Sop CV

HANDBOOK
HANDBOOK CVCU
CVCU
LENTA
LENTA FERNANDO
FERNANDO
Dedicated to CVCU
April, 2010
Dedicated to mykynaocca
SINDROMA KORONER
AKUT
SINDROMA KORONER
AKUT ( SKA )
5 SUBSET/MANIFESTASI IHD :
- Silent angina ( asimtomatis )
- Angina Pektoris Stabil ( APS )
- Angina Pektoris tak stabil ( APTS )
- Infark miokard NSTEMI ( Non Q )
- Infark miokard ST Elevasi ( STEMI /Q
YANG TERMASUK SKA : APTS, NSTEMI

SKA : bentuk peralihan antara stenosis stabil
( APS ) ke stenosis
yang dinamik
UA/NSTEMI bisa menjadi
APS atau STEMI

Tergantung keberhasilan terapi
Karakteristik Nyeri :
APS :
nyeri dicetuskan aktifitas ttt
Dalam 30 hr tdk ada perubahan frekuensi,
lama, fc pencetus
Lama nyeri </= 15 menit
APTS :
o Terdapat perubahan pola : frekuensi, durasi,
beratnya nyeri & fc pencetus ( PROGRESIF &
CRESENDO ), perlu obat dg dosis lebih besar
o Rest angina
o Lama > 20 menit
o Angina berat onset baru ( CCS III )
Nyeri > 20 menit : sudah sebabkan infark .

NSTEMI & STEMI , nyeri > 20 menit
POLA EVOLUTIF EKG pada Infark :

1.Hiperakut T ( jrg terlihat krn tjd dlm waktu
singkat )
2.Elevasi segmen ST ( mula2 gel T msh (+),
lama2 ST depresi/elevasi dan gel T terbalik )
3.Mulai terbentuk gel Q yg makin lama makin
dalam
4.ST segmen akhirnya isoelektrik lagi dg gel T
terbalik
ST Elevasi : hrsnya smkn menurun

Kecuali bl tjdEvolusi
Berdasarkan ANEURISMAInfark VENTRIKEL(2
mll EKG : mgg
msh elevasi
1.Infark akut :) perub terjadi dlm bbrp menit /
Perjalanan
jam Gel Q : 1. menetap atau 2. Lama2
menghilang
2.Recent Infark : perub tjd dlm bbrp hari / mgg
3.Old Infark : Jk terlihat Gel Q atau hanya
terlihat progresifitas gel R yg jelek
DIAGNOSIS INFARK :
o Ax : karakteristik nyeri dada ( > 20 mnt, tak
berhub dg aktif & tdk hilang dg nitrat )
o Perubahan khas EKG
o Perub enzim > 1 kali
CKMB meningkat ( tjd stlh 4 jam )
Troponin T lebih spesifik
- Ditegakkan jika memenuhi 2 dari 3 kriteria

- Perubahan EKG lebih dulu dp perub enzim
SEHINGGA pengobatan Trombolitik tdk perlu
tunggu enzim. OK trombolitik hrs < 12 jam
( bahkan sebaiknya < 6 jam=golden period )
PRINSIP TERAPI Dedicated to mykynaocca
APS : Goal : keseimbangan suplai & demand
- Perbaiki suplai : ACEI, CCB, Nitrat
- Menurunkan demand : B Bloker, KI :
asma
- Kurangi risiko trombosis : antiplatelet
UA / NSTEMI : Sama dg APS + stabilisasi plaq
( double
platelet =Aspirin/Ticlopidin
+ Clopidogrel )
STEMI : Sama dg diatas
+Heparin+ REFERFUSI
/ LMWH
REFERFUSI : 1. Trombolitik ( Streptokinase )

2. PTCA
POST TROMBOLITIK :
1.Infark anterior : HEPARIN ( tanpa yg BOLUS
lagi LHO )
2.Infark inferior : Biasanya tdk diberikan ok
risiko bleeding besar ( tapi ya di ICU tetap
HEPARIN
AMI > 12 jam :
- Heparin bolus 5000 U slnjtnya 1000 U jam
- ASA 160 / 24 jam
- ISDN 10 mg / 8 jam ( sss kan tensi )
- Ticlopidin 250/24 jam atau Plavix 1 tab / 24 jam
- Laxadin syr CI / 24 jam atau Bisacodyl 2 tab / 24 jam
- Diazepam 5 mg / 24 jam (p.r.n)
- Puasa 8 jam diet cair 1300 kkal naikkan bertahap
NOTE :
Dosis heparin 500, 750, 1000, 1250, 1500 sss PTTK
Monitor PTTK / 12 jam. EKG / 24 jam
Diberikan selama 4 5 hari
PTTK : < 1,5 dari standar Heparin

dinaikkan 250 U
1,5 2 x dari standar tetap
> 2 x dari standar Heparin
diturunkan
CT normal : 0 10, BT normal : 1 5
Bl CT BT normal, heparin bisa dimulai dgn
dosis 1000 IU/jam
Dapat juga digunakan :

LMWH risiko perdarahan kecil, tdk perlu
HEPARIN 1 vial = 5 cc = 25 .000 IU
monitor PTTK
SP Program x Pengenceran = . ml / jam
Vol obat yg di sedot x 5000
Heparin di encerkan dalam D 5 % menjadi 20 cc atau 50 cc
INFUS PUMP + INFUS DRIP

I. Program x vol infus = . ml /jam
Vol obat disedot x 5000
II. Vol infus x fc ttsan ( 20 or 15 ) = tts/ menit

60 menit
Dosis Heparinisasi dg UFWH :

Bolus 60 IU / kg BB. Max 400 UI
Selanjutnya : 12 UI/kgBB, Max 1000 UI
Infark < 12 jam : TROMBOLITIK dg :

STREPTOKINASE
Sediaan 1 vial: 1.500.000 unit
Dosis:
Larutkan bubuk di D5%/NaCL 0,9% 5 cc
Masukkan dlm NaCl/D5% 50-100 cc
Diberikan selama 60 menit i.v di titrasi
Monitor:
Rekam EKG dan cek CKMB sebelum pemberian
Rekam EKG 10-15 mnt pertama
Selanjutnya Rekam EKG tiap jam dlm 4 jam I selanjutnya
tiap 24 jam atau jk ada indikasi.
HATI2 : hipotensi & anafilaktik
PROTOKOL PEMBERIAN STREPTASE
KI MUTLAK :
Kecurigaan diseksi aorta
Perdarahan gastrointestinal baru ( terbukti )
Kejadian stroke baru ( < 6 bulan )
Kejadian trauma mayor atau bedah baru ( < 1 bulan )
KI RELATIF
o Kehamilan
o Menstruasi
o Punksi arteri atau baru cabut gigi
o Resusitasi jantung paru yang lama
o Hipertensi tidak terkontrol
o Alergi thd streptokinase (gunakan Reteplase rPA atau
Alteplase )
o Pemberian streptokinase > 5 hari sebelumnya
( gunakan Reteplase rPA )
o Retinopati diabetik proliferasi
o Gg hemostasis ( Trombo < 20.000, > 50.000 dg
perdarahan ) atau
mendapat antikoagulan warfarin.
Yanfile
JIKA NYERI DADA >> :
Morfin (untuk AMI anterior)

o Sediaan 1 ampul: 1 cc = 10 mg
o Dosis : 2,5 mg bila masih kesakitan dapat
diulang per 10
menit max 7,5 mg
o 1 cc dioplos sp 10 cc
o Efek bradikardi
Untuk edema paru dosis 2,5 5 mg /jam
total 30mg/hari
Lebih diutamakan efek sedasi.
Pethidin(AMI posterior & inferior) ciri
bradikardi
Punya atrofin like effect takikardi
Inferior biasanya diikuti bradikardi
Sediaan 1cc=50 mg
Dosis : 12,5 mg dpt diulang per 10 mnt max
37,5 mg
yans file
LOKASI INFARK &
KOMPLIKASI
Infark Inferior ( II,III,aVF) PDA

