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INTRODUCTION OF INTRODUCTION OF ANESTHESIA ANESTHESIA Departement of Anestesiology and Reanimation , School of Medicine, S t Ut Ui it Sumatera Utara University

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Page 1: INTRODUCTION OF ANESTHESIA - USU …ocw.usu.ac.id/.../rps138_slide_introduction_of_anesthesia.pdf · INTRODUCTION OF ANESTHESIA Departement of Anestesiology and Reanimation , School

INTRODUCTION OF INTRODUCTION OF ANESTHESIAANESTHESIA

Departement of Anestesiology and Reanimation , School of Medicine,

S t Ut U i it1

Sumatera Utara University

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HistoryHistory fof

Anesthesia

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3Living Made Easy: Prescription for Scolding Wives [1830]

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Hinkley, an American portrait painter who studied at the Paris Ecole des Beaux Arts, in 1882 began his

painting of the ether demonstration as a speculative work and took 11 years to complete it.

4The Hinkley painting today hangs in the

Francis A. Countway Library of Medicine at Harvard Medical School in Boston. .

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Ether Monument, Boston Public GardenPhotographs from the Detroit Publishing Company, 1880-1920

American Memory Collection aLibrary of Congress

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History of Anesthesia History of Anesthesia

A history of anesthesia or "pain killing" techniques A history of anesthesia or pain killing techniques throughout history

Anesthesia, historical background and the word's originPain, however useful as a warning signal designed to keep living

organisms from damaging themselves too badly becomes useless organisms from damaging themselves too badly, becomes useless agony when operations must be performed.

Attempts to control pain were many. The use of alcohol or some f f h t t b ll d h ti ld A t form of what came to be called hypnotism was old. Acupuncture

was used in the Orient. The new chemistry also contributed nitrous oxide, which, when inhaled, served to suppress the

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ppsensation of pain.

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Year 1846

10The Ether Dome, Boston, Massachussets, USA

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1846, Boston MassachussettsThe first clinical useThe first clinical useof ether as anesthetic

W ll TG MWilliam TG Morton

Inventor and revealer of anesthetic inhalationBefore whom in all time surgery was agony

By whom pain in surgery was averted and annuled Since whom science has control of pain

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Since whom science has control of painH. Bigelow

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Dr William Morton a Boston dentist and former partner ofDr. William Morton, a Boston dentist and former partner of Dr. Horace Wells was one of the first to use ether as an

anesthesia. I 1846 j t t ft H W ll ’ th tiIn 1846, just two years after Horace Wells’ anesthetic success with nitrous oxide, Dr. William Morton (1819-68), constructed

the first anesthetic machine. Morton’s simple device was a glass globe housing an ether-

soaked sponge so all the patient had to do was merely to inhale the vapor through one of two outlets.

Morton’s invention was put to the test on October 16, 1846, in the surgical amphitheater of the Massachusetts General Hospital

in Boston when a twenty-year-old man was successfullyin Boston when a twenty year old man was successfully anesthetized so a tumor could be painlessly removed from what one source said was his neck and another indicated was from his

jaw.

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jaw.

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Anesthesiology is a blessed profession

• When God created Eva from Adam’s rib ………. first, He put Adam into a deep sleep…………….

• The beginning of mankind started with anesthesia• The beginning of mankind started with anesthesia

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Ether :- good narcosisgood a cos s- good analgesia- good muscle relaxation

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KemajuanIlmu Bedah

a

nsfu

si

biot

ika

s t e

s i

Tran

Ant

ib

A n

e s

N u t r i s i

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andand .…..TODAY

A h i i h f d l f hAnesthesia is now much safer and more pleasant for the patient than it was 50 years ago. Factors contributing to the improvements include a fuller understanding of physiology andimprovements include a fuller understanding of physiology and pharmacology, better preoperative assessment and preparation of patients …… Improvements in anesthesia have allowed

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surgeons to attempt more complicated operations on increasing number of patients …...... M.Dobson

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EndoscopicEndoscopic surgery

Trauma surgeryg y

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Many techniques originally developed for use during anesthesiaare now widely recognized as applicable to the care of a variety ofcritically ill patients, for example those with severe head injuries, asthma tetanus or neonatal asphyxia Skills such as the rapidasthma, tetanus or neonatal asphyxia. Skills such as the rapid assessment and management of unconscious patients, control ofairway, endotrachel intubation,…. cardioplumonary resuscitation h h i i i i h i

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have their origins in anesthesia, but are now recognized as essential for all doctors.

