AIRWAY

Volume TIDAL: jumlah udara tiap 1x pernapasan (6-8 cc/kg

BB)
Volume SEMENIT volume tidal x freq napas per menit
(n= 4-6 liter (dewasa)/ menit
>61 = hiperventilasi
<41 = hipoventilasi

PENILAIAN JALAN NAPAS

 Gunakan seluruh indra Distal larynx sampai bronchiolus terminalis

- Lihat : niak dinding dada
- Dengar: dengkur (terhalang otot lidah), kumur PERBEDAAN ANATOMI DEWASA VS ANAK
(benda cair: vomit, blood), stridor
(bengkak/obstruksi ISPA), ronchi, wheezing, tdk
ada samsek (obstruksi total)
- Rasakan aliran udara napas : abnormal chest
movement
 Apakah jalan napas terbuka?
 Lindungi C-spine (tulang leher)

Posisi ideal:

JALAN NAPAS BAGIAN ATAS

Fungsi: SUMBATAN ISPA

 Passage udara Etiologi

 Menghangatkan o Lidah
 Filter o Benda asing
 Melembabkan o Proses radang
 Proteksi (refleks muntah, batuk) Manifestai klinis:
 Bicara  Snoring
 Gurgling
 Stridor

SUMBATAN ISPB

o Rale/crepitation
o Wheezing
o Stridor

TANDA SUMBATAN PD KORBAN SADAR

 Kesulitan bicara (laryngitris, difteri)

 Kesulitan napas
hidung= berakhir di larynx  Korban batuk dengan kuat dengan kedua tangan
memegang leher
 Bila kondisi berlanjut, penderita akan lemas
JALAN NAPAS BAGIAN BAWAH sampai berhenti napas

ETIOLOGI
Px tdk sadar/tdk respon nyeri GCS <9)

 Lidah jatuh ke belakang

 Benda asing
 Trauma leher
TATALAKSANA:
PRINSIP: Buka-bersihkan-pertahankan
BUKA
Teknik manual u/ membuka A (px tdk sadar)=
-modifikasi jaw thrust
-head tilit KI px trauma
-chin lift KI pd tx traumamenekan farynx
-jaw lift  u/ px trauma. Mengurangi mobilitas leher.
Kecurigaan trauma pada servikal (jatuh dari ketinggian,
trauma berat kepala)
BERSIHKAN
-Manual finger swap (bareng dg head tilt chin lift
jawtrust)
-Suction sedot. Tdk boleh>10 detik karena dpt menyedot
udara  resiko hypoxia
PERTAHANKAN
 Oral airway Oropharyngeal tube (OPA/OPT)
- I = px tdk sadar GCS <8
- Ukuran: anak telinga (tragus) sd. Sudut mulut/
angulus mandibula sd simphisis mandibula
- Pemasangan: direct (tounge blade)/indirect(up
sliding)
- KI px reflex muntah tinggi
 Nasal airway Nasopharyngeal tube (NPT)
- Ukuran= 12F-36F
- Komplikasi= epistaksis, aspirasi, hipoksia
- Ujung miring harus sesisi septum nasi
- Ukuran: mengukur diameter pipa px= jari
kelingking px
- u/ kasus sulit di kombinasi dgn OPA
 Laryngeal mask (LMA)
- Backup u/ ET atau u/ oprasi pd pediatrik
Bila butuh kontrol pernapasan dlm waktu lama butuh
ventilatoroperasi
DEFINITIVE AIRWAY
Indikasi= bila prosedur non invasif gagal/tdk dpt dilakukan
(ada trauma maksilofasial berat)
Prosedur non invasif
 Endotracheal tube
- tdk boleh > 5 hari (bila butuh lebih 
trakeostomi)
- Teknik: cek balon, lubrikasi bagian distal,
masukkan entroduser, masukkan ETT dg
laryngoskop, plester ETT dg kuat, kaji status
pernapasan
- Ukuran= (d= 7-8mm) (a= kuku ibu
jari/kelingking/cuping hidung/pita broselow)
 Intubasi endotracheal metode laringoskopik
orotracheal
Indikasi
- Gagal mempertahankan jalan napas
- Gagal oksigenasi/ventilasi
 Manuver sellick (tambahan)
- Penekanan dg jari pd kartilago krikoid
- Cegah = muntah dan distensi lambung
- KI= bilaada cedera tl leher (C Spine)
Prosedur non invasif
 Surgical bila semua cara lain gagal. krikotiroidotomi,
trakeostomi
TATALAKSANA PASIEN SADAR
1. Abdominal thrust (heimlich manuver)
2. Bila collaps pijat jantung (CPR)
BREATHING
 Proses masuk keluarnya udara (oksigen masuk dlm
darah dan keluarmya gas CO2 ke udara bebas dg
adekuat. Dmn perubahan kadar kedua gas tsb (dlm
plasma dan udara bebas) merupakan faktor
penting.
Contoh kasus: tidak sadar, terdengan suara mendengkur,
tdk merespon nyeri, auskultasi terd1engar suara
ronchiseluruh lapang paru. Terlihat retraksi interkosta dan
kesan napas cepat
KOMPONEN  Volume dada mengecil
 Tekanan intrathorakal meningkat
 Batang otak  medula oblongata (disekitar
 Udara pernapasan scr pasif keluar
foramen magnum) ex: fraktur/ disloasi servikal
 Inervasi
 Dinding dada termasuk didalamnya : tl (rusuk
dan dada) dan otot pernapsan
 Jar paru parenkim (cont: penyakit pneumonia)