Gagal ventrikel kanan
Blok ok a. coronaria kanan mendarahi
miokard dikanan
Infark Anterior
o Anteroseptal ( V1-V3 ) LAD
o Anterolateral ( I, aVL, V5, V6 ) LCx
o Anterior Ekstensif ( I, aVL, V1-V6 ) LAD, LCx
Komplikasi :
Gagal jantung
Aritmia maligna
Trombus di apex
GAGAL JANTUNG PADA

AMI
PATOFISIOLOGI GAGAL JANTUNG PADA AMI
IMA transmural
Fungsi sistolik <
Pre load >
Backward failure After load >
Impedance
Cardiac output
Tabel 1. Pembagian kelas klinik menurut Killip
Kelas klinik Dapatan klinik

I Tak ada tanda gagal jantung
II Gagal jantung ringan / Moderat,
ronki terdengar hingga < 50 %
dari lapangan paru
III Edema paru, ronki > 50 %
IV lapangan paru
Syok kardiogenik (TD sistolik <
90 mmHg, denyut jantung
meningkat, akral dingin,
produksi
Dikutib dari Wolk MJ, Scheidt S, Killip Turine
1972 1 cc / Kg BB / jam
PRINSIP
PENANGANAN
UMUM :
: Reperfusi miokard
Perbaiki pertuk gas
Koreksi hipoksia
KHUSUS : Kontraktil miokard

Pre load , After load
Impedance , Oedem paru
PENERAPAN : Sesuai Kls Klinik

PRINSIP :
Mudah dipantau
Dosis dapat dititrasi
Aksi pendek
Akses parentral
OBAT KONTRAKTIL MIOKARD
Klp Katekolamin & derivat :

Dobutamin : Card Output
Pre load Lung edem

Dopamin : bila hipotensi (+)
Penghambat PDE :
Amrinon & Milrinon
Klp Digitalis : bila AF (+)
OBAT PRE LOAD

Kelompok nitrat
Venodilatasi Redistribusi (+)
Pre load
Efek arterial sekunder
Diuretika : pre load , elektrolit ,
CO , SRA , impedance
Kombinasi gagal + dobutamin
OBAT AFTER LOAD & IMPEDANCE
IMA : after load & Impedance

bersifat relatif
Klp vasodilator arteri ???
Klp penghmbt aktifitas SRA :

Kaptoril : aksi paling pendek
Indikasi : disfungsi sistolik (+)
Syarat : TDS 100 mmHg
OBAT KONGESTI PARU
Kelompok nitrat
Dilatasi V sistem + paru
Redistribusi Kongs paru

Diuretika : vol eks sel
Indik : ret garam & air
Morfin : simpatikolitik
Pomp resp + flebot farmakolo (+)
venous return
PRINSIP TATALAKSANA
Tabel 2. Obat-obat tambahan untuk GJ akibat IMA berdasarkan kelas killip
Kelas klinik Obat tambahan
I Kaptopril
II Kaptopril, nitrat (parentral)
III Kaptopril, nitrat (parentral), morfin,
furosemid (parentral), dobutamin,
IV dopamin (dosis rendah)
Nitrat (parentral), furosemid (parentral),
dobutamin, dopamin (dosis tinggi),
digitalis (?)
IMA Disf sistol GJ
Tujuan terapi : beban ,
kongs paru ,
kontraktil
Urutan obat : kurangi beban,
bila gagal baru kontraktil
Bila semua gagal LVAD
ARITMIA
APPROACH :
1.Macam disritmia ( nilai EKG 12 lead )
2.Ada tdknya ggg hemodinamik ancam jiwa
3. Manifestasi : - kelainan jtg organik
- gg ekstra kardial ( ggg elektrolit, obat,
tirotoksikosis )
4. Terapi yg terbaik ? Co : pada AF tdk sll hrs konversi ke
sinus
SA AV Berkas his cab ka/ki serabut
purkinye
FREKUENSI yg dihasilkan :
SA : 60 100 x / mnt
AV : 40 60 x / mnt
Ventrikel : 20 40 x / mnt
Panjang Gel Normal :
PR int : 0,10 0,20
QRS compl : 0,04 0,12
NSR
A
Flutter
SINUS BRADIKARDI
A Fibrilasi
SINUS TAKIKARDI SVT
VT VF
AV Block 2 First Degree
AV Block 2 Second Degree
Third Degree Heart Block
Dedicated to mykynaocca Asystole

VES
multifokal
VES salvo
VES
R on T
PENANGANAN
ARITMIA
SVT :
Gel P tersembunyi dlm gel T ok frekuensi
sgt cepat
( 151 250 x / menit )
Terapi : ( versi UPJ )

TANPA GGG HEMODINAMIK
o Manuver valsava ( masagge sin
karotikus ). Hati2 : jk ada bruit : ada
plak,bl dimasagge Ruptur SYOK
o Jika tdk berhasil :
ATP 6 mg bolus cepat tanpa pengenceran
( < 3 dtk )
Tunggu 5 menit : tdk berhasil : ulang 12
CARA LAIN : Dedicated to mykynaocca
Diltiazem, Digoxin, Amiodaron
ISOPTIN ( VERAPAMIL ) 5 mg IV ulang tiap 5
menit
Bisa juga DRIP : 10 cc D5% + 1 ampul ISOPTIN
dg Syringe s/d
RATE terkontrol.
Lalu Lanjutkan ISOPTIN oral 80 mg / 8 jam
DENGAN GGG HEMODINAMIK:

KARDIOVERSI start 50 J ( syncronized)
TERAPI SVT dg Hemodinamik stabil ( VERSI ICU )
MgSo4 40%
Cara Pemberian : 3-5-6-24
Dosis 3 gram habis dalam 5 menit
Selanjutnya Dosis 6 gram dalam 24 jam
ATRIAL FIBRILASI
Gel P tak teratur, tdpt perbedaan interval &
tinggi gel P
Tjd ok peningkatan iritabilitas semua sel jantung
dlm atrium ( byk t4 yg memulai impuls ) tdk
semua dihantarkan ( depolarisasi atrium tdk
sempurna ), hanya timbul getaran shg gel P
hanya seperti garis gelombang
Dlm menghitung frekuensi, yg dihitung adalah
RESPON VENTRIKEL ( dihitung jumlah QRS
complek dlm lead II panjang )
Frek gel P : 380 600 / mnt
Respon Ventrikel : N ( 60 -100x/mnt ), CPT ( >
100 x /mnt )
Jenis AF : - Paroksismal : tanpa

pengobatan, berhenti
PRINSIP PENGOBATAN AF :
HEMODINAMIK BAIK
1.Kontrol Rate
2.Konversi ke sinus
3.Prevensi stroke / Tromboemboli
HEMODINAMIK TERGANGGU : DC SYOK
KONTROL RATE : ( VERSI UPJ )