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Working togetherS & A th i lSurgery & Anesthesiology

|extends the boundaries of life and death

19Massive Crush Injury - Hb 2

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PengembanganIntensive Care / ICUIntensive Care / ICU1975 Anestesiologi RSCM1977 Anestesiologi RSDS

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Prolonged Life SupportProlonged Life Supportdi ICU

|adalah bagian dari

Resusitasi

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MagillGuedelMacIntoshE t iEpstein

Archie Brain

L M A

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Resusitasi Jantung ParuACLSACLSATLSsemua perlu intubasi trachea

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semua perlu intubasi trachea

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Sekolahnya 4 tahun, 120 SKS + MKDU

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Anestesia

• Keadaan yang ditandai hilangnya kesadaran dan / atau persepsi nyeri (bersama atau terpisah)p p y ( p )

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Anestesia

• Keadaan yang ditandai hilangnya kesadaran dan / atau persepsi nyeri (bersama atau terpisah)

• Dapat dilakukan secara temporer dengan– obat anestesia umum– obat anestesia lokal / regional– akupunkturakupunktur– hipnosis– stimulasi listrik

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stimulasi listrik

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Kapan anestesia diperlukan?

• Menghilangkan nyeri pembedahan & trauma• Menghilangkan nyeri akut lain:

– proses persalinan– proses diagnostik medik tertentu

• Menghilangkan nyeri kanker• Menghilangkan nyeri khronis (ischemia dll)g g y ( )• Menghilangkan rasa cemas pada anak

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Apakah anestesia berbahaya?

• Ya– menyebabkan depresi nafas, jantung, sirkulasi,menyebabkan depresi nafas, jantung, sirkulasi,

fungsi otak, hati, usus, ginjal dan sistim imun• TidakTidak

– jika semua perubahan diawasi dan dikendalikan maka bahaya dapat di-minimal-kana a ba aya dapat d a a

• Dengan anestesia yang baik risiko mati adalah 1: 10 000

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adalah 1: 10,000

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Throughout America there are thousands ofThroughout America there are thousands of doctors—working in hospitals, clinics and private offices—who hurt and even fatally injure patients y j pthrough incompetence or carelessness yet remain

in active practice.

In Denver, Richard Corbett Leonard, 8, died during a routine ear operation because the

anesthesiologist allegedly fell asleep.

From an article, “Why Some Doctors May Be Hazardous to Your Health”, by Bernard Gavzer in the April 14 1996 issue of Parade Magazine

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Bernard Gavzer, in the April 14, 1996, issue of Parade Magazine

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Mortality associated w/ anesthesia• Lund & Mushin (1982)-6 days 1:10 000Lund & Mushin (1982) 6 days 1:10,000• Forrest (1990)-7 days 1:10,000• Pedersen (1994)-30 days 1: 2,500Pedersen (1994) 30 days 1: 2,500• MHA (Maryland Hosp Assoc 1999)-

National Aggregate Data

– Class I 1:10,000– Class II 3:10,000– Clas III 28:10,000– Class IV 230:10,000

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Anestesiamenghambat hantaran impulse nyeri atau

menghilangkan persepsi nyeri

• Suntikan im atau iv • Anestesia umum

• Inhalasi (dihisap nafas)

• Dengan suntikan syaraf • Anestesia regional / conduction block

• Dengan suntikan di tempat operasi

conduction block

• Anestesia (infiltrasi) lokal

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p p

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Anestesia umum

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Anestesia umumblok otak = syaraf pusat

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Anestesi umumMorfin pada reseptorMorfin pada reseptor

Ketamin pada jalur thalamus-cortex

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Anestesia regionalblok serat syaraf

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OA I h l iKetamine

OA Inhalasi

S i l bl kSpinal block

Plexus & NerveBlock

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Anestesia regionalAnestesia regional

P d j f di l k i• Pada ujung syaraf di lokasi (local infiltration block)

• Pada serabut syaraf• Pada serabut syaraf (nerve block)

• Pada berkas syaraf dekat medula spinalis y p(plexus block)

• Pada medula spinalis ( i/ id l bl k d b h id bl k)(peri/epidural block dan subarachnoid block) = spinal anesthesia