PERAN OTAK DALAM VENTILASI DIFFUSI

o Pengendali utama ventilasi  Ph cairan otak   pergerakan udara pd alveoli – pulmonary capilary bed
menggenangi batang otak komponen: alveolus// basement membrane (interstitial
o Jd batang otak memegang peran utama space)// capillary wall
Kontrol Ventilasi
A. ALVEOLUS
Kimia mekanik  100jt alveoli @paru
Primary : pH cairan otak  Strech reseptors pd paru  Single cell thickwall
berhubungan dg PaCO2 (herring breurreceptors)  Langsung berhub dg pulmonary capillary
(arterial level of C02) mencegah pengembangan  Pertukaran gas mll diffusi
Secondary: O2 terlarut dlm berlebihan paru
Mekanisme:
darah arteri (Pao2) 
Konsentrasi tinggi  rendah (terus menerus sampai dicapai
hypoxic drive
konsentrasi = SEIMBANG)

B. MEMBRAN BASALIS
 Meliputi = dinding kapiler + alveoli
 Bagian terpenting= INTERSTITIAL SPACE yg
terdapat antara dinding kapiler dan alveoli
 Drainase = via PEMB LYMPHE
INERVASI
Menghubungkan batang otak dengan pernapsan:
 N. Phrenicus  diaphragma (C4-C6)
 N. Spinal thoraca calis  musculus intercostalis
(T1-T12) apabila nyeri dapat menyebabkan takut
napas dan menurunnya fungsi breathing

CHEST WALL C. DINDING KAPILER

 Bila menebal proses difusi akan terganggu
 Menciptakan : negative intrathoracic pressure
 Bila rusak, difusi jg terganggu
- Diaphragma (80%)
- Meningkatkan thoracic diameter PENILAIAN
 Udara masuk ke airway u/ mengisi space udara yg
baru terbentuk 1. KECEPATAN
Normal respiratory rates
INSPIRASI
Adult = 12-20/min Chldren = 18-24/min
 Peningkatan volume intratorakal Infants = 22-36/min Newborn = 40-60/min
 Tekanan negatif
 Dilatasi brochioli 2. IRAMA :
 Udara masuk ke jalan napas/alveoli (kec. Reguler 
Terdapatnya lubang pada dinding dada) bila 1 (inspirasi) : 2 (ekspirasi) = normal
bila 1 (insprasi) : 1 (ekspirasi) =sesak
irreguler
tangan kaku/kejang  fungsi otak tdk spasmefungsi
otak tdk ada
3. KUALITAS
o Pengembangan dada= simetris
o Usaha bernapas= kontraksi otot bantu napas
EKSPIRASI o Bunyi napas= ronchi halus-kasar
 Diaphragma dan musculus intercostalis relax 4. KEDALAMAN
 o Volume tidal = 6-8 cc/kg C. FACE MASK DGN O2 RESERVOIR BAG
o Death space +- 150cc  Konsentrasi O2>60%
o Ventilasi semeit: hypo/hyperventilation  Konsentrasi kira2 10% @liter
 Pada aliran10liter/menit, konsentrasi hampir 100%

TANDA GEJALA PERNAPASAN TIDAK ADEKUAT

 Sesak : bercakap pendek2 (tidak full)

 Laju napas >> atau <<
 Irreguler
 Kualitas: pengembangan rongga dada tidak simetris,
ada suara napastambahan, retraksi D. HIGH FLOW SYSTEM
 Kedalaman : hyper/hypoventilation
 Air entertaiment system
TATALAKSANA  Venturi system
 Enclosuresystem
Bila penderita tdk bernapas / gasping (napas satu2) maka  Fixed FiO2 (WYSWYG)
secpatnya identifikasi sumbatan jalan napas, bila tdk ada
lakukan bantuan pernapasan.