1.LANOXIN 0,5 mg / 0,25 mg diencerkan dg D5% 10
cc Injeksi lambat ( 10 mnt ). Jika HR <
100x/mnt STOP ganti oral
@ 1 amp = 0,5 mg. MONITOR EKG lead II
Jika TABLET :
Digoksin Loading Dose : 2 : 1 : 1 tiap 6 jam Sljutnya
maintena (1/2 tb/12 jam)
Keuntungan : Absorbsi 100 %. Hati2 : intoksikasi Digitalis
2. AMIODARON : mungkin dpt konversi ke sinus,
TERAPI AF DI ICU sama dengan SVT (jk tdk ada
Lanoxin) :
20 % MgSO4 ( Mg : 42 mEq/25 ml , So4 : 42 mEq/25 ml ) @ 25
cc
40 % MgSO4 (Mg : 83 mEq/25 ml , So4 : 83 mEq/25 ml ) @ 25
cc
Sediaan 1 vial : 10 gr = 2,5 cc 1cc : 400 mg
Cara Pemberian : 3-5-6-24
Dosis 3 gram habis dalam 5 menit
Selanjutnya
CARA LAIN u/ Dosis
SVT6 gram
/AF (dalam
VERSI24 ICU
jam )
Cordaron/Amiodaron : memperpanjang potensial
aksi
Sediaan 1 ampul: 3cc=150 mg
ES : - fibrosis paru
Dosis: - ggg fs hati
Injeksi 150 mg bolus dilanjutkan
- ggg hormon tiroid
Dilanjutkan 600 mg dalam jangka
24 panjang
jam sbbkan : sinus bradika
simtomatik
Atau
240 mg dalam 6 jam dilanjutkan
360 mg dalam 18 jam
VES
o Impuls berasal dari daerah dibwah AV, tjd lbh
awal dari komplek yg sebenarnya.
o Saat tjd VES, atr tdk berdepolarisasi Gel P (-).
Jk ada depolarisasi, P tersembunyi didlam QRS
komp
o QRS lebar & bizzare ( > 0,12 det )
o Initial defleksi berlawanan dg komplek yg
sebenarnya.
o Jenis : Bigemini : VES tjd tiap selang 1 komplek ( N-VES-N-
VES dst )
Trigemini : N-N- VES
Quadrigemini : N-N-N-VES
Salvo ( ganda ) : VES berurutan yg tdk dipisahkan
oleh irama dasar
( N-VES-VES-N )
Kej VT : ada 3 VES /> dlm 1 deret
o VES MALIGNA :
- > 5 / menit
VES :
Bila Frekuensi irama dasar BRADIKARDI, VES dpt
merupakan
upaya jantung me + frekuensi jtg agar sirkulasi
adekuat.
Tdk semua VES memerlukan pengobatan .
Dianggap berbahaya jika :
- VES Maligna
- Kejadian VT
- Hemodinamik tak stabil
TERAPI : ( ICU / UPJ )

JIKA HEMODINAMIK BAIK
LIDOKAIN / XYLOCAIN : memperlambat

repolarisasi
Bolus 1 1,5 mg / kg BB diencerkan . Ulang tiap 3
menit dengan dosis dss awal. Max 3 mg/kgBB
VT
asal dari 1 tempat di ventrikel ( Frek : 41 250 )
Gel P (-)
QRS lebar & bizzare
VF :
asal dari byk tempat di ventrikel
tdk ada waktu depol/gel P (-) & repol/ QRS (-), PR
int (-), PP
RR int (-)
grs2 gel kacau
TORSADE : VT yg mendekati VF
PENGELOLAAN VT :
Umum : - rawat ICU
- O2 2 3 ltr/mnt
- Infus line D5%
- diet Lunak
KHUSUS :
Hemodinamik baik : XYLOCAIN : Bolus 1 1,5 mg / kg
BB diencerkan
tunggu 15 mnt
Hemodinamik BURUK :
Pulse (+) : DC shock 50 100 J ( sincronized:
deteksi QRS )
Pulseless : terapi sss VF, DC shock 200 300 J
asincronized 360 J
ditambah ADRENALIN 1 mg bolus 3x
ulang tiap 1 s/d
5 mnt
BLOK ( ggg penghantaran impuls ) Dedicated to mykynaocca
- Blok sinoatrial
- BLOK AV :
1.AV blok derajat I : P sinus,QRS comp&T
normal,PR int > 0,20 det
Terapi : -
2. - AV blok derajat II, Mobitz tipe I : P sinus, QRS

comp &T
normal, PR int memanjang scr progresif shg bs
terdpt gel P yg
tdk diikuti QRS
Terapi : SA 2 ampul.
- AV blok derajat II, Mobitz tipe II: P sinus, QRS
comp &T
normal, PR int sama dg denyut berkurang
( dropped beat ) dg
blok 2 ; 1, 3 : 1 dll
BRADIARITMIA Dedicated to mykynaocca
o Sulfas Atrofin 0,4 atau 0,5 mg iv tiap 5 menit, max
2,4 mg
o SA 1 ampul = 1 cc = 0,25 mg
o SA dosis kecil berefek BRADIKARDI, dosis > 2 mg berefek
TAKIKARDI
ATAU :
ALUPENT ( ORCIPRENALINE ) ampul iv bolus , bl
respon (+) teruskan drip : 5 amp + 500 cc D5%
Adrenalin
12 tts / menit
Dosis 0,1 mikrogram/kgBB/mnt dinaikkan bertahap tiap 10
Sediaan
mnt bl Alupent tab : 20 mg
HR blm naik. Max 0,4 mikrogram / kgBB/mnt. Sasaran HR
100x/mnt
Sediaan: 1 amp: 1 cc= 1 mg
SP : Program x BB x Pengenceran x 60 mnt
x ampul x 1000
Indikasi :
- Blok dengan ggg hemodinamik
- AV blok derajad III/ blok total
- Jk respon (+) Adrenalin tapp off selanjutnya ganti Efedrin
MGSO4 utk EKLAMSI

MGSO4 40 %
Bolus 4 gram iv (40-80 mg/kgBB)
Lanjutkan 1 gr/jam sampai 24 jam bbs kjg
Bila kejang ekstra MgSO4 2 gram iv bolus
Dihentikan bila:
Urine < 30 cc/jam Antidotum :
Glukonas Calcicus
Depresi nafas(RR<16x/mnt)
Reflek patela turun
ANTIHIPERTENSI yg srg pd Eklamsi :

Metyldopa 250
GAWAT DARURAT HIPERTENSI

( GDH )
GDH perlu rawat intensif

Tujuan rawat hindari organ rusak
Kriteria : Hipertensi & organ target
Penentu : organ target ?
PATOFISIOLOGI
Pre load
After load Kontrak jnt
Frek jantung
Curah jantung
Auto regul
Tekanan darah
Viabilitas Perfusi jaringan

TAHAP PENURUNAN TEK DRH GDH
Tek darah awal
2 jam
MAP 25 %
6 12 jam
Td diast :
110 100 mmHg
bbrp hari
+ OATDTO
Normotensif
MAP ( Mean Arterial Pressure )

Sistolik + 2 x Diastolik
3
Sasaran : 2 jam I : MAP 75 % dari nilai awal
6 jam I sasaran diastolik 110 mmHg
Misal :
TD saat datang : 200 / 140 mmHg
MAP : 200 + ( 2 x 140 ) = 160
3
Sasaran 2 jam I : 75 % x 160 = 120 mmHg
( diastolik )
PRINSIP PEMILIHAN OBAT GDH
o Titrasi, pemantauan, klinik ?

Farmakologik : aksi, potensi, pulih asal,
spesifitas, efek samping ?
Fasilitas / personal ?
Pilihan utama : Nitroprusid

Alternatif : Vasodilator vena
Penghambat adrenergik,
Penghambat SRA, antagonis Calsium
Diuretika ?
PENANGANAN GDH ( versi campuran ) :

o Konvensional : Clonidin (catapres) IV 2 x, jika
gagal drip 7 - 9
ampul dlm D5% 10 tts evalusi ketat.
Sediaan : amp : 0,15 mg, tab : 0,075 mg
Atau
o NITRAT
o Diltiazem ( HERBESSER )
Dosis : 5 15 mikrogram /kgBB/menit.
Dinaikkan 2,5 mikro
sss respon TD.
o Sediaan : 1 ampul ; 10 mg
o Pada Hipertensi saat operasi :
Herbesser : 10 mg iv pelan selama 1 menit,
diikuti drip 5 15
mikrogram /kgBB/menit.
EDEMA PARU
AKUT
3 mekanisme agar interstitium & alveolus kering:

1. Tekanan onkotik plasma lebih besar drpd tekanan
kapiler pulmoner (25 vs 7-12)
2. Jaringan ikat& barrier seluler relatif impermeabel
thd protein plasma
3. Sistem limfatik yang baik
PROSES :
Stage 1 terjadi peningkatan perpindahan cairan
ke dalam intetestital paru, karena aliran limfatik
juga meningkat & tidak terjadi peningkatan
volume interstitial.
Stage 2 Kapasitas limfatik tidak mampu
mengeluarkan cairan, cairan terakumulasi dalam
ruang intertstitial yang mengelilingi bronkiolus
dan vaskuler paru ( rontgent : edema interstitial)
Stage 3 karena cairan terus meningkat, terjadi
ETIOLOGI
I. Altered capillary permeability
A. Infectious pulmonary edema (viral or bacterial)

B. Inhaled toxins
C. Circulating toxins
D. Vasoactive substances (histamine, kinins)
E. Disseminated intravascular coagulation
F. Immunologic reactions
G. Radiation pneumonia
H. Uremia
I. Near-drowning
J. Aspiration pneumonia
K. Smoke inhalation
L. Adult respiratory distress syndrome
II. Increased pulmonary capillary pressure.

