L.S. = 30
 Etidocaine L.S. = 140
 90 % Axolemma consist of lipid
 Protein binding
 Higher Protein binding  Longer duration
 Procaine P.B. = 5
 Bupivacaine P.B. = 95
 10 % axolemma consist of protein
 p Ka
P Ka as pH at which its ionized and non ionized are
in complete equilibrium
L.A. with pKa closer to tissue pH  more rapid
onset
 p Ka lidocaine = 7,7
 Bupivacaine = 8,3
IDEALLY LOCAL ANASTETIC DRUGS

1. No iritating tissues
2. No damaging nervous tissues
permanently
3. Margin of safety  Wide
4. Onset of action  short and Duration of
action  long
5. Soluble in water – stable as solute – can
be sterilized without change
 Intrinsic vasodilator activity

 Influence potency and DOA

 Vasodilator  leading to rapid diffusion from the
site of action and shorter duration when drugs
are administered alone.
 By adding epinephrine, rate of LA absorption and
diffusion ↓  ↓ systemic toxicity and ↑ DOA.
 All local anesthetic  vasodilation except
Cocaine
 Base upon potency and
duration of action

1. Low Potency & short duration o.a.

 Procaine
 chloroprocaine
2. Intermediate potency & duration o.a.
 Lidocaine
 Mepivacaine
 Prilocaine
3. High potency & long duration o.a.
 Bupivacaine
 Tetracaine
 Etidocaine
Toxicity of local anesthetic

 Systemic toxicity
Excitation
CNS
Depression
Hypotension
CVS
CV collaps
 Local irritation
Neural damage Chloroprocaine

Miscellanous
Allergy Ester compound
Met.Hb.emia Prilocaine
Addiction Cocaine
↑Neonatus toxicity mepivacaine
 Systemic toxicity

L.A. agent are relatively free of side effect, if :

1. In appropriate dosage  toxic excessive dose
2. In appropriate anatomical location  toxic
reaction  following :
- accidental i.v. injection
- subarachnoid inj. of large dose
 Systemic toxicity

 CNS is more susceptible than CVS

 Adverse effect involving CVS tend to be more

serious and more difficult to manage
 CNS toxicity

CNS is more susceptible to the systemic actions of

L.A. than CVS

 Tinnitus
 Light headedness
 Confusion
 Circumoral numbness
 Drowsiness  unconscious
 Twitching & tremors muscles of face & distal
extremities  convulsion
 Respiratory arrest
 Bupivacaine : Etidocaine : Lidocaine =
4 : 2 : 1

 Convulsive threshold is inversely related to the

PaCO2 level.

PaCO2  convulsive threshold

pH  convulsive threshold
 CVS toxicity
 Cardiac :
 Negative inotropic action
more potent  more depress contractility  more
difficult to resuscitate
 Ventricular fibrillation  bupivacaine

 Vascular : biphasic action

 Lower dose  vasoconstriction
 Increase dose  vasodilatation

No correlation between L.A. potency and vascular smooth

muscle effect
 Hypotension initially as a result of
decrease in SV  CO

Later on vasodilatation  CV collaps