E. VENTURI MASK
 Memberi O2 dlm konsentrasi yg tetap
 Sering digunakan u/ pasien PKKOK Retensi CO2
 Konsentrasi O2 yg ada: 24%, 35%, 40%, 60%, 80%
F. BAG VALVE MASK
Indikasi: ventilasi tdk adekuat
Ukuran bag:
o Bayi= 240ml
o Anak = 500ml
o Dewasa = 1600ml
1. PEMBERIAN OKSIGEN
Aliran O2
A. NASAL CANULA
o 5-10 L/ mnt u/ bayi
 Sist aliran rendah
o 10-15 L/ mnt u/ anak & dewasa
 Konsentrasi O2 KIRA2 4% u/ setiap penambahan 1
liter/menit
 Aliran 1-5 ltr/menit memberikan konsentrasi O2
24-44%

EVALLUATION EFEFFECTIVENESS
B. SIMPLE MASK Bagaimana mengetahui bahwa ventilasi berhasil:
 Aliran O2> 5 Liter / menit
 Dianjurkan aliran 8-10 liter/menit  Chest movement
 Konsentrasi O2 40-60%  Lung sound
 Epigastric sound/ abdominal distention
 Patient response
 o Jantung  mesin pompa

PATOFISIOLOGI

Untuk mencapai aliran volume o2 yg baik yg diikat o/ hb

dan yg larut dlm plasma:

DO2 (Oxygen delivery) = [1.39 x hb x SaO2 + (0.002 X PaO2]

X CO
Hb = eritrosit
SaO2= saturasi O2 (min 92%)
PaO2= tekanan parsial 02
PENENTUAN NAPAS ADEKUAT/TIDAK (n)=900-1000ml/menit
1. Semua px tdk sadar  potensi ancaman usaha Oxygen Consumption
napas adekuat VO2= CO x (Ca O2 – CvO2) x 10
2. Bila korban bernapas  ada distress napas? (frek (n)= 250 ml
napas meningkat, keterlibatan otot pernapasan
berlebih normalnya kontraksi otot tdk terlihat) Keseimbangan supply dan demand
3. Apakah px bs menjawab?  bila sesak,hanya dpt (CaO2 –CvO2) atau C (a-v) O2
menjawabdg kata (n) 4-6ml/dl
4. Napas cepat, dalam, reguler lbh baik dari
Keseimbangan DO2-VO2 = 750 ml  cadangan O2 di
lambat,dangkal, tdk teratur
sirkulasi (vena)
5. Laju pernapasan lambat(<10 x/menit) dan cepat
esktraksi O2 kejaringan (VO2/DO2)= 20-30%
(>30x/menit) telah tjd masalah pd px. Faktor =
sistem pernapasan/komponen lain (jalan Stroke volume= EDV (end diastole volume)= ESV (End
napas/sirkulasi)/kelainan metabolik asidosis (syok)/ systemic volume)
kelainan susunan saraf pusat (n) EDV Dewasa = 20ml
(n) ESV= 50ml

Blood Pressure= Cardiac Output x tahanan perifer

Tambahan:
o Gagal napas:
HYPOXIA (kekurangan 02): membiru
BRADIPNU: RR<12/10, CO2naik, Ph darah turun (asam),
02 blm tentu turun (tdk membiru) biasanya poisoned
o Ph darah normal = 735-745
o RR cepat= tidal volume kecil
o Apabila pasien dg napas tdk adekuat (masih ada
napas) tdak perli resque breathing bantu naikkan
tidal volume saat inspirasi
o Sampai kapan bantuan breathing dilakukan?  sampai
ada napas spontan
o Kapan evaluasi breathing dilakukan? setelah 1 menit
bila ada carotis resque breathing
tidak ada carotis  CPR
SIRKULASI
SISTEM CARDIOVASKULAR:
 kesatuan pembuluh darah, darah dan jantung yg
dibutuhkan u/ tjdnya alran darah spontan dan adekuat
dalam membawa o2 sampai ke sel
Cardiac output= stroke volume x heart rate (nadi)
Nadi (n)= 60-100  Dikontrol sist saraf otonom
Stroke volume dipengaruhi oleh:
 preload= volume akhir diastok  volume pd pem darah
vena
 afterload= tegangan dinding ventrikel pd akhir sistolik
tegangan/tahanan pem darah
[transmural pressure x radius / 2 x wall thickness]
 contractlity
dpt menurun karena = acidosis, hypoxia, hypocalcemia
ditingkatkan dengan= adrenaline/nor adrenaline,
dobutamine/dopamine, calcium
MAP (Mean arterial pressure) = Parameter Kontrol dinamik
MAP= tekanan diastol + ([tekanan sistol-diastol]/3)
MAP= (CO x SVR) + SVP
MAP= CO x SVR
ditentukan oleh= CO,SVR (systemic vascular resistance),
CVP [flow, pressure, resistance]