A. Cardiac causes
1. Left ventricular failure from any cause
2. Mitral stenosis
3. Subacute bacterial endocarditis
B. Noncardiac causes
1. Pulmonary venous fibrosis
2. Congenital stenosis of the origin of the pulmonary veins
3. Pulmonary venoocclusive disease
C. Overinfusion of fluids
III. Decreased oncotic pressure

Hypoalbuminemia from any cause
(renal, hepatic,
nutritional, or protein-losing enteropathy)
IV. Lymphatic insufficiency
V. Mixed or unknown mechanisms

A. High-altitude pulmonary edema
B. Neurogenic pulmonary edema (CNS trauma,
subarachnoid bleeding)
C. Heroin overdose (also other narcotics)
D. Pulmonary embolism (very rare)
E. Pulmonary parenchymal disease
F. Eclampsia
G. Cardioversion
H. Postanesthetic
I. Cardiopulmonary bypass
Symptom
dyspnea
tachypnea
orthopnea
tachycardia
hypertension
thoracic oppression
cold extemities with cyanosis or not
cough with a frothy or pink sputum
extensive use of accessory muscles of respiration
moist rales with or without wheezing .
At begining of the process , when edema is only in the

interstitium, patients can present only tachydyspnea
and dry cough
When the pulmonary fluid accumulation is very intense
and fastly installed , patients present an intense
dyspnea, cyanosis, and elimination of large amount
Diagnosis
1. Pemeriksaan darah: darah rutin dg
dif count, eletrolit, BUN, kreatinin dan
konsentrasi protein serum
2. Urianalisis dan pemeriksaan
mikroscopik urin: dapat ditemukan
proteinuria
3. Analasis gas darah arteri: pertama
terjadi penurunan PO2 and PCO2.
Kemudian terjadi penurunan PO2
sedangkan PCO2 meningkat. Bila nilai
PO2 < 50 mmHg and PCO2 > 50 mmHg
merukakan keadaan yang berat dan
memerlukan ventilasi mekanik
4. X foto thorax PA dan lateral

o INTERSTITIAL EDEMA Kerley B lines,
garis horizontal yang mengarah ke
lateral pada lapangan paru bawah,
setidaknya panjang 2 cm, dekat
pembuluh darah dapat mencapai tepi
paru.
o ALVEOLAR EDEMA "butterfly"
pattern, ditandai dengan bayangan yang
dominan pada sentral dengan daerah
yang bersih pada lobus perifer.
5. ECG:
6. Tes lain
o Kateteisasi jantung kanan dapat
dilakukan untuk mengukur tekanan
kapiler pulmoner, yang umumnya
miningkat (> 25 mmHg) pada edema
PENGOBATAN
Anamnesis yang jelas, pemeriksaan fisik dan
tes laboratororium untuk mengetahui
penyebab, sehingga dapat diobati secara
spesifik.
Posisi setengah duduk pernafasan lebih
mudah dan untuk mengurangi aliran vena ke
jantung
Oksigen 100% diberikan dengan masker
untuk memastikan oksigenasi yang cukup.
Morfine (2 - 5 mg IV bolus, yang dapat
diulang hingga maksimum15 mg) ><
naloxone (0.8 to 2.0 mg IV bolus)
Furosemide (40 to 100 mg IV bolus)
venodilaytasi dan kemudian sebagai
Nitroglycerine sublingual tablets atau IV drip

(0.4 mg)(NTG dapat diulang dua kali tiap
interval 5 menit ki: SBP < 120 mmHg
Digoxin (0.25 mg IV lambat) dapat diberikan

jika terdapat atrial fibrilation dan rapid
ventricular response merupakan faktor yang
ikut berperan terjadinya edema
Agonis beta-adrenergic inhalasi atau

aminofilin IV dapat diberikan untuk
mengobati bronkospasme
Aminofilin juga meingkatkan aliran plasma

renal, eksresi sodium, kontraksi jantung dan
menimbulkan venodilatasi,sehingga
menurunkan resistensi vaskuler perifer.
keduanya dapat menginduksi takikardi dan
supraventricular arrhythmia.
Tindakan lain untuk menurunkan

preload adalah flebotomi +/- 500 ml
darah dan plasmapheresis.
Jika tidak bisa dilakukan, dapat
dipasang torniquet pada anggota
gerak bawah jika tidak ada obstruksi
arterial ( 15 -20 menit)
Pada kasus edema non kardiak, harus
diobati penyebab utama,
mempertahankan fungsi respirasi dan
pertimbangkan pemberian NSAIDS.
GAGAL JANTUNG AKUT

( ACUTE HEART FAILURE )
Acute heart failure ( AHF ) : Dedicated to mykynaocca
sindroma klinik yang ditandai dengan :
penurunan cardiac output
hipoperfusi jaringan
peningkatan tekanan kapiler paru (PCWP) dan
kongesti jaringan.
Dapat terjadi dengan / tanpa penyakit jantung

sebelumnya.
Disfungsi jantung dapat :

o disfungsi diastolik
o disfungsi sistolik
o gangguan irama
o ketidakseimbangan antara preload dan afterload.
Keadaan ini membahayakan jiwa dan memerlukan

terapi SEGERA
Clinical
Clinicalsigns:
signs:Shock,
Shock,hypoperfusion,
hypoperfusion,
Congestive
Congestive heart failure, acutepulmonary
heart failure, acute pulmonaryedema
edema
Most likely problem
Most likely problem ??
Acute
Acutepulmonary
pulmonary Volume
Volumeproblem
problem Pump
Pumpproblem
problem Rate
Rateproblem
problem
edema
edema
11ststAcute
Acutepulmonary
pulmonaryedema
edema Administer
Administer: :
Furosemide iv 0.5 1.0 mg/kg Fluids Bradicardia
Furosemide iv 0.5 1.0 mg/kg Fluids Blood
Blood Bradicardia Tachycardia
Tachycardia
Morphine iv 2 4 mg Blood transfusions See algorithm See algorithm
Morphine iv 2 4 mg Blood transfusions
Nitroglycerin SL Cause-specific interventions Pressure?? See algorithmSee algorithm
Pressure
Nitroglycerin SL Cause-specific interventions
Oxygen/intubation as needed Consider
Oxygen/intubation as needed Considervasopressors
vasopressors
Systolic Systolic
SystolicBP
SystolicBPBP nd Systolic
SystolicBP
BP Systolic
SystolicBPBP Systolic
SystolicBPBP >>100 mmHg
BP
BP
BP defines22nd
defines <<7070mmHg
mmHg 7070toto100
100mmHg
mmHg 7070toto100
100mmHg
mmHg 100 mmHg
Line
Lineofofaction
action Signs/symptoms
Signs/symptoms Signs/symptoms
Signs/symptoms No sign/symptoms
No sign/symptoms
(see below)
(see below) ofofshock
shock ofofshock
shock ofofshock
shock
Systolic
SystolicBPBP nd Systolic
SystolicBP
BP Systolic
SystolicBP
BP
BP
BP defines22nd
defines <<7070mmHg
mmHg 7070toto100
100mmHg
mmHg 7070toto100
100mmHg
mmHg >>100 mmHg
100 mmHg
Line
Lineofofaction
action Signs/symptoms
Signs/symptoms Signs/symptoms
Signs/symptoms No sign/symptoms
No sign/symptoms
(see below)
(see below) ofofshock
shock ofofshock
shock ofofshock
shock
Norepinephrine iv Dopamine iv Dobutamine iv Nitroglycerin iv

