Anda di halaman 1dari 40

Workshop Anestesia Regional

CPD
PP. PERDATIN

OBAT ANESTETIK LOKAL

1
1

tujuan
Memahami struktur kimia dasar
anestetik lokal
Memahami mekanisme kerja anestetik
lokal
Memahami pengaruh sifat kimia
anestetik lokal dan aplikasi klinisnya
Memahami toksisitas anestetik lokal
dan cara mengatasinya
2
2

Perkembangan
anestetik lokal

3
3

dimana
obat
anestetik
lokal
bekerja ??

4
4

Klasifikasi saraf tepi

5
5

OBAT ANESTETIK LOKAL


Obat-obat yg scr reversibel menghambat
konduksi impuls saraf, baik di saraf pusat
maupun saraf perifer
Efek yg dihasilkan berkaitan dgn konsentrasi
obat pada tempat kerja/lokasi saraf yg
diblokade
Autonom sensorik motorik
rendah

(konsentrasi obat)

tinggi
6
6

STRUKTUR KIMIA

7
7

STRUKTUR KIMIA
(Gugus lipofilik)

(Gugus hidrofilik)

(amida)

(ester)
8
8

ester

STRUKTUR
KIMIA
amida

9
9

MEKANISME KERJA

Berikatan dgn kanal Na


Shg kanal Na tdk bs diaktifkan lagi
Permeabilitas Na menurun
Tdk terjadi influks Na jika ada stimulus
Potensial ambang (threshold potential)
tdk akan tercapai
Tdk terjadi depolarisasi
10
10

PHYSIOLOGY
RESTING POTENTIAL

11

11

FISIOLOGI PENJALARAN
IMPULS SARAF

12
12

MEKANISME KERJA
ANESTETIK LOKAL

13
13

MEKANISME KERJA
ANESTETIK LOKAL

14
14

MEKANISME KERJA
ANESTETIK LOKAL

15
15

SIFAT KIMIA & APLIKASI


KLINIS
Lipid solubility = banyaknya atom
karbon potensi
Protein binding lama kerja/durasi
pKa mendekati pH fisiologik onset
pH = fraksi tdk terionisasi onset

16
16

METABOLISME
Gol.Ester:
Pseudocholinesterase (plasma
cholinesterase)
Metabolit: PABA reaksi alergi

17
17

METABOLISME
Gol.Amida:
hepar: enzim mikrosom dealkilasi
hidrolisis
metabolit dari Prilocaine & Benzocaine
methemoglobin

18
18

KECEPATAN ABSORPSI
trgantung lokasi blok regional & ajuvan
Lokasi blok :
cepat

a b s o r p s i

Intravena
Trakheal
Interkostal
Kaudal
Paraservikal/paravertebral
Epidural
Pleksus Brakhial
Sciatic/femoral
Subkutan

lambat
19
19

PENYEBARAN OBAT &


BLOKADE

Saraf bermielin lebih cepat mengalami


blokade dibandingkan yg tdk bermielin
dgn ukuran yg sama
onset

B
C , A
A
A
A
recovery

20
20

onset

PENYEBARAN OBAT &


BLOKADE
Blok simpatis
(vasodilatasi perifer & suhu kulit meningkat)

Blok nyeri & Sensasi suhu


Blok proprioseptif
Blok sensasi raba dan penekanan
Blok motorik
recovery
21
21

PENYEBARAN OBAT &


BLOKADE
Obat AL menyebar dari
sekeliling jaras saraf,
difusi ke dalam jaras
saraf sesuai gradien
konsentrasi, dari jaras
saraf terluar sp ke
paling dalam

22
22

TOKSISITAS
Lokal
TNS
Cauda equina syndrome

Sistemik
Kardiovaskular
Respirasi
Susunan saraf pusat,dll

Efek lain-lain:
Alergi s.d anafilaktik
Hematologi (methemoglobin), dll
23
23

TOKSISITAS
Toksisitas sistemik terjadi jika kadar
puncak obat AL dalam darah mencapai
konsentrasi yang cukup untuk
menghambat konduksi impuls pada
organ-organ tertentu shg terjadi
gangguan fungsi organ

24
24

TOKSISITAS
Faktor yg mempengaruhi:
1. Injeksi AL intravena
2. Dosis obat
3. Kecepatan absorpsi (lokasi, ajuvan
vasokonstriktor)
4. Biotransformasi & eliminasi
5. Usia, berat badan, status sehat
6. Kehamilan

25
25

TOKSISITAS

26
26

TANDA & GEJALA


TOKSISITAS
Susunan Saraf Pusat
Ringan s.d sedang: light-headedness,
dizziness, tinnitus, circumoral numbness,
abnormal taste, confusion and drowsiness
Berat : kejang tonik-klonik s.d hilang
kesadaran scr cepat, koma, depresi nafas
s.d henti nafas

27
27

TANDA & GEJALA


TOKSISITAS
Kardiovaskular
Ringan s.d sedang:
takikardia & hipertensi (AL plus adrenalin),
bradikardia & hipotension (AL minus adrenalin)

Berat : henti jantung


biasanya diperlukan 4-7x dosis yg
mengakibatkan kejang
Henti jantung krn efek depresi langsung pd
miokardium
28
28

TANDA & GEJALA


TOKSISITAS
Aritmia:
prolonged PR, QRS, and QT intervals
potentiating reentrant tachycardias with
aberrant conduction
cardiac resuscitation of such patients may
be difficult and prolonged (30-45 min)

29
29

BERAPA DOSIS MAKSIMUM?