KOMPONEN

o Pemb darah  pipa (n)= 65mmHg-95mmHg/150 darah bs terdistribusi ke

o Darah/plasma  isi organ2
<65= filtrasi glomerulus meurun anuria  Produksiurin
>150= fungsi sawar darah otak berhenti cerebral  Saturasi O2 darah arteri
autoregulation tdk berfungsi (sel rusak)  Lactate level
 pH mucosa GT(lambung)
Arterial pulse pressure= perubahan terakanan aortamax
selama sistole (saat katub aorta membuka sampai dicapai
TATALAKSANA
tekanan aorta tertinggi)
 fluid hipovolemik
PP (pulse pressure) monitor kecukupan volume  intropes  cardiogenik (adrenalin)
intravaskular  vasokonstriksi
PP= sistole-diastole  vasodilatasi
PP< volume intravaskular kurang
ditentukan oleh: compliance of aorta & stroke volume
makin kaku aorta PP melebar
makin compliant aorta PP menyempit

CVP (Central vein pressure)

CVC (cateter vena central) parameter lbh akura ttpi
invasif didapatkan CVP (Central vein pressure)
(n) CVP= 12-18cmH20/8-12mmHg
bila kurang kurang volume intravaskular tx fluid
(kristaloid 20ml/kgBB atau koloid 10ml/kgBB) Evaluasi
perbaikan:
membaik  cairan selanjutnya dipertimbangkan
memburuk stop bs jd syok cardiogenik

TARGET PARAMETER RESUSITASI PADA JAM PERTAMA

(sampai 6 jam pertama)

1. A (Airway)= dijamin bebas/paten

2. B (Breathing)= bantuan napas sampai ventilator
datang
3. C (Circulation)
 Evaluasi volume intravaskular
(CVP=8-12mmHg)
 MAP=65mmHg-95mmHg
 Saturasi O2 (SaO2>95%, min 92%)
 Dukungan obat2an bersifat inotropik, kronotropik,
vasoaktif
 Nadi= <120x/menit
 SaO2 pd vena sentral 70-75%  bila tdk
pertimbangkan transfusi sampai Hb 10gr/dL

TANDA GAGAL SIRKULASI:

 Pompa: pulsus alternan, suara gallop, ronchi basal

basah, peningkatan tekanan vena jugularis,
penurunan MAP
 Isi pompa (defisit): tanda2 dehidrasi, CRT > 2 dtk,
prosuksi urin turun, PP<<isi pipa (overload):
distensi vena leher, ronchi
 Pipa: edema, ascites (ada cairan di perut), akral
dingin
Ronchi cairan paru keluar

EVALUASI KLINIS PERFUSI JARINGAN

 Tingkat kesadaran
 Temperatur extremitas/akral
 Absence of extreme takikardi
 Absence of extreme hyppotensi
SHOCK AND FLUID RESUSCITATION
 shock= clinical expression of circulatory failure that
result in inadequate cellular o2 utilization
 diagnosis based on: clinical, hemodynamic, and
biochemical signs
 Kondisi dmn perfusi jar dan organ tdk adekuat yg
mengarah pd suatu keadaan hipoperfusi dan
hipoksia seluler yang berakhir dg semua gejala sisa

COMPENSATED SHOCK (SIGN)

 kutan skin is cold and clammy, with
vasoconstriction and sianosis= low flowstates)
 renal (urin output <0,5 ml/kg/hour)  caused by
hypovolemia, hypoxia, and circulating
catecholamines
 Weakened peripheral pulses
 Weakness and lightheadedness
 takikardi  MAP <70 mmHg caused by the
effect od catecholamines on the heart as the brain
increases the activity of SNS
 Hyperlactatemia  abnormal cellular o2
metabolisme (>1.5 mmol/liter)  kondisi akut KLASIFIKASI
 Pucat (pallor)  caused by catecholamine induced 1. HYPOVOLEMIK
vasoconstrction and/loss of circulating RBC - Paling sering dijumpai  semua shock awalnya
 Diaphoresis (sweating) effect of catecholamines diterapi seperti hipovolemik sampai dibuktikan
on sweat glands tidak
 Thirst  caused by hypovolemia (low fluid amount - Evaluasi dilakukan bersamaan dg tatalaksana
in blood vessels) - Hipotensi sering menyertai syok, normotensi bisa
 Tachypnea (elevated respiratory rate) disertai syok  syok tingkat sel (bila px dlm
keadaan normal punya hipertensi)
Semua hal di atas adalah kompensasi tubuh menghadapi 2. CARDIOGENIC
shock tahap selanjutnya adalah  HIPOTENSI tubuh tdk 3. OBSTRUCTION
bs mantain perfusi  kondisi shock decompensated  Tanda: low CO, hence, inadekuat trasport O2
4. DISTRIBUTIVE SEPTIK & ANAFILAKTIK
DECOMPENSATED SHOCK (SIGN)
 Menurunnya systemic vascular resistance, altered
 Hypotensi  caused byhypovolemia O2 extraction
 Altered mental status (confusion, restlessness,
unconciousness)  caused by decreases cerebral
perfusion
 Cardiac arrest  caused by critical organ failure to
blood/fluid loss