Norepinephrine iv Dopamine iv Dobutamine iv Nitroglycerin iv
0.5
0.5 3030mcg/min
mcg/min 551515mcg/kg/min
mcg/kg/min 222020mcg/kg/min
mcg/kg/min 10102020mcg/min
mcg/min
Consider
Consider
Nitroprusside iv
Nitroprusside iv
0.1-5
0.1-5mcg/kg/min
mcg/kg/min
22ndnd- -Acute
Acutepulmonary
pulmonaryedema
edema
Nitroglycerin / nitroprusside if BP > 100mmHg
Nitroglycerin / nitroprusside if BP > 100mmHg
Dopamine if BP 70 100 mmHg, signs/symptoms of shock
Dopamine if BP 70 100 mmHg, signs/symptoms of shock
Dobutamine if BP > 100 mmHg, no signs/symptoms of shock
Dobutamine if BP > 100 mmHg, no signs/symptoms of shock
Further
Furtherdiagnostic
diagnostic/ /therapeutic
therapeuticconsideration
consideration
Pulmonary artery catheter
Pulmonary artery catheter
Intra-aortic balloon pump
Intra-aortic balloon pump
Angiography for AMI / ischemia
Angiography for AMI / ischemia
Additional diagnostic studies
Additional diagnostic studies
1. Gagal jantung kongestif akut dengan tanda dan gejala AHF yang
ringan dan tidak memenuhi kriteria cardiogenic shock, pulmonary
oedema atau hypertensive crisis.
2. Hypertensive AHF : tanda dan gejala gagal jantung disertai

tekanan darah yang tinggi dan radiologis thorax menunjukkan
edema paru akut.
3. Edema Pulmo (verified by chest X-ray) disertai severe respiratory

distress, dengan ronki basah diseluruh paru dan orthopnoe,
dengan saturasi O2 biasanya < 90 % pada suhu ruangan sebelum
terapi.
4. Syok Kardiogenik : keadaan dimana terjadi hipoperfusi jaringan

yang diakibatkan oleh gagal jantung.
Tidak ada definisi yang jelas mengenai parameter hemodinamik
namun biasanya ditandai dengan : penurunan TD (systolic BP
<90mmHg atau MAP Turun >30mmHg) & atau Oliguria
(<0.5ml/kg/h), with a pulse rate >60b.p.m. dengan atau tanpa
kongesti organ.
5. High output failure biasanya pada keadaan : high heart rate

(caused by arrhythmias, thyrotoxicosis, anaemia, Paget's disease,
iatrogenic or by other mechanisms),dengan perifer hangat,
Medical treatment Dedicated to mykynaocca
1. Morphine , jika ingin diambil efek sedasi
2. Vasodilators in the treatment of AHF (first line terapy)
3.Calcium antagonists TIDAK DIREKOMENDASIKAN
4. ACE-inhibitors TIDAK DIINDIKASIKAN untuk stabilisasi
awal.
5. Diuretik
6. Inotropik
Indications and dosing of vasodilators in AHF
Vasodilator Indication Dosing Main side Other

effects
Glyceryl Tolerance on
trinitrate, 5- Acute heart failure, when blood Start 20 g/min, Hypotension, continuous
mononitrate pressure is adequate increase to 200 g/min headache use
Tolerance on
Isosorbide Acute heart failure, when blood Start with 1 mg/h, Hypotension, continuous
dinitrate pressure is adequate increase to 10 mg/h headache use
Hypotension,
Hypertensive crisis, cardiogenic isocyanate Drug is light
Nitroprusside shock combined with intoropes 0.35g/kg/min toxicity sensitive
Bolus 2 g/kg +
Acute decompensated heart infusion 0.015
OBAT- OBATAN
RESUSITASI
EPINEPHRINE
Meningkatkan :
Resistensi vaskuler sistemik
TD diastolik & sistolik
Electrical activity in the myocardium
Coronary and cerebral blood flow
Strength of myocardial contraction
Myocardial oxygen requirements
Automaticity
INDIKASI :
Cardiac arrest from : VF or Pulseless VT
unresponsive to initial
countershocks, asystole, PEA
Symptomatic bradycardia
DOSIS & CARA PEMBERIAN :
o 1 mg IV, repeated every 3-5 minutes
o During cardiac arrest and symptomatic bradycardia
profound hypotension :
continuous infusion, 30 mg Epinephrine HCl added to 250
mL of normal saline
ATROPINE
A parasympatholytic drug
Enhances both sinus node automaticity and AV conduction via
its vagolytic action
INDIKASI :
Initial therapy for symptomatic bradycardia
In 1st degree AV block, Mobitz type I AV block and brady-
asystoloc cardiac arrest :
excessive vagal stimulation.
Without cardiac arrest : 0.5 1 mg,IV. Repeated at 5 minutes
interval.
Brady-asystolic cardiac arrest : 1 mg IV. Repeated every 3 5
minutes.
HATI - HATI :
Induce tachycardia
Administered with caution in the setting of myocardial
infarction
Excessive doses can cause : anti-cholinergic syndrome of
delirium, tachycardia,
come, flushed, hot skin and blurred vision
LIDOCAINE Dedicated to mykynaocca
Suppresses ventricular arrhythmias by decreasing automaticity
Terminates re entrant ventricular arrhythmias
Elevates the fibrillation threshold
INDIKASI :
Ventricular ectopy, wide complex tachycardias, ventricular
tachycardia and VF.
Pulseless VT and VF that is refractory to electrical therapy and
epinephrine.
Patient with significant risk factors for malignant ventricular
arrhythmia.
DOSIS & CARA
Routine PEMBERIAN
prophylactic :
Lidocaine therapy in patient with AMI can
Initial
no longerdose
be : 1,0 1,5 mg / kg I.V. bolus
Via ETT : 2 2,5 x IV dose
recommended.
Second bolus : 0,5 0,75 mg / kg after 10`
Additional bolus : 0,5 0,75 mg/kg every 5 ` -10` (if arrhythmia
persists), until total
dose: 3 mg/kg.
Continuous iv infusion: 2-4 mg/min (spontaneous circulation).
HATI - HATI :
Neurological change
Myocardial & circulatory depression
ADENOSINE
Slows conduction through the AV node
Interrupts AV nodal re entry pathways
Restores normal sinus rhythm in patients with PSVT
Short-lived pharmacologic response
INDIKASI :
Terminating SVT that involve a re-entry pathways including
the AV node

Initial dose : 6 mg rapid bolus over 1-3 followed quickly by
20 ml saline flush
Repeat dose : 12 mg, if no response within 1 2 minutes
Patients taking theophylline are less sensitive
HATI HATI :
Flushing, dyspnea, chest pain ( usually resolve within 1 2
minutes )
Transient bradycardia and ventricular ectopy
Produce few hemodynamic effects
VERAPAMIL
Inhibits slow channel activity on cardiac and vascular
smooth muscles
Slows conduction & prolongs refractoriness in the AV
node
Slows the ventricular response to atrial flutter and
fibrillation
Potent direct negative chronotopic and negative
INDIKASI
inotropic:
Terminates SVT by direct effects on the AV node
Slows ventricular response to atrial flutter and fibrillation