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Nerve block

Pl bl k41

Plexus blockEpidural block Subarachnoid block

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Peridural blockSubarachnoidSubarachnoid

block

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Obat anestesia = obat berbahayadosis kecil = anestesia

dosis besar = fatal

• Pentothal, lidocain, N2O, halothan, sevoflurane, d fl d l d i i i ikdesflurane dalam dosis tinggi semua mematikan– coma yang dalam– tekanan darah turun hebat– henti jantung

• Pavulon, Esmeron, Tracrium, Succinylcholine = obat pelumpuh otot

43

– henti nafas (apnea) perlu nafas buatan

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Pentothal PavulonKCl

Obat anestesia

=

Obat eksekusi mati

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Obat anestesia umum

• Ether • Bau (+) menyengat, terbakar, murah

• Halothane• Enflurane

• Harum, gg liver, aritmia• Harum <, gg ginjal, convulsi

• Isoflurane• Sevoflurane

• Harum <, sadar cepat, mahal• Harum>, sadar cepat, mahal >>Sevoflurane

• Desflurane

, p ,• Harum<<, sadar cepat, mahal >>

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Sistem anestesia

Pvaporizerbreathing tubes

canister sodalime(CO2 absorber)

Flowmeteroksigen

(CO2 absorber)

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Sumber gas O2, N2O Vaporizer etherg ,

Flowmeter pengatur gas

Vaporizer halothane

50Vaporizer enflurane

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otak

Uap obat inhalasi

Alveoliparu

Art.carotis int..p

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Kapiler paruObat intravena

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Mekanisme anestesia umum inhalasiMekanisme anestesia umum inhalasi

• TAHAP INDUKSI & MAINTENANCE• Uap OA kadar tinggi dihisap masuk alveoli paru p gg p p→ kadar OA alveolair tinggi → menembus membran alveoli-kapiler → masuk darah kapiler

k d d l k il i i i k l i l h→ kadar OA dalam kapiler tinggi → sirkulasi oleh jantung kiri ke otak → menembus kapiler di j i t k → k l l t k → k d OAjaringan otak → masuk sel-sel otak → kadar OA dalam sel otak tinggi → pasien menjadi tidak sadar

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sadar

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Mekanisme anestesia umum inhalasiMekanisme anestesia umum inhalasi

• TAHAP RECOVERY• Bila uap OA dihentikan → kadar alveolair• Bila uap OA dihentikan → kadar alveolair

turun → OA dalam darah pindah ke l l i k d OA d l d halveolair → kadar OA dalam darah turun →

OA dalam sel otak pindah ke darah →kadar OA dalam otak turun → pasien sadar kembali

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Mekanisme anestesia umum parenteralMekanisme anestesia umum parenteral

• TAHAP INDUKSI & MAINTENANCE• Injeksi obat masuk vena ke jantung kananInjeksi obat masuk vena ke jantung kanan

lalu ke jantung kiri → sirkulasi oleh jantung kiri ke otak → menembus kapiler dikiri ke otak → menembus kapiler di jaringan otak → masuk sel-sel otak →kadar OA dalam sel otak tinggi → pasienkadar OA dalam sel otak tinggi → pasien menjadi tidak sadar

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Mekanisme anestesia umum parenteralMekanisme anestesia umum parenteral

• TAHAP RECOVERY• Bila suntikan OA dihentikan → redistribusi• Bila suntikan OA dihentikan → redistribusi,

metabolisme dan ekskresi OA → kadar OA intravena turun → OA dalam sel otakintravena turun → OA dalam sel otak pindah ke darah → kadar OA dalam otak

i d k b liturun → pasien sadar kembali

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Urutan proses anestesia umum

• Puasa: mengosongkan lambung

• Premedikasi: memberi sedatif analgesia tenangPremedikasi: memberi sedatif, analgesia tenang

• Induksi: memberi loading dose obat anestesia

M i• Maintenance: memelihara kadar obat anestesia

• Recovery: menunggu siuman kembali

• Post-op care: menunggu normal kembali

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Anestesia menyebabkan depresi fungsi vital• Nafas:

– sumbatan jalan nafas,sumbatan jalan nafas, – mengurangi nafas (hipoventilasi)– henti nafas