HIPOPERFUSI

CLINICAL SIGN OF ACUTE HEMORRHAGIC SHOCK


EARLY SHOCK
 Loss= 15%-25% of blood volume
 Moderate takikardi, pallor, narrowed pulse pressure,
thirst, weakness, delayed capillary refill
 Body still compensating
LATE SHOCK
 Loss = 30%-45% of blood
 Hypotensi first sign of late shock
 Body’s ability to compensate the physical insult has
failed
 Aggresive assessment must be provided
CARA MENGENALI SHOCK
INITAL APPROACH TO PATIENT IN SHOCK
 Early  adekuat hemodynamic support
 Identifikasi  perbaiki sebab
 Resusitasi VIP rule
Ventilate (oxyen administration)
- Segera, menghindari pulmonary hypertension
Infuse (fluid resuscitation)
- Improve microvascular blood flow and increase
CO (termasuk u/ px cardiogenik)
- Used to determine a patient actual responce to
fluid, limiting adverse effect
- 4 component fluid challange tets:
1. Type of fluid must be selected
2. The rate of fluid administration must me
defines  300-500ml/20-30 menit
3. Object increase in systemic arterial
pressure/decrease in heart rate/increase
urine output
4. The safety limited measurement of CVP,
diameter IVC with USG
- Can be repeated as required, STOP in case non
response (avoid fluid overload)
Pump (administration pf vasoactive agent)
TIPS KHUSUS:
 Semua px shock harus dirujuk ke RS
 Waspada gejala samar pd px geriatri dan
pediatri
GOALS OF HEMODYNAMIC SUPPORT
 Restoring MAP (65-70mmhg
 SCVO2 MIN 70% 6 jam pertama
 Lactat level turun 20%
VASOACTIVE AGENTS
 Vasopressor= norepinephrine (FIRSTCHOICE)
Dose: 0,1-0,2 mikrogrm/kg/minute
 Intropic agent= dobutamine, phosphodiesterase type
III inhibitor (milrionone, enoximone, combie inotropic
+ vasodilating)
 Vasodilator agent = nitrate
May increase CO withput myocardial demand for O2
MECHANCAL SUPPORT
 Intraaortic balloon counterpulsaton (IABC) 
reduce left ventricular afterload & increase
coronary blood flow (non beneficial in cardiogenic
shock)
 Venoarterial extracorporeal membrane
oxygenation (ECMO)  used as temporary life
saving in patient witj reversible cardiogenci shock/
as bridge to heart transplantation
GOAL OF TREATMENT
APPROPRIATE TREATMENT:
Hemodynamic stabilization
Fluid infusion
Administration of vasoactive agent
SYOK (tambahan)
TATALAKSANA
 Rawat di area critical care,bila ragu kerjakan tilt test
(hipotensi orthodontik)
 Kontrol jalan napas beri o2 100% (dg masker non
breathing)
 Pasang 2 jalur intravena dg jarum besar pd fossa
antecubiti u/ shock hipovolemik
 Beri kristaloid min 1 liter diinfuskan dlm 1 jam 
evaluasi (pulse oximetry,ECG, non invasive blood
pressure)lebih lanjut = koloid/whole blood
 Pasang kateter urin
 Kultur darah
 Antibiotik
LAB
 DL, urea/elektrolit/creatinin
 Troponin T dan enzim jantung
 Faal hemostasis dg screening DIC
 Chest X ray
 EKG
CATATAN LAB
 Hematokrit (Hct) adalah tes yg paling tidak reliable 
nilai bs normal di fase awal, peningkatan bs tjdpd px
minum alkohol akut krn diuretik
 Hitung neutrofil absolute tdk spesifikdan sensitive
pd syok septik  bs jd meningkat/normal/rendah
 Setelah evaluasi,support dg obat inotropik u/ menjaga
tekanan darah
- IV dopamine 5-10mikrogram/kg/min
- IV dobutamine 5-10  khususnya u/ cardiogenik
- IV norephinephrine  titrasi sampai dapatkan
efek yg diinginkan
SHOCK (DR YUDI)
PRINCIPLES:
 Maintain airway
 Maintain oxygenation and ventilation
 Control bleeding where possible
 Maintain circulation  adequate heart rate &
intravaskular volume
TREATMENT MANAGEMENT
 Drug first choice  adrenaline (short term) has
inptropic and vasocontrictor effect
 Monitor BP with arterial line
 Adrenaline infused va central venous catheter
 Adrenaline 6mg diluted in 100ml dextrose 5% and run
initially at 3-10ml/hr
HEMORRHAGIC SHOCK
 Adekuat ventilasi/oksigenasi
 Control hemorrhage (isotonic kristaloid solution (10-
20ml/kg)
 Red blood cell infusion (5-10ml/kg)
 Px trauma (GCS<9)  PRBC
CARDIOGENIK SHOCK
 Oksigen
 Vasopresor dan inotropik support  norephinephine
(0.5 mg/min) & dobutamne (5mg/kg/min)
 Consider intra-aortic balloon pump
counterpulsation u/ shock refractory
SEPTIC SHOCK
 Oksigenasi
 Kristaloid 20ml/kg & titrate infusion
 Antimikrobial terapi  drainase
surgical/debridemen
 PRBC infusion u/ hb <8g/dl
 Bila masih gagal 
 vasopresor = dopamine 5-15mg/kg/min atau
norephinephrine 0.5mg/min
ANAPHYLAXIS SHOCK
 severe, life threatning, generalised or systemic
hypersensitivity reaction
 systemic reaction of multiple orga system to antigen
induced igE-mediated immunologic mediator release
in previously sensitized individual
 manifestasi: respratory distress, laryngeal edema
(berbahaya), brochospasme, vascular collapse
 di kutan: urtikaria, pruritus