Initial dose : 2,5 5 mg bolus over 1-2 minutes,slowly
Repeat dose : 5 10 mg in 15-30 minutes after first dose
5 mg bolus, every 15 minutes, until response or total dose
30 mg
HATI HATI :
Atrial flutter / fibrillation with WPW syndrome
VT , may induce hypotension or VF
Hypotension , A-V block
AMIODARONE Dedicated to mykynaocca
Effective for supraventricular arrhythmia, ventricular

arrhythmia
Ventricular rate control
Pharmacological cardioversion
Alter conduction through accessory pathway
Adjunct to electrical cardioversion of refractory PSVT
( II a)
Pharmacological cardioversion of atrial fibrillation ( II a)
Atrial tachycardia ( II b)
INDIKASI :
Ventricular rate control of rapid atrial arrhythmia in
patients with severely impaired LV function, and in
patients with accessory pathway conduction.
Cardiac arrest with pulseless VT or VF ( after
defibrillation and epinephrine )
hemodinamically stable VT
polymorphic VT
Wide-complex tachycardia of uncertain origin
AMIODARONE
Initially, 150 mg. I V. over 10 minutes,Repeated 150 mg, as

necessary, for recurrent or
resistant arrhythmia
Followed by 1 mg / min infusion (6 hrs). Then, 0,5 mg / min
Max. daily dose : 2 grams
In cardiac arrest due to pulseless VT or VF :

o Initially , 300 mg, rapid infusion, diluted in 20-30 ml saline or
D5W.
o Repeated, 150 mg for recurrent or refractory VT/VF.
o 1 mg / min ( 6 hrs ), then 0,5 mg/min. Max. daily dose: 2
grams
HATI HATI :
- Hypotension
- Bradicardia
- Heart block
VASOPRESSIN
Non-adrenergic peripheral vasoconstrictor
Half-life 10 20 minutes (longer than epinephrine)
During CPR increases coronary perfusion pressure, vital

organ blood flow, VF median frequency, cerebral
oxygen delivery
INDIKASI :
Shock-refractory VF ( II b)

40 U, I.V. single dose, 1 time only
Sod. Bicarbonate Dedicated to mykynaocca
Buffer agent
CO2 generated, during CPR when the transport of CO2 to and
from the lung is
decreased
INDIKASI :
Tissue acidosis resulting acidemia during cardiac arrest and
CPR, it depends on the duration of cardiac arrest and the level
of blood flow during CPR
1 mEq/kg, I V bolus as initial dose
Give half dose every 10 minutes.
Check acid base status with blood gas analysis
May be administered by continuous infusion: use 5%
NaHCO3 solution
HATI HATI :
PCO2 should be emphasized
Negative inotropic
Hypernatremia and hyperosmolality
DOPAMINE
Low dose (1-2 microgram/kg/min) : stimulate
dopaminergic receptors to produce cerebral, renal and
mesenteric vasodilation but venous tone is increase
In dose 2 10 microgram/kg/min : increase cardiac

output and only modest increase the systemic vascular
resistance
At dose greater than 10 microgram/ kg/min: renal,
peripheral arterial, mesenteric and venous
vasoconstriction with marked increase in systemic
vascular resistance, pulmonary vascular resistance
and further increase in preload.
INDIKASI :
Significant hypotension in the absent of
hypovolemia
Hypotension occurs with symptomatic bradicardia,

or after return to
spontaneous circulation
DOPAMINE Dedicated to mykynaocca
Initial rate of infusion is 15 microgram/ kg/min, the infusion

rate maybe increased
until BP, urine output improve
Final dose range : 5 20 microgram/ kg/min
Use volumetric infusion pump to ensure precise flow rate.
HATI HATI :
Increased HR may induce arrhythmia
Even at low doses can exacerbate pulmonary congestion and
compromise cardiac
output
Nausea and vomiting are frequent side effects especially in high
dose
Cutaneous tissue necrosis if extravasation
Inactivated in alkaline pH; do not added to solution containing
sodium bicarbonate
Aminophyline, phenytoin and sodium bicarbonate can be
administered over a short
period through the same venous catheter.
DOBUTAMINE Dedicated to mykynaocca
Inotropic effect ; increases cardiac output
Decrease peripheral vascular resistance
Less induces tachycardia than dopamine or isoproterenol
Increase renal and mesenteric blood flow by increasing
cardiac output
Combination with Dopamine
INDIKASI :
Pulmonary congestion with low cardiac output
Hypotensive patients with pulmonary congestion
Left ventricular dysfunction that can not tolerate vasodilators

Should be mixed in D5W or normal saline
Dose range : 2 20 microgram/kg/minute
HATI HATI :
May cause tachycardia, arrhythmia, fluctuation in BP
Can provoke myocardial ischemia
MORPHIN SULPHATE Dedicated to mykynaocca
Reduce anxiety
Reduce pain and ischemia
Increase venous capacitance
Decrease systemic vascular resistance
Lead to reduced oxygen demands, less ischemia and
infarct extension
INDIKASI :
o Pain and anxiety associated with AMI
o Acute cardiogenic pulmonary edema
o 1-3 mg, at frequent intervals as often as every 5 min.

o GOAL : eliminate pain
HATI HATI :
Respiratory depressant
Excessive narcosis can be reverse by : Naloxone ( 0.4
0.8 mg )
Hypotension and inappropriate heart rate response
NITROGLYCERIN
Decrease the pain of ischemia
Increase venous dilation
Decrease venous blood return to the heart
Decrease preload and oxygen consumption
Dilates coronary arteries
Increase cardiac collateral flow

Sublingual: 0.3 0.4 mg, repeat every 5 min.
Spray inhaler, repeat every 5 min.
I.V. infusion : 10 20 microgram/min; increase by 5 10
microgram/min every 5 10 min.
Goal : pain relief and lowered blood pressure.
HATI HATI :
Extreme caution if systolic < 90 mmHg.
MAP decreases to 10% if the patient normotensive, 30%
if the patient
hypertensive.
Headache, blood pressure drop, syncope, tachycardia.
Right ventricular infarction
ASPIRIN
Anti-platelet aggregation
Block the formation of thromboxane A2
Reduce overall mortality from acute MI
Reduce nonfatal reinfarction
Reduce nonfatal stroke
KAPAN DIBERIKAN :
As soon as possible !
Standard therapy for all patients with new pain
suggestive of acute M I
Give within minutes of arrival
160 320 mg tablet, as soon as possible
Emergency or pre-hospital
RKP / CPR
CPR
|
pijat jantung 100 x pm
nafas 12 x pm atau
sinkronisasi 15:2
(satu atau dua penolong)
|
pasang monitor ECG
siap DC-shock
| |
VF/VT Asystole / PEA
| |
DC shock CPR terus 3 mnt
DEFIBRILATION
DC shock
Un - Synchronized Synchronized
VF / VT Pulseless AF - SVT
Asystole-withness
kardioversi
PERSIAPAN ALAT / OBAT
1. Mesin DC shock
2. EKG monitor
3. Jelly elektrode
4. Alat / obat resusitasi
5. Oksigen
6. Peralatan suction dengan
kateter suction
Cardiac arrest = carotis (-)

check ECG
VF / VT pulseless = ada gelombang
khas
shockable rhythm, harus segera DC-
shock
Asystole = ECG flat, tak ada

gelombang
UN-shockable
PEA = EMD = ada gelombang mirip

ECG normal
UN-shockable
Asystole (ECG flat)
PEA (ECG ada kompleks tetapi carotis
(-) |
CPR 3 menit
Intubasi, iv line,
adrenalin 1 mg / 3-5 menit
1-1-1 / 1-3-5 mg
|
| |
Asystole / PEA ROSC
( Recovery of
Spontaneous Circulation )
CPR 3 mnt | |
bradycardia normal
atropin 1-1-1 sp 3 mg / obat klasDedicated to mykynaocca
Cardiac arrest =
carotis (-)
Asystole
= ECG flat,
tak ada gelombang
UNshockable
CPR + adrenalin
(+atropin?)
ROSC < 10%
( Recovery of
Spontaneous
Circulation )
PEA =
EMD
ada gelombang mirip ECG
normal
TETAPI nadi carotis tidak teraba
terapi sama seperti Asystole
P-ulseless E-lectro
E-lectrical M-echanical
A-ctivity D-issociation
VT / Ventricular Tachycardia
|
| |
carotis (+) carotis (-)
Lidocain
DC shock
1 mg/kg iv
200 Joules
cepat
VF / VT
pulseless
Bentuk gelombang khas
shockable, harus segera DC-shock
CPR menunggu DC-shock, CPR saja sukar ROSC
DC-shock < 5 mnt bisa mencapai > 50% ROSC
tanpa DC-shock akan memburuk jadi asystole
VT = Ventricular Tachycardia VF = Ventricular Fibrillation

