R EG IO N A L

A N ES TH ES IA
Iswandi Darwis, MD
FACULTY OF MEDICINE
LAMPUNG UNIVERSITY

ANESTHETIC DRUGS
DRUGS THAT CAUSED
ANESTESIA

NO PAIN
SENSATION
1. GENERAL ANESTHETICS
2. LOCAL ANESTHETICS

A N ES TH ETIC S
ESSENTIAL TO SURGICAL PRACTICE
- Analgesic
- Amnesic
- Unconsciouc
- Muscle Relaxation
- Suppresion Reflexes
HISTORY
THEORY

AD JU N CTS TO AN ESTH ETICS

PREANESTHETICS MEDICATION
-

ANTICHOLINERGICS
ANTIEMETICS
ANTIHISTAMINES
BARBITURATES
BENZODIAZEPINES
OPIOIDS

MUSCLE RELAXANTS
- ATRACURIUM
- SUCCINYL KHOLINE
- VECURONIUM

Anesthesia
General

Local

I.V
I.M
Inhalation

Topical
Infiltration
Field Block
Nerve Block
Spinal
Epidural
Intra Venous

COMBINATION

GENERAL ANESTHESIA :
Impulse still reach to CNS

Cortisol
Catecholamine
Tachycardia
Blood sugar

REGIONAL ANESTHESIA :
Impulse less/not reach to CNS
Segmental blockade T5 L1
Block sympathetic system
Cortisol N / less
Catecholamine N / less

General sensory
Anesthesiacortex
All sensation loss cerebral
Unconscious
Subarachnoid
Local/Regional
Anesthesia
Partial sensation loss
Conscious
Nerve Ending
Epidural

Medulla Spinalis

ADVANTAGES :
Simple, Cheap
Non explosive
No pollution
Post op care relative easy
Conscious aspiration risk (-)
Blood loss
Autonomic & endocrine response

DISADVANTAGES :
Patient prefer unconscious
Not practical if several injection are

needed
Fear that the effect of drug vanished
the surgery not finished
Side effect so severe death

G EN ERAL AN ESTH ETICS

INHALED
-

ENFLURANE
HALOTHANE
ISOFLURANE
METHOXYFLURANE
N2O
SEFOFLURANE

INTRAVENOUS
METHOHEXITAL
THIAMYLAL
THIOPENTAL

BARBITURATES

DIAZEPAM
LOKAZEPAM
MIDAZOLAM

BENZODIAZEPIN

FENTANYL
MORPHINE

OPIOIDS

DROPERIPIL + FENTANYL
NEUROLEPTIC

ETOMIDATE
KETAMINE
PROPOFOL

LocalAnesthetic 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

Max:Single
dose

Potency

Cocaine

4-10% Topical

Slow 30

150 Mg

Procaine

Infiltration 1%
Epidural 2%
Plexus block 2%
Spinal 10%

Slow
30-45

500 Mg EPI
600 Mg + EPI
1012 Mg/Kg

Low

Chloro
procaine

Infiltration 1%
Epidural 2%
Plexus block 2%

Rapid
45-60

600 Mg EPI Interme

diate
650 Mg + EPI
10-15 Mg/Kg

Tetracaine

Topical 0,5-1%
Infiltr 0,1-0,2%
Epidrl 0,4-0,5%
Spinal 1%

Slow
180-300

100 Mg
2 Mg/Kg

High

Agent

Concent: Clinical
use

Onset &
Duration

Max:Single
dose

Potency

Xylocaine

Infiltr 0,5-1%
Epidural 1-2%
N.block 1-1,5%
Topical 4%
Spinal 5%

Rapid
60-120

300 Mg EPI Interme

diate
500 Mg + EPI
7-8 Mg/Kg

Prilocaine

sda

Slow
60-120

175 Mg EPI Interme

diate
250 Mg + EPI
3-4 Mg/Kg

Bupivacaine

Infilt 0,25-0,5%
N.blok 0,5-0,75%
Spinal 0,5%

Slow
>180>300

175 Mg EPI
250 Mg + EPI
3 4 Mg/Kg

High

Etidocaine

Infiltr 0,5%
N.blok 0,5-1%
Epidrl 1-1,5%

Rapid
>180 >300

300 Mg EPI
400 Mg + EPI
4-5 Mg/Kg

High

Metabolism

Allergy

ESTER.C

Hydrolyzed in Plasma
(Ps.Choline)

(+)
PABA

AMIDE.C

Degradation in the Liver

(-)

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

ID EALLY LO CAL AN ASTETIC

D RU G S
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 duration of action
Degree of vascular absorption is related

to blood flow through the area

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 (0,2 1,5% )

1. Systemic toxicity

Excitation
CNS
Depression
Hypotension
CVS
CV collaps

 Local irritation

Neural damage

Chloroprocaine

Miscellanous
Allergy
Ester compound
Met.Hb.emia
Prilocaine
Addiction
Cocaine

System ic 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

System ic toxicity
CNS is more susceptible than CVS
Adverse effect involving CVS tend to

be more serious and more difficult to

manage

CN S 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

: 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
- increase dose

vasoconstriction
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

Respect Others,
then They will
Respect You More

HANUPIS