PELATIHAN RESUSITASI

PEDIATRIK TAHAP LANJUT

SYOK

KOMISI RESUSITASI PEDIATRIK

UKK PEDIATRI GAWAT DARURAT IDAI

APRC
 DEFINISI SYOK
SINDROM KLINIS AKIBAT KEGAGALAN SISTEM
SIRKULASI UNTUK MENCUKUPI :

 NUTRISI PASOKAN METABOLISME

 OKSIGEN UTILISASI JARINGAN TUBUH

FASE: KOMPENSASI
DEKOMPENSASI
IREVERSIBEL DEFISIENSI O2 SELULER
 Etiologi Syok

Type Primary Insult Common Causes

Hypovolemic Decreased 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
Cardiogenic Decreased contractility Congenital heart disease,
myocarditis, dysritmia
Dissociative O2 not released from CO poisoning,
hemoglobin methemoglobinemia
 FUNGSI SISTEM SIRKULASI

 JANTUNG CURAH JANTUNG METABOLISME

 PEMB. DARAH ALIRAN DARAH ADEKUAT JARINGAN
 VOL. DARAH O2 DELIVERY

METABOLIT

DO2 = CO x CaO2 ELIMINASI

CaO2 = (1,34 x Hb x sat O2) + (0,003 x PaO2) DI ORGAN
PEMBUANGAN
Pengaturan curah jantung dan tekanan darah

Preload Contractility Afterload

Heart rate Stroke volume

Cardiac output Systemic vascular resistance

Blood pressure
 Distribution of CO & VO2
in a Healthy Resting Normal Subject

% Total AVDO2 % Total

Organ CO vol % VO2
GI tract and liver 24 4.1 25
Skeletal muscle 21 8.0 30
Kidney 19 1.3 7
Brain 13 6.3 20
Skin 9 1.0 2
Heart 4 11.4 11
Other organs 10 3.0 5
Adapted from Wade OL, Bishop JM: Cardiac output and regional blood flow, Oxford, Blackwell, 1962
 Extracel. Fluid Low Output Cardiac Failure Intra vasc. Vol. due to
Volume Pericardial Tamponade Oncotic Pressure
Constrictive Pericarditis Capillary Permeability

CARDIAC OUTPUT

Activation receptor of ventricular & arterial

Non-osmotic Stimulation of Activation of the

Vasopressin Sympathetic Nervous Renin-Angiotensin-
Stimulation System Aldosterone System

RENAL WATER PERIPHERAL & RENAL RENAL SODIUM

RETENTION ARTERIAL VASC. RESISTANCE RETENTION

MAINTENANCE OF EFFECTIVE
ARTERIAL BLOOD VOLUME
 FRANK STARLING`S LAW
5

POSITIVE SYMPATHOMIMETIC
AMINES
INOTROPY
4 XANTHINES
D GLUCAGON
CARDIAC GLYCOSIDES
3
C

2
B
NEGATIVE
INOTROPY HYPOXEMIA
1 ACIDOSIS
A
VOLUME INFUSION HYPOGLYCEMIA
ENDOTOXEMIA
0 5 10 DRUG TOXICITY
CENTRAL VENOUS PRESSURE (Toor)
Oxyhemoglobin saturation The Oxygen-hemoglobin Dissociation Curve

H+
2,3-DPG
CO2
Pi

H+
2,3-DPG
CO2
Pi

PaO2
 Shock

Hypotension

  Preload

Cellular hypoxia

 Intravasculer volume  Myocardial contractility

Anaerobic metabolism

 Membrane permeability

Metabolic by-products:
- lactic acid
- myocardial depressant factor
- endogeneous catecholamines
- adenine nucleotides
 STADIUM SYOK

 KOMPENSASI
 DEKOMPENSASI
 IREVERSIBEL (PRETERMINAL)
PERJALANAN KLINIS BERSIFAT PROGRESIF
 FASE I: KOMPENSASI
 KOMPENSASI TEMPORER
  SIMPATIS,  SVR,  TEKANAN NADI
 DISTRIBUSI SELEKTIF ALIRAN DARAH
  RETENSI NA & AIR
 KLINIS : * TAKHIKARDIA
* GADUH GELISAH
* KULIT PUCAT DINGIN
* PENGISIAN KAPILER >>
 FASE 2: DEKOMPENSASI
 KOMPENSASI MULAI GAGAL
 HIPOPERFUSI  HIPOKSIA JAR.  METAB. ANAEROBIK
 GGN. METAB. SELULER
 PELEPASAN MEDIATOR : * VASODILATASI 
* PERMEABILITAS 
* DEPRESI MIOKARD 
* GGN KOAGULASI 
 KLINIS : TAKHIKARDIA  TEKANAN DARAH 
TAKIPNU  PERFUSI PERIFER 
ASIDOSIS (+) OLIGURI (+)
TINGKAT KESADARAN 
 FASE 3: IREVERSIBEL
 KOMPENSASI GAGAL
 CADANGAN ENERGI TUBUH 
 KERUSAKAN/KEMATIAN SEL  DISFUNGSI ORGAN
MULTIPEL
 KLINIS : * T.D TAK TERUKUR * NADI TAK TERABA
* TINGKAT KESADARAN * ANURIA (+)
* GAGAL MULTI ORGAN
DAN KEMATIAN
 Manifestasi Klinis Syok