30
30

TOKSISITAS
Penatalaksanaan
ABC resusitasi
atasi kejang (midazolam, pentotal,
propofol)
Resusitasi cairan
Vasopressor & inotropik
Anti aritmia
Lipid emulsion
31
31

BUPIVACAINE-ASSOCIATED CARDIAC ARREST


Bolus 1 ml/kg/min lipid emulsion 20%
Starting infusion of 0,25 ml/kg/min
Repeated bolus every 5 minutes, 2-3 times if
needed
Weinberg G, et al
-Reg. Anesth. Pain med.2003;28:198-202
-Reg. Anesth. Pain med.2004;29:74-5

32

GUIDELINES FOR THE MANAGEMENT OF SEVERE


LOCAL ANAESTHETIC TOXICITY
The Associa<on of Anaesthe<sts of Great Britain & Ireland 2007

Sign of severe toxicity


Sudden loss of consciousness, with of without
tonic-clonic convulsions
Cardiovascular collapse : sinus bradycardia,
conduc<on blocks, asystole and ventricular
tachyarrytmias may all occur
Local anaesthe<c (LA) toxicity may occur some
<me aCer the ini<al injec<on
33

GUIDELINES FOR THE MANAGEMENT OF


SEVERE LOCAL ANAESTHETIC TOXICITY
The Associa<on of Anaesthe<sts of Great Britain & Ireland
2007

34

GUIDELINES FOR THE MANAGEMENT OF SEVERE


LOCAL ANAESTHETIC TOXICITY
The Associa<on of Anaesthe<sts of Great Britain & Ireland 2007

Immediate management :
Stop injec<ng the LA

Call for help

Maintain the airway and, if necessary, secure it with a


tracheal tube
Give 100% oxygen and ensure adequate lung ven<la<on
(hyperven<la<on may help by increasing pH in the presence
of metabolic acidosis)
Conrm or establish intravenous access
Controle seizures : give a benzodiazepine, thiopental or
propofol in small incremental doses
Assess cardiovascular status throughout
35

GUIDELINES FOR THE MANAGEMENT OF SEVERE


LOCAL ANAESTHETIC TOXICITY
The Associa<on of Anaesthe<sts of Great Britain & Ireland 2007

Management of cardiac arrest associated with LA


injec<on:
Start cardiopulmonary resuscita<on (CPR) using
standard protocols
Manage arrhythmias using the same protocols,
recognising that they may be very refractory to
treatment
Prolonged resuscita<on may be necessary; it may be
appropriate to consider other op<ons :
Consider the use of cardiopulmonary by pass if available
Consider treatment with lipid emulsion
36

GUIDELINES FOR THE MANAGEMENT OF SEVERE


LOCAL ANAESTHETIC TOXICITY
The Associa<on of Anaesthe<sts of Great Britain & Ireland 2007

Treatment of cardiac arrest with lipid emulsion :


(approximate doses are given in red for a 70-kg pa<ent)

Give an IV bolus injec<on of IntralipidR 20% 1.5 ml/kg


over 1 min
Give a bolus of 100 ml

Con<nue CPR
Start an intravenous infusion of IntralipidR 20% at 0.25
ml/kg/min
Give at a rate of 400 ml over 20 min

Con$nue........
37

GUIDELINES FOR THE MANAGEMENT OF SEVERE


LOCAL ANAESTHETIC TOXICITY
The Associa<on of Anaesthe<sts of Great Britain & Ireland 2007

Con$nue......
Treatment of cardiac arrest with lipid emulsion :

(approximate doses are given in red for a 70-kg pa<ent)


Repeat the bolus injec<on twice at 5 min intervals if an
adequate circula<on has not been restored
Give two further boluses of 100 ml at 5 min intervals

ACer another 5 min, increase the rate to 0.5 ml/kg/min if an


adequate circula<on has not been restored
Give at a rate of 400 ml over 10 min

Con<nue infusion un<l a stable and adequate circula<on


has been restored
38

GUIDELINES FOR THE MANAGEMENT OF SEVERE


LOCAL ANAESTHETIC TOXICITY
The Associa<on of Anaesthe<sts of Great Britain & Ireland 2007

Remember :
Con<nue CPR throughout treatment with lipid
emulsion
Recovery from LA-induced cardiac arrest may take
> 1 h
Propofol is not a suitable subs$tute for IntralipidR
Replace your supply of Intralipid 20% aCer use

39

TERIMA KASIH

40
40