• Sirkulasi:– tekanan darah turun– nadi tak teratur– henti jantung

• Kesadaran:– menurun sampai coma

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Perubahan pCO2 akibat anestesia

90

(hipoventilasi)pCO2 arteria

60

70

80Enflurane

Isoflurane

40

50

60Halothane

20

30

40

0

10

58

0 MAC 1.0 MAC 1.5 MAC

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Perubahan cardiac output akibat anestesia

120

(depresi sirkulasi)% awake value

80

100Isoflurane

60

80

EnfluraneHalothane

40

0

20

59

1.0 MAC 1.5 MAC 2.0 MAC

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Perfusi, nadi dan tekanan darah harus di monitor selama anestesia

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Waktu induksi

Jari rabanadi

Mata lihat nafas Waktu maintenancenadiTelinga dengar jantung

Monitoring selama anestesia

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g

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62Edmond I Eger 1985

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Pasien trauma kepala dengan tekanan intra-kranial tinggi||

Perlu obat anestesia yang tidak meningkatkan TIKlebih tinggi lagi

63

gg gselama Dr Bedah Syaraf tidak dapat dekompresi

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Perubahan hormonal akibat anestesiaakibat anestesia

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Perlu monitorResusitator

Perlu monitor- tekanan darah- ECG- suhu- saturasi O2- kedalamanstadium anestesia

Perlu alat untuk bertindakPerlu alat untuk bertindak- resusitator- defibrilator

i65

- respirator

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Perbandingan sifatPerbandingan sifat

ether halothan sevofluran desfluran

Induksi sukar mudah sangatmudah

sukar

Titikdidih

36.2 50.2 58.5 22.8

Bl d/Blood/gaspart.coeff

12.1 2.3 0.68 0.42

T k 460 243 160 66966

Tek.uappada 20C

460 243 160 669

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VOLATILE ANESTHETICSETHER

HALOTHANETHRANEETHRANE

ISOFLURANSEVOFLURAN

67DESFLURAN

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Induksi inhalasi dengan ether perlu waktu 20-30 menit

Induksi dengan sevoflurane sangat cepat (cukup 1 2 nafas saja)68

Induksi dengan sevoflurane sangat cepat (cukup 1-2 nafas saja)

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Induksi inhalasi halothane3-5 menit dan dapat dipercepat

Induksi inhalasi desfluranebisa cepat tetapi > 25% pasienb t k d l →

69

dengan suntikan pentothal iv batuk dan spasme larynx →harus dibantu propofol iv

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Dijaga agarDijaga agarmuntah tidak masuk paru(aspirasi)

MASA RECOVERY

DijDijaga agarwaktu gelisah tidak jatuhNafas dibantu oksigen

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Tekanan darah dipantau

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PengembanganIntensive Care / ICUIntensive Care / ICU1975 Anestesiologi RSCM1977 Anestesiologi RSDS

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Anestesiologi & Reanimasisangat kompleks

||dimana multiple variables bekerja cepat dalam

hitungan menit dan detik

dan dalam range mati-hidupnya seorang pasien

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Penyulit buruk adalahCARDIAC ARRESTCARDIAC ARREST- karena penyakitnya sendiri- karena pembedahannyap y- karena anestesianya

Penyulit terburuk adalahMALIGNANT HYPERTHERMIAHYPERTHERMIA

obat cuma satu (dantrolene)

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efeknya belum tentuDipicu succinyl - halothan

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Goodgeneral anesthesia

on

rcos

is

alge

sia

rela

xatio

Nar

Ana

Mus

cle

rM

Stress Free

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Narcosis dan analgesia

Anestesi umumKetamin pada jalur thalamus-cortex

Morfin pada reseptorreseptor

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Analgesia

Nerve block

Pl bl k76

Plexus blockEpidural block Subarachnoid block

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Muscle relaxation

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Setelah 161 tahun pengembanganSetelah 161 tahun pengembangan Anestesia

• 1. Pemahaman fisiologi, farmakologi, pato-fisiologi serta pato-farmakologi

2 V i k• 2. Vaporizer yang akurat• 3. Pelumpuh otot dan antagonisnya• 4. Narkotik sintetik dan antagonisnya• 5. Obat inhalasi “inert” desflurane, xenon• 6. Respirator canggih dan analisa gas darah• 7. Sarana monitoring fungsi vital yang teliti

78• 8. Dll masih banyak lagi

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Operasi mikroskopikjangka panjangjangka panjang

| Perfectly still

Pengembangan79

PengembanganVaporizer yang akurat

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Pengembanganblok regional yang andalg y g

- Jarum spinal # 29 - Celiac plexus block, - Cervical peridural

Depresi minimal80

Depresi minimal,bahkan untuk janin

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What are e tr ing to sa ?What are we trying to say ?