 di GIT: nausea, vomit, cramp, diarrhea
ALLERGIC REACTION
ANTIGENinduced antibody formation
antigens enter body by injection,ingestion, inhalation,
absorption
MAST CELL
- in all subcutaneous/submukosal tissue
- include= conjunctiva, upper/lower repiratory, gut
BASOPHILS
-circulated in blood
HISTAMIN
- three types:
H1= act on H1 receptors to cause
- smooth muscle contraction
- increased vascular permeability
- prostaglandin generation
H2= to cause
- increased vascular permeability
-gastric acid secretion
-stimulation of suppressor lymphocytes
-decreased PMN enzym release
-release of more histamine from mast cells and basophils
H3= to cause Methylprednisolone 125mg IV
-inhibition of central, peripheral nervous system transport
neurotransmiter release 3. SEVERE (ANAPHYLAXIS)
-inhibition of further histamine formation release  Mild + moderate + shock/hipoperfusi
 Tx:
PATOFISIOLOGI
 AB: High cons O2// Ventulation, ETT
antigen enters body antibody produced attach to
Concider inhaled beta agonists
surface of mast or basofil cells mast cells become
 C large bore IV NS X 2
sensitized
Titrate fluid to perfusion w/ bolus therapy// ECG
antigen reenters bodyattach to antibodies on mast or
monitor
basophil cells mast cell degranulates, release (histamin,
 Treat as pre arrest patient
leukotrienes, SRS-A, ECF)
 Epinephrine 0.5-1 mg 1:10.000 IV prn
VASODILATION Hipotensi unresponsive to fluid and epinephrine 
dopamine 10mcg/kg/min
 Decreased peripheral vascular resistance Broncoconstriction unresponsive to epi
 Hypotensi aminophylline
 Takikardi  Diphenhydramine 50mg IV
 Peripheral hipoperfusi  Methylprednisolone 125 mg Iv
 Consider MAST if unresponsive to fluid
INCREASED CAPILLARY PERMEABILITY
 Rapid trasnport
 Tissue edema, urtikari, itch
OBSERVED 6-8 HOURS!
 Layrnx edema
 Fluid leakage from vascular space hypovolemik TRIGGERS
shock
 lactam antibiotik  sering
SMOOTH MUSCLE SPASM  hymoneptera stings
 drugs  muscle relaxant,antibiotik, NSAID, aspirin,
Bronchospasme respiratory distress, tight chest,
beta blockers, adrenal insufficiency
wheezing
 food allergy nuts
GI Tract spasme nausea, vomit, cramp,diarrhea
 latex hypersensitivity
Bladder spasmurinary urgency, urinary incontinence
 idopathic  non igE mediated
ANAPHYLACTIC REACTION
DIAGNOSIS
Leukotrienes
 riwayat alergi, atopi, atau asma
 Potent bronchoconstriction, increased vascular
 klinial: tanda dan gejala
permeability, coronary vasokonstriksi
 leukosit suspension
 Slower onset than histamin
 igE
 Last longer than histamin
 Elevation of tryptase level in serum
ALLERGIC REACTION
CLINICAL MANIFESTATION
1. MILD
 Urtikari, eritema, rhinitis, conjunctivitis, mild  First manifestation skin (pruritus, eritema, urtikari)
bronchoconstriction, usually localized, NO  Respiratory  cough, chest tightness, dyspnea dll
SOB/hipotensi/hipoperfusi, self treated  Other lightheadedness, nasal congestion, cramp dll
 Tx:  Physical urtikari, angiodema,rhinitis, takipnea,
often at home. Diphenhydramine 25-50mg PO/IM takikardi, hipotensi, laryng stridor, hipersalivasi,
may consider cimetdine/rantidin, prednisone, hoarseness
inhaled beta-angonist ABC PROBLEM
2. MODERATE
 Mild symptiom + Dyspnea (wheezes), AIRWAY
angioneurotic edema, systemic (not localized), NO
 Airway swelling,throat,tongue swelling
hopotensi/hipeperfusi
(pharynx/larynx oedem)
 Tx:
 Difficult breathing andswallow
High flow O2
IV NS  titrated to systolic BP 90mmhg  Hoarse voice
ECG Monitor  Stridor  upper airway obstruction
Beta agonists BREATHING
Diphenhydramine 25-50mg IM/IV
  Shortness breath  increase RR ADRENALINE (EPINEPHRINE)
 Tired
 Use to: ease breathing difficulty, restore adequate CO,
 Confusion by hypoxia
Reduce oedem, Dilates bronchial airways
 Sianosis blue
 Workbest but its not without risk  terutama u/
 Respiratory arrest
Intravena (IM jarang)
CIRCULATION
IM ADRENALINE
 Pale, clammy
 Monitor response to adrenaline  pulse,BP, ECG,
 Takikardi
pulse oximetri
 Hypotension, faint, dizzy,collapse
 Benefit:
 Kesadaran turun
- Greater margin of safety
 Myocardial iskemik
- Dont required IV access
 Cardiac arrest
- IM route easier to learn
TATALAKSANA  Best site: antrolateral aspcet of the middle third of the
depends on: tigh
 Subcutaneous route not recommended less
1. Location effective
- Out of hospital  call ambulance  Repeat if there is no improvement  5 minutes
2. Training and skills of rescuers intervals
3. Number of responders
- Single  ensure that help is coming
- Several action takens simultaneously
4. Equipment and drugs available
- Resucitation equipment and drugs
- Monitoring : pulse oximetry, non invasive blood
pressure, 3-lead ECG