DC shock
1. Switch ON
Oles paddles dengan
jelly ECG tipis rata
Pasang paddles pada

posisi apex
danparasternal
(boleh terbalik)
2. Charge 200 Joules

(Non-synchronized) DC
Perintahkan : shock
Awas semua lepas dari
pasien!
nafas buatan berhenti
sternum
dulu
bawah bebas,
samping bebas, atas apex
bebas, saya bebas!
3. Shock!! siap charge
(tekan dua tombol lagi bila
paddles bersama) irama masih
shockable
Biarkan paddles tetap
DC shock 200
ROSC
Joules
| |
masih VF/VT ROSC
ROSC carotis (+)
| |
200/300 JoulesROSC pertahankan
oksigenasi
| pertahankan
tensi
CPR 1 menit, intubasi,
masih iv line, adrenalin 1 mg
VF/VT
intravena, intra-trachea, intra-osseus
|
RESUME
DC shock 200
CPR 1- menit,
200/300 - 360
Joules intubasi,
iv line, adrenalin 1 mg
ROSC
|
masih VF/VT
ROSC
|
CPR 1 menit, adrenalin 1 mg, obat klas IIa

| | ROSC
Masih
DC shock VF/VT
360 - 360 - 360 Joules
| |
Adrenalin, Atropin, Lidocain,

Vasopresin
Intra-venous
Intra-tracheal / trans-tracheal
dosis 2-3 x intravena
Intra-osseus
TIDAK intra-cardial
menghentikan pijat jantung
sukar pastikan intra-ventrikuler
kena miokard nekrosis
kena a. coronaria infark
DRUGS
adrenalin 1-1-1 / 3-5 menit

atropin 1-1-1 / 3-5 menit
Na-bik hanya 1 mEq/kg dan
paling
akhir
cardiac arrest membandel ???
Hipoksia
4H Hipovolemia
Hiperkalemia
Hipotermia
Tamponade jantung
Tension
4T pneumothorax
Thromboemboli
paru
Toxic overdose
MA B-block, Ca-block
Digitalis, Tricyclic
AD
GAGAL NAFAS
GAGAL NAPAS
Gangguan signifikan kapasitas

perubahan gas dalam sistem respirasi,
bisa merupakan gagal oksigenasi dan
gagal ventilasi (Praveen Kumar).
Suatu keadaan yang mengancam
kehidupan akibat tidak adekuatnya
pengambilan 02 dan pengeluaran CO2.
Ditandai dengan penurunan mendadak
PaO2 < 50 mmHg, dan peningkatan
mendadak
Pa CO2 > 50 mmHg
Klasifikasi Gagal Napas
I. Gagal Napas Tipe I

(Kegagalan oksigenasi, Hipoksia arterial)
tergantung dari tekanan parsial 02 :
1. Tek. Parsial O2 dalam udara respirasi
2. venttilasi per menit
3. Kuantitas darah yang melewati kapiler paru
4. Saturasi O2
5. Difusi membran alveoler
6. Ventilasi-perfusi
PaO2 < 60 mmHg
Penyebab gagal napas tipe I :

- ARDS
- Asma
- Udema Paru
- COPD
- Fibrosis intersisial
- Pneumonia
- Pneumothoraks
- Emboli Paru
- Hipertensi Pulmonal
II. Gagal Napas Tipe II
Kegagalan Ventilasi = Hiperkapnia arteri
Peningkatan tekanan parsial CO2 dalam darah arteri (Pa CO2 > 46
mmHg)
Penyebab gagal napas tipe II :

- Infark / perdarahan batang otak
- Miastenia gravis
- SGB
- Multiple sklerosis
- Flail Chest
- Amiotropik lateralis sklerosis
Gagal Napas Tipe III

Kombinasi kegagalan oksigenasi dan kegagalan ventilasi (= kombinasi
hipoksemia dan
hiperkarbia, PaO2 menurun dan PaCO2 menigkat).
Peningkatan perbedaan PAO2 PaO2
Penyebab :
1. ARDS
2. Asma
3. COPD
oo
VENTILATOR
Ventilator ~ ventilasi
Ventilasi = keluar masuknya udara dari atmosfer ke alveolus
Ventilator = menghantarkan (delivery) udara
udara/gas
/gas TEKANAN
POSITIF ke dalam paru
Ventilasi semenit = TV x RR (frekuensi
(frekuensi nafas)
nafas )
TV = 5-7 cc/kgBB
cc/ kgBB
RR = 10 12 kali/menit
kali/ menit
Compliance = Pengukuran dari elastisitas paru dan dinding

dada
Nilai compliance mengekspresikan adanya perubahan volume
akibat perubahan dari tekanan (pressure)
Compliance rendah = Stiff lung - edema paru
paru,, efusi pleura,
obstruksi,, distensi abdomen dan pneumotoraks
obstruksi
Compliance tinggi = penurunan elastisitas resistensi pada inspirasi
dan penurunan kemampuan mengeluarkan udara waktu ekspirasi
(COPD)
Kriteria tradisional untuk bantuan ventilasi mekanik
PARAMETER INDIKASI VENTILASI NORMAL RANGE
Mekanik (RR) > 35x/m 10-20x/m
TV (cc/kg) <5 5-7
Oksigenasi (PaO2- <60 dg FiO2 0,6 75-100 (air)

mmHg)
P(A-aDO2) mmHg > 350 25-65(FiO2 1.0)
Ventilasi (PaCO2- > 60 35-45
mmHg)
TUJUAN KLINIS / INDIKASI PEMAKAIAN

VENTILASI MEKANIK
GAGAL NAFAS HIPOKSEMIK:
Reverse hypoxemia dgn pemberian PEEP dan konsentrasi O2
tinggi (ARDS,edema paru atau pneumonia akut)
GAGAL NAFAS VENTILASI:
Reverse acute respiratory acidosis
- Koma : trauma kepala, encefalitis, overdosis, CPR
- Trauma med spinalis, polio, motor neuron disease
- Polineuropati, miastenia gravis
- Anesthesia (relaksan u/operasi, tetanus, epilepsi)
STABILISASI DINDING DADA:
Flail chest
MENCEGAH ATAU MENGOBATI ATELEKTASIS
TUJUAN FISIOLOGIS
MEMPERBAIKI VENTILASI ALVEOLAR

MEMPERBAIKI OKSIGENASI ALVEOLAR
(FiO2, FRC,V'A)
MEMBERIKAN PUMP SUPPORT ( ME
WOB)
Consensus conference on mechanical ventilation, Int Care Med 1994,

20:64-79
Indications for
Mechanical Ventilation
Oxygenation abnormalities
Refractory hypoxemia
Need for positive end-
expiratory pressure (PEEP)
Excessive work of
breathing
Types of Ventilator Breaths

Volume-cycled breath
Volume breath
Preset tidal volume
Time-cycled breath
Pressure control breath
Constant pressure for preset time
Flow-cycled breath
Pressure support breath
Constant pressure during inspiration
Modes of Mechanical
Ventilation
Consider trial of NPPV