•Reversibility• Anesthesia is a physiological trespassing

– Awake - Coma - Awake Againg– Breathing - Apnea - Breathing Again

• Every change in Anesthesia is• Every change in Anesthesia is made reversible

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1 582

1.5

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i 161 h b A iIsi 161 tahun pengembangan Anestesia

• Menjadi disiplin ilmu kedokteran yang mandiri :• Menjadi disiplin ilmu kedokteran yang mandiri : Anestesiologi & Reanimasi

• Melahirkan disiplin ilmu baru : Intensive CareIntensive Care

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Anestesiologi & ReanimasiAnestesiologi & Reanimasi• Pengetahuan berdasar reversibilityPengetahuan berdasar reversibility

– Apakah nafas berhenti itu reversible?– Apakah jantung berhenti itu reversible?Apakah jantung berhenti itu reversible?– Apakah coma itu reversible?

Apakah renal failure itu reversible?– Apakah renal failure itu reversible?• Prevent a premature death mendasari upaya

“ i i”– “resusitasi” – “reanimasi”

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– reversing the dying process

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Resusitasi primitif|

ResuscitologyResuscitology|

Patophysiology of Dying and Reanimation

(Peter Safar et al)|

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|Public Access Defibrillation

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Resuscitation CycleResuscitation Cycle

• Basic Life Support– (A-B-C, 1968, Safar etal)(A B C, 1968, Safar etal)

• Advanced Life SupportDefinitive airway– Definitive airway

– Artificial VentilationDC Sh k & D– DC Shock & Drugs

• Prolonged Life Support

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– Intensive Care (G-H-I)

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Definitive Diagnosis& Definitive Therapy& Definitive Therapyof surgical pathology

LIFE SUPPORTAi hi

SpesialisBedah

Airway, BreathingCirculation, Brain

(BLS-ALS-PLS) Spesialis Anestesiologi & Reanimasi

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& Reanimasi

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Perlu dibedakan antaraPerlu dibedakan antara

KNOWLEDGEKNOWLEDGE

Anestesiologi& Reanimasi Bedah PROFESSIONAL

COMPETENCECOMPETENCE

BedahAnestesiologi& Reanimasi

90Selalu bekerja sama

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Trias AnesthesiaTrias Anesthesia1.Sedation

N2OVolatile anestheticsVolatile anesthetics

(Ether, Halothane, Ethrane, Isoflurane, Sevoflurane Desflurane etc)Sevoflurane, Desflurane, etc)

iv-anesthesia(penthotal ketamine propofol midazolam(penthotal, ketamine, propofol, midazolam,

etomidate, etc)

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Trias AnesthesiaTrias Anesthesia

2. Analgesia,2. Analgesia,Narcotic-analgetic

(morphin, petidin, fentanyl, sufentanyl alfentanyl etc)sufentanyl, alfentanyl, etc),

N2O

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Trias AnesthesiaTrias Anesthesia

3. Relaxation,3. Relaxation,Muscle relaxan

( succinylcholine, pancuronium bromide atracurium vecuroniumbromide, atracurium, vecuronium

rocuronium, etc)

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ROUTINE PREOPERATIVE LABORATORY EVALUATION OFROUTINE PREOPERATIVE LABORATORY EVALUATION OFASYMPTOMATIC, APPARENTLY HEALTHY PATIENTSASYMPTOMATIC, APPARENTLY HEALTHY PATIENTS

� Hematocrit of hemoglobin concentrationAll menstruating womenAll patients over 60 years of ageAll patients who are likely to experience

significant blood loss and may require transfusion

�Serum glucose and creatinie ( or blood urea nitrogen )concentration : All patients over 60 years of age

�Electrocardiogram : all patients over 40 years of age�Electrocardiogram : all patients over 40 years of age�Chest radiograph : all patients over 60 years of age

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THE ANESTHETIC PLANTHE ANESTHETIC PLAN