PATIENT SELF MANAGEMENT:

 Benadryl 50mg p.o INTRAVENOUS ADRENALINE (specialist only)

 Sign anaphylaxis subkutan ephinephrine  Greater risk in px with spontaneous circulation 
 If short breath/wheezing use aerosolized hypertensi, takikardi, arrhytmia, myocardial iskemik
epinephrine  Monitoring
 Diluted 1:10.000
PENANGANAN MINIMUM:
AUTOINJCETOR ADRENALINE
 Early recognation
 Call for help  Given to px with risk
 Initial assessment based on ABCD  Dose: 0.15 and 0.3mg
 Adrenaline therapy (if indicated)
 Investigaton and followup FLUIDS (GIVE ASAP)

 If there is IV access infuse fluid ASAP

1. Patient positoning  Rapid IV fluid challange = 20ml/kg (child) / 0.5-1L
 Sit up px w/ breathing prob (adult) kristaloid/hartmann/saline
 Lying flat/ without leg elevaton  low BP /  If IV imposible  intraosseous route
circulation prob
 If px faint  dont sit / stand them cause ANTIHISTAMIN (after initial resuscitation)
cardiac arrest
 H1 antihistamin  clorphenamine slowly IV/IM
 Pregnant lie on left side
 Dose:
2. Remove triggers
 Stop drugs suspected (IV infusion, gelatin
solution, antibiotik), Stinger, Food induced
 Dont delaydefnitive treatment if removing
triggers is not feasible
 Cardiorespiratory arrest following  CPR  STEROID
ensure help coming  use adrenalin  IM
 Corticosteroid shorten protracted reaction
route for adenaline not recommend after
 Inject hydrocortisone IM/IV
cardiac arrest occured
 Dose:
BRONCHODILATOR

 Salbutamol (inhaled/IV)
 Ipratropium (inhaled)
 Aminophylline (IV)
 Magnesium (IV)

CARDIAC DRUGS

 Glucagon for px taking beta blocker

 Atropine  px severe brakikardi after anafilaksis

INVESTIGATION EG, ECG, Chest Xray, urea/elektrolit,

ABG

MAST CELL TRYPTASE

 Anaphylaksis  increased tryptase

 Significantly after 30 min/more, peak 1-2 hour after
onset
 Back to normal= 6-8 jam
 Min: 1 sample at 1-2 hours after symptom
(ideal = 3x)

DISCHARGE FROM HOSPITAL

 Observation 24jam
PERAN CAIRAN PADA RESUSITASI PERIOPERATIF
PraOperatif  resusitasi/stabiltasi, obat
BODY WATER Operasi
Pasca Operasi resusitasi, obat,nutrsi

MACAM CAIRAN:

1. Non elektrolit glukosa 5%/dextrose 5%--> tdk bs

diberikan banyak
2. Elektrolit RL, PZ, KAEN, Asering dll
3. Koloid dextran, HES, Gelatin, darah, albumin
4. Resusitasi RL, NS, Ringer acetat

COMPOSTION OF FLUID MAINTENANCE

A. Jumlah cairan
dewasa = 500cc/kgBB/24 jam
Anak = 10 kg I ------- 1000cc/KgBB/24jam
10 kg II ------- 50cc/kg BB/24 jam
> ------- 20cc/kgBB/24 jam
B. Tetesan/menit
C. Macam cairan
---(kebutuhan)--- Na+---- 3-5 meq/kgBB/24 jam