Determine patient needs
Goals of mechanical ventilation
Adequate ventilation and
oxygenation
Decreased work of breathing
Patient comfort and synchrony
SPONTANEUS
SPONTANEUS VENTILATION
VENTILATION
Continuous
Continuous Positive
Positive Airway
Airway Pressure
Pressure
(CPAP)
(CPAP)
No
No machine
machine breaths
breaths delivered
delivered
Allows
Allows spontaneous
spontaneous breathing
breathing atat elevated
elevated baseline
baseline
pressure
pressure
Patient
Patient controls
controls rate
rate and
and tidal
tidal volume
volume
Assist-Control
Assist-Control Dedicated to mykynaocca
Ventilation
Volume
Volume or
or time-cycled
time-cycled breaths
breaths + + minimal
minimal ventilator
ventilator rate
rate
Additional
Additional breaths
breaths delivered
delivered with
with inspiratory
inspiratory effort
effort
Advantages:
Advantages: reduced
reduced work
work ofof breathing;
breathing; allows
allows patient
patient
to
to modify
modify minute
minute ventilation
ventilation
Disadvantages:
Disadvantages: potential
potential adverse
adverse hemodynamic
hemodynamic effects
effects
or
or inappropriate
inappropriate hyperventilation
hyperventilation
Pressure-Support
Pressure-Support
Ventilation
Ventilation
Pressure assist during spontaneous inspiration with flow-cycled
breath
Pressure assist continues until inspiratory effort decreases
Delivered tidal volume dependent on inspiratory effort and
resistance/compliance of
lung/thorax
Pressure-Support Ventilation
Potential
Potential advantages
advantages
Patient
Patient comfort
comfort
Decreased
Decreased work
work of
of breathing
breathing
May
May enhance
enhance patient-ventilator
patient-ventilator synchrony
synchrony
Used
Used with
with SIMV
SIMV to
to support
support spontaneous
spontaneous breaths
breaths
Pressure-Support Ventilation
Potential
Potential disadvantages
disadvantages
Variable
Variable tidal
tidal volume
volume ifif pulmonary
pulmonary resistance/compliance
resistance/compliance
changes
changes rapidly
rapidly
If
If sole
sole mode
mode of
of ventilation,
ventilation, apnea
apnea alarm
alarm mode
mode may
may be
be only
only
backup
backup
Gas
Gas leak
leak from
from circuit
circuit may
may interfere
interfere with
with cycling
cycling
Synchronized Intermittent Mandatory Ventilation (SIMV)
Volume
Volume oror time-cycled
time-cycled breaths
breaths at
at a
a preset
preset rate
rate
Additional
Additional spontaneous
spontaneous breaths
breaths at
at tidal
tidal volume
volume and
and
rate
rate determined
determined byby patient
patient
Used
Used with
with pressure
pressure support
support
Potential
Potential advantages
advantages
More
More comfortable
comfortable for
for some
some patients
patients
Less
Less hemodynamic
hemodynamic effects
effects
Potential
Potential disadvantages
disadvantages
Increased
Increased work
work of
of breathing
breathing
ntrolled Mechanical Ventilation
Preset rate with volume or time-cycled breaths
No patient interaction with ventilator
Advantages: rests muscles of respiration
Disadvantages: requires sedation/neuro-muscular
blockade, potential adverse hemodynamic effects
piratory Plateau Pressure (IPP)
Airway pressure measured at end of inspiration with no gas

flow present
Estimates alveolar pressure at end-inspiration
Indirect indicator of alveolar distension
High inspiratory plateau pressure
- Barotrauma
- Volutrauma
- Decreased cardiac output
Methods to decrease IPP
- Decrease PEEP
- Decrease tidal volume
Inspiratory Time: Expiratory Time Relationship (I:E ratio)
Spontaneous
Spontaneous breathing
breathing I:E
I:E =
= 1:2
1:2
Inspiratory
Inspiratory time
time determinants
determinants with
with volume
volume breaths
breaths
Tidal
Tidal volume
volume
Gas
Gas flow
flow rate
rate
Respiratory
Respiratory rate
rate
Inspiratory
Inspiratory pause
pause
Expiratory
Expiratory time
time passively
passively determined
determined
I:E Ratio during Mechanical Ventilation
Expiratory
Expiratory time
time too
too short
short for
for exhalation
exhalation
Breath
Breath stacking
stacking
Auto-PEEP
Auto-PEEP
Reduce
Reduce auto-PEEP
auto-PEEP by by shortening
shortening inspiratory
inspiratory time
time
Decrease
Decrease respiratory
respiratory rate
rate
Decrease
Decrease tidal
tidal volume
volume
Increase
Increase gas
gas flow
flow rate
rate
Permissive
Hypercapnia
Acceptance
Acceptance of
of an
an elevated
elevated PaCO
PaCO22,, e.g.,
e.g., lower
lower tidal
tidal volume
volume
to
to reduce
reduce peak
peak airway
airway pressure
pressure
Contraindicated
Contraindicated with
with increased
increased intracranial
intracranial pressure
pressure
Consider
Consider in
in severe
severe asthma
asthma and
and ARDS
ARDS
Critical
Critical care
care consultation
consultation advised
advised
Auto-PEEP
Auto-PEEP
Can
Can be
be measured
measured on on some
some ventilators
ventilators
Increases
Increases peak,
peak, plateau,
plateau, and
and mean
mean airway
airway pressures
pressures
Potential
Potential harmful
harmful physiologic
physiologic effects
effects

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HANDBOOK

YANG TERMASUK SKA : APTS, NSTEMI

APS atau STEMI

Nyeri > 20 menit : sudah sebabkan infark .

POLA EVOLUTIF EKG pada Infark :

ST Elevasi : hrsnya smkn menurun

- Ditegakkan jika memenuhi 2 dari 3 kriteria

REFERFUSI : 1. Trombolitik ( Streptokinase )

PTTK : < 1,5 dari standar Heparin

Dapat juga digunakan :

INFUS PUMP + INFUS DRIP

II. Vol infus x fc ttsan ( 20 or 15 ) = tts/ menit

Dosis Heparinisasi dg UFWH :

Infark < 12 jam : TROMBOLITIK dg :

Morfin (untuk AMI anterior)

Infark Inferior ( II,III,aVF) PDA

GAGAL JANTUNG PADA

Fungsi sistolik <

Pre load >

Backward failure After load >

Tabel 1. Pembagian kelas klinik menurut Killip

Kelas klinik Dapatan klinik

KHUSUS : Kontraktil miokard

PENERAPAN : Sesuai Kls Klinik

OBAT KONTRAKTIL MIOKARD

Klp Katekolamin & derivat :

Pre load Lung edem

OBAT PRE LOAD

IMA : after load & Impedance

Klp vasodilator arteri ???

Klp penghmbt aktifitas SRA :

Redistribusi Kongs paru

SINUS TAKIKARDI SVT

AV Block 2 Second Degree

Third Degree Heart Block

Dedicated to mykynaocca Asystole

Terapi : ( versi UPJ )

DENGAN GGG HEMODINAMIK:

Jenis AF : - Paroksismal : tanpa

HEMODINAMIK TERGANGGU : DC SYOK

KONTROL RATE : ( VERSI UPJ )

TERAPI : ( ICU / UPJ )

LIDOKAIN / XYLOCAIN : memperlambat

2. - AV blok derajat II, Mobitz tipe I : P sinus, QRS

MGSO4 utk EKLAMSI

ANTIHIPERTENSI yg srg pd Eklamsi :

GAWAT DARURAT HIPERTENSI

GDH perlu rawat intensif

Viabilitas Perfusi jaringan

MAP ( Mean Arterial Pressure )

o Titrasi, pemantauan, klinik ?

Pilihan utama : Nitroprusid

PENANGANAN GDH ( versi campuran ) :

3 mekanisme agar interstitium & alveolus kering:

A. Infectious pulmonary edema (viral or bacterial)

II. Increased pulmonary capillary pressure.

III. Decreased oncotic pressure

V. Mixed or unknown mechanisms

At begining of the process , when edema is only in the

4. X foto thorax PA dan lateral

Nitroglycerine sublingual tablets atau IV drip

Digoxin (0.25 mg IV lambat) dapat diberikan

Agonis beta-adrenergic inhalasi atau