PremedicationType of anesthesiaType of anesthesia

GeneralAirway managementInductionMaintenanceMaintenanceMuscle relaxation

Local or regional anesthesiaTechniqueAgentsAgents

Monitored anesthesia careSupplement oxygenSedation

Intraoperative managementIntraoperative managementMonitoringPositioningFluid managementSpecial techniquesSpecial techniques

Postoperative managementPain controlIntensive care

Postoperative ventilation

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Postoperative ventilationHemodynamic monitoring

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PREOPERATIVE PHYSICAL STATUS CLASSIFICATION ofPATIENTS ACCORDING TO THE AMERICAN SOCIETY OF ANESTHESIOLOGIST

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AMERICAN SOCIETY OF ANESTHESIOLOGISTAMERICAN SOCIETY OF ANESTHESIOLOGISTAMERICAN SOCIETY OF ANESTHESIOLOGISTAMERICAN SOCIETY OF ANESTHESIOLOGISTCLASSIFICATION AND PERIOPERATIVE MORTALITY RATESCLASSIFICATION AND PERIOPERATIVE MORTALITY RATES

CLASSCLASS MORTALITY RATEMORTALITY RATECLASSCLASS MORTALITY RATEMORTALITY RATE

1 0,06 - 0,08 %

2 0,27 - 0,4 %

3 1,8 - 4,3 %

4 7,8 - 23%

5 9,4 - 51 %

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Labour PainLabour Pain,Pathway and Mechanismy

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CCauses1 First stage: uterine contractions and dilatation of the 1. First stage: uterine contractions and dilatation of the

lower uterine segment and cervix to allowpassage of the fetus.

d f h2. Second stage: greater pressure of the presenting part on pain-sensitive pelvic structures anddistension of surrounding structures.g

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Pathways1 Uterus and cervix: mainly via A delta and C fibers 1. Uterus and cervix: mainly via A-delta and C fibers

passing in the sympathetic nerves to thesympathetic chain; referred to the T10–L1 dermatomes.

2. Vagina and pelvic outlet: via A-delta and C fibers passing in the parasympathetic bundle in thep g p y p

pudendal nerves; referred to the S2–S4 dermatomes.

3 Other: contributions from the ilioinguinal 3. Other: contributions from the ilioinguinal, genitofemoral, and perforating branch of the posteriorcutaneous nerve of the thigh; somatic pain experienced

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in the L2–S5 dermatomes.

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Features.1Over 90% of women experience severe/unbearable labor

pain, although recollection fades with time

2. Typically, pain is similar to other types of visceral pain, i.e., intermittent, severe, and colicky; it starts in the lower

abdomen and back, spreading to the perineum and thighs (Lowe 2000).

3. Pain may be influenced by the factors already listed above, in particular by social, societal, and cultural aspects.

Certain cultures are more emotive and expressive than other Certain cultures are more emotive and expressive than other, more stoic ones, leading possibly to differences in pain behavior rather than in the extent of pain felt. Fatigue and

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general debility, common in late pregnancy, may also contribute to the experience of labor pain.

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Consequences of labor painConsequences of labor painA. Understand that labor pain may have adverse

physiological and psychological consequences:physiological and psychological consequences:

1. Respiratory: causes hyperventilation, leading to p y yp ghypocapnia and respiratory acidosis.

2. Cardiovascular: increases cardiac output and blood pressure via sympathetic activity; this may be

problematic in cardiac disease and pre-eclampsia. Increased venous return associated with uterinecontractions may also contribute.y

3. Neuroendocrine: increases maternal catecholamine secretion with risk of uteroplacental

constriction.

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constriction.

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4. Gastrointestinal: effect of labor on gastric emptying and acidity is unclear although delayed emptying andacidity is unclear, although delayed emptying and

increased acid secretion have been suggested. Opioids are well known to induce gastric stasis

5. Psychological: severe labor pain has been implicated in contributing to long term emotional stress withcontributing to long-term emotional stress, with

potential adverse consequenceson maternal mental health and family relationships.

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B. Understand also that pain during labor may have benefits:

1. Indicates to the mother and those assisting labor/delivery that contractions are occurring.y g2. May have positive connotations regarding

childbirth, related to societal/cultural influences.3 M i di t bl ( t i t3. May indicate problems (e.g. uterine rupture,

placental abruption).

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Thank you Thank you for listeningg

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