CONTOH

ISOTONIC INFUSION

HYPOTONIC INFUSION

HYPERTONIC INFUSION

TATALAKSANA
Dehidrasi  def cairan  hypoxia sel ATP turun
 rehidrasi  evaluasi (nadi, tensi, urine, warna,jumlah)
 CAIRAN U/ MEMASUKKAN OBAT

 Pemberian berulang
 Syarat:
- Cairan harus mengalir  pelan2 
thrombus/embolus (-)
- Tetesan/menit asal menetes
- Cairan elektrolit/non
- Pemberian pada vena besar

MAX HENTI JANTUNG = 4 MENIT  kerusakan otak

permanen
SYOK HIPOVOLEMIK
Hipoxia sel + gangguan perfusi
kompensasi tubuh:
- RAA sistem (vasokonstriksi perifer)
CPR
- Kulit/akral dingin  Jantung berhenti  BLS
- Dingin/basah (keringat)  Henti jantung 4 menit  kerusakan permanen otak
Tensi rendah, nadi cepat kecil
URUTAN BLS MENURUT AHA
Resusitasi:
Airway
- Cairan elektrolit grojok, evaluasi
Breathing look (dinding dada), listen (suara napas), feel
- N, RR, Akral
(hembusan napas)
- Kesadaran
Circulation  meraba nadi karotis
- Produksi urine
Namun 2010 dirubah mjd CAB (u/ korban serangan
PATOGENESIS
jantung koroner)
Perdarahan  hipovolume  o2 sel turun syok
5 RANTAI KEHIDUPAN AHA (CHAIN OF SURVIVAL)
Masalah:
1. Secepatnya mengenal px henti jantung dan hub
 awal jumlah cairan intravaskular berkurang ambulan 118
 jumlah cairan ntersisiel dan intrasel tetap, blm 2. Lakukan prosedur RJPO kualitas tinggi (high quality
mengisi intravaskular CPR)
 kesan, hb tetap, karena blm dilusI 3. Lakukan terapi kejut listrik (rapid defibrilation)
 tx resusitasi = mengisi cairan intravaskuler 4. Pertolongan kegawatan jantung dan pemb darah
(kalo pake RL 1cc darah = 3-4 cc RL) tingkat lanjut (advanced) segera dimulai dalam
ambulan
PERLU DIINGAT 5. Manajemen perawatan penderita setelah kembali
ke sirkulasi spontan (intergrated post cardiac
1. Volume darah efektif (Effective blood flow [EBV])
arrest care) yang terntegrasi
Laki2 70-75cc/kgbb
Wanita 60-65 cc/kgbb
Anak 90-100 cc/kgbb
2. 15% EBV/F hilang  hypoxia +  nadi meningkat
3. 25% EBV/F hilang hipotensi

CONTOH: PROSEDUR RJP (1 PENOLONG DEWASA)

1. SAFE AND RESPON

- Periksa daerah sekitar (aman)
- Periksa kesadaran (tanya)
- Bila tdk sadar  langkah 2
2. AKTIFKAN EMS
- Minta org hub 119 (ambulan) dan suruh bawa
AED
- Periksa karotis. Tidak teraba  cardiac arrest
(henti jantung)
3. KOMPRESI DADA
 - Lakukan kompresi dada u/ memulai RJPO.
Rasio kompresi: ventilasi (30:2) tiap siklus, dan
dilakukan 5 siklus. Stop dan cek karotis
- Bila bl teraba  RJPO 5 siklus lagi cek nadi
LANDMARK
- Stop RJP, periksa pernapasan 3M (merasakan,
mendengarkan, melihat). Bila negatif (blm napas),
berikan bantuan napas.
- Buka jalan napas (headtilt chin lift), mulai rescue
breathing 8-10 tiup per menit

5. RESCUE BREATHING
- 8-10 tiupan per menit dg berhitung sbb: tiupan
pertama , hitung satu ribu –enam ribu
- Setelah 10 tiupan, evaluasi nadi dan 3M
bersamaan
- Bila adekuat stop rescue breathing

6. POSISI RECOVERY
Observasi sampai ambulan datang
POSTUR
RJP SISANYA BACA BPSL AJAYAA REK :’)

HAND POSITION AND POSTURE:

- Dominant hand over the center of the px’s chest
corrspond to the lower half sternum
- Heel of the hand in the midline and aligned w/ the
long axis of sternumfocuses the compressive force
on sternum & decrease chance rib fracture
- Place non dominant hand on top of the first hand
both hand are overlapped and paralel
- Finger should be elevated off the px’s ribs min
compressive force over the ribs & avoid compressive
force over xiphisternum or upper abdomen (min
iatrogenic injury)

KAPAN STOP:

- Nadi adekuat
- Penolong lelah
- Ambulan datang menggantikan
- Empiris RJPO 20-30 menit, tiap 5 siklus cek nadi

4. NADI TERABA