2

Etiologi Syok
Type Primary Insult Common Causes
HypovolemicDecreased circulating Dehydration,
hemorrhage,
blood vol capilarry leaks
Distributive Vasodilation -> venous Sepsis, anaphylaxis,
pooling -> decreased preload drug
intoxication,
spinal cord injury
Obstructive Obstruction of cardiac Cardiac tamponade,
tension
filling/out flow pneumothoracx,
pulmonary embolus
3

disease,
Cardiogenic Decreased contractility Congenital heart

4
5
6
7
8
9
10
11
12
13
 FASE I: KOMPENSASI
KOMPENSASI TEMPORER

SIMPATIS, SVR, TEKANAN NADI
DISTRIBUSI SELEKTIF ALIRAN DARAH
RETENSI NA & AIR
KLINIS : * TAKHIKARDIA
* GADUH GELISAH
* KULIT PUCAT DINGIN
14
* PENGISIAN KAPILER >>

FASE 2: DEKOMPENSASI
KOMPENSASI MULAI GAGAL
HIPOPERFUSI HIPOKSIA JAR. METAB.
ANAEROBIK GGN.
METAB. SELULER
PELEPASAN MEDIATOR : * VASODILATASI
*
PERMEABILITAS
*
DEPRESI MIOKARD
15
 *
GGN KOAGULASI

16
 KLINIS : TAKHIKARDIA TEKANAN DARAH
TAKIPNU

17
18
19
20
 TATALAKSANA RESUSITASI
SYOK
RESUSITASI AWAL
OKSIGEN 100% + VENTILATORY SUPPORT
PASANG AKSES VASKULER (90 DETIK)
FLUID CHALLENGE (20 ml/kg BB)
SECEPATNYA < 10 MENIT
DPT DIULANGI 2-3 KALI

KRISTALOID/KOLOID

21
PEMANTAUAN AWAL
RESPON THD FLUID CHALLENGE
PANTAU PROD. URIN (KATETER)
STAT. LAB/PENUNJANG

Monitoring
State of consiousness-Glasgow Coma
Scale
Respiratory rate and character

Cardiovascular parameters

Skin and core temperature difference

Pulse rate and volume

Blood pressure
22
Pulse oximetry

Capillary perfusion time
Central venous pressure - should be monitored in

a patient where there has been poor response to

fluid therapy or with established shock.
Urinary output - urine bag, or preferably
catheter; output should be 1-2 ml/kg body
weight

RESUSITASI LANJUT
BILA FLUID CHALLENGE NON
RESPONSIVE
INTUBASI & VENT. MEKANIK
23
 PASANG CVP & LOADING HATI-HATI
KOREKSI EFEK INOTROPIK NEGATIF
Hb < 5 g/dl PRC 10 ml/kg BB (Ht 40-50
vol %)
OBAT INOTROPIK

24
25
26
 Stadium syok septik dan manifestasi
klinis
Stadium Tanda Klinis Gang fisiologis Biokimiawi

Warm Shock perfusi perifer (N)

Smv
O2 hipokarbia
(Hiperdinamik) kulit hangat kering VO2 hopoxia
HR nadi bounding
CO kadar laktat

suhu / (tak stabil) SVR
hiperglikemia
RR , gg. kesadaran

Cold Shock sianosis CO

hipoxia
27
 (Hipodinamik) kulit dingin lembab SVR asidosis
metab
nadi kecil, lemah CVP
koagulopati
HR , Oliguria Smv O2 hipoglikemi
shallow breathing pe kesadaran

TATALAKSANA SYOK SEPTIK

AB BROAD SPECTRUM SESUAI KULTUR
RESUSITASI CAIRAN : KOLOID/KRISTALOID
OBAT INOTROPIK : DOBUTAMIN + DOPAMIN
ISOPRENALIN/ADRENALIN

28

SVR VASODILATASI PERIFER
KOREKSI : - HIPO/HIPERGLIKEMI - ASAM BASA
- ELEKTROLIT
TATALAKSANA SYOK
ANAFILAKTIK
STOP ALERGEN PENYEBAB + ADRENALIN (IM)
AIR WAY & RESPIRATION ADEKUAT
WHEEZING NEBULASI
ADRENALIN/SALBUTAMOL
OBSTRUKSI INTUBASI/SURGICAL AIRWAY

29

SYOK BERLANJUT : KOLOID + INOTROPIK

 SIRKULASI & HEMODINAMIK
VASOPRESOR : ADRENALIN (10 g/kg BB)
FLUID LOADING : KRISTALOID (20 ml/kg BB/IV-IO)
RE ASSESSMENT ABC RESUSITASI
WHEEZING (+) NEBULASI SALBUTAMOL
BILA PERLU (+) HIDROKORTISON (IV)
(+) AMINOPILIN/SALBUTAMOL
DRIP
TATALAKSANA SYOK
KARDIOGENIK
OKSIGENASI ADEKUAT
30
 KOREKSI GGN ASAM BASA & ELEKTROLIT
KURANGI RASA SAKIT & ANSIETAS

ATASI DISRITMIA JANTUNG

KELEBIHAN PRELOAD : DIURETIKA
KONTRAKTILITAS: FLUID CHALLENGE SESUAI
CVP/POAP
OBAT
INOTROPIK (+)

BEBAN AFTERLOAD (SVR ) :
VASODILATOR
KOREKSI PENYEBAB PRIMER
31
Key points in management
Remember BP and pulse are unreliable
indicators in early septic shock
Look for minor degrees of mental
impairment
(anxiety, restlessness)
Do not delay treatment, try to prevent the
onset of hypotension, metabolic acidosis,
and hypoxia
Give adequate fluids early in treatment,
especially colloids

32
 Do not use inotropic agents until the patient
has received adequate fluid therapy
Monitor blood glucose, gases, and pH, and
treat appropriately

33
34