Clinical Signs Compensated Uncompensated Irreversible

Blood loss (%) Up to 25 25 - 40 > 40

Heart rate Tachycardia + Tachycardia ++ Tachy/bradycardia

Systolic BP N N or falling Plummeting
Pulse volume N/  +  ++
Capillary refill N/  +  ++
Skin Cool, pale Cold, mottled Cold, deathly pale
Respiratory rate Tachypnoea + Tachypnoea ++ Sighing rsp.
Mental state Mild agitation Lethargic Reacts only to pain
Uncooperative or unresponsive
GANGGUAN PERFUSI PERIFER
 CORE > PERIFER TEMP. ~ > 2O C
 CAPILLARY REFILL >> :
* NAIL BED PRESS
* BLANCHING SKIN TEST
 PRODUKSI URIN 
(N) BAYI = 2 ml/kg/jam
ANAK = 1 ml/kg/jam
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
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
 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
 Pulse oximetry
 RESUSITASI LANJUT
BILA FLUID CHALLENGE NON RESPONSIVE
 INTUBASI & VENT. MEKANIK
 PASANG CVP & LOADING HATI-HATI
 KOREKSI EFEK INOTROPIK NEGATIF
Hb < 5 g/dl  PRC 10 ml/kg BB (Ht 40-50 vol %)
 OBAT INOTROPIK
 PEMANTAUAN LANJUT
 CARI PENYEBAB SYOK (CXR, KONSULTASI)
 EVALUASI FUNGSI SIST. ORGAN LAIN :
 ATN/PRE RENAL FAILURE
 ARDS
 CARDIAC FUNCTION
 GGN. KOAGULASI/DIC
 ORGAN-ORGAN LAIN
 CHILD IN SHOCK

(1) OXYGEN (2) CRYSTALLOID

20 ml/kg)
IMPROVEMENT

NO IMPROVEMENT

NO IMPROVEMENT (3) CRYSTALLOID - INCREASE MABP

(20 ml/kg) - NORMALIZATION HR
- IMPROVED PERFUSION
- URINE OUTPUT > 1 ml/kg/hr
URINARY CATHETER

ESTABLISH CVP ESTABLISH ETIOLOGY,

OBSERVATION

CVP < 5 Torr CVP > 5 Torr

CRYSTALLOID INFUSION NO IMPROVEMENT 1. CORRECT

ACIDOSIS
UNTIL CVP - 5 Torr
2. Co. GLUCOSE

3. INTROPIC
IMPROVEMENT ABG, HT, NaK, GLUC Ca, SUPPORT
SWAN GANZ CATHETER

ESTABLISH ETIOLOGY CO, RAP, PAP, POAP

CONFIRM SOURCE
OF FLUID LOSS
CENTRAL VENOUS PRESSURE
Stop pemberian
Le Veen HH: Surg Gynecol Obstet 1980; 150:139-149
 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

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

MOSF bergantung sistem Koma susai

yang terkena ARDS, CHF, RF jenis
GI bleeding/DIC organ failure
 TATALAKSANA SYOK SEPTIK
 AB BROAD SPECTRUM  SESUAI KULTUR
 RESUSITASI CAIRAN : KOLOID/KRISTALOID
 OBAT INOTROPIK : DOBUTAMIN + DOPAMIN
ISOPRENALIN/ADRENALIN
  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
 SIRKULASI & HEMODINAMIK
 VASO PRESOR : ADRENALIN (10 mg/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
 SYOK BERLANJUT : KOLOID + INOTROPIK
 TATALAKSANA SYOK KARDIOGENIK
 OKSIGENISASI ADEKUAT
 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
 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
 Do not use inotropic agents until the patient has
received adequate fluid therapy
 Monitor blood glucose, gases, and pH, and treat
appropriately
 SEQUENCE OF THERAPEUTIC MANEUVERS (VIPPS)

Priority Mnemonic Therapy Purpose

1 V Ventilate Adequate O2&CO2
exchange
2 I Infuse Vascular Access
Blood, fluid &
electrolite balance
3 P Pump Restoration cardiac
performance
4 P Pharmacologic Improved perfusion
by vasoactive agents
5 S Specific/ Medical & surgical
Surgical management of
primary causes