PELATIHAN RESUSITASI

PEDIATRIK TAHAP LANJUT

SYOK

KOMISI RESUSITASI PEDIATRIK

UKK PEDIATRI GAWAT DARURAT IDAI

APRC 1
 DEFINISI SYOK
 
SINDROM KLINIS AKIBAT KEGAGALAN SISTEM
SIRKULASI UNTUK MENCUKUPI :
 
 NUTRISI PASOKAN METABOLISME
 OKSIGEN UTILISASI JARINGAN
TUBUH
 
FASE: KOMPENSASI
DEKOMPENSASI
IREVERSIBEL DEFISIENSI O2
SELULER 2
 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
3
Cardiogenic Decreased contractility Congenital heart
 FUNGSI SISTEM SIRKULASI
 
 JANTUNG CURAH JANTUNG
METABOLISME
 PEMB. DARAH ALIRAN DARAH ADEKUAT
JARINGAN
 VOL. DARAH O2 DELIVERY
 

METABOLIT
2 = CO x CaO2
O2   = (1,34 x Hb x sat O2) + (0,003 x PaO2)
4
Pengaturan curah jantung dan tekanan darah

Preload Contractility
Afterload

 
 
Heart rate Stroke volume

 
 
Cardiac output Systemic vascular resistance

 
5
Blood pressure
6
 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
7
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 8

RENAL SODIUM
 FRANK STARLING`S LAW
5

POSITIVE SYMPATHOMIMETIC
AMINES
INOTROPY
4 XANTHINES
STROKE VOLUME

D GLUCAGON
CARDIAC GLYCOSIDES
3
C

B
2
NEGATIVE
INOTROPY HYPOXEMIA
1
A ACIDOSIS
VOLUME HYPOGLYCEMIA
INFUSION ENDOTOXEMIA
0 5 10 DRUG TOXICITY
9
CENTRAL VENOUS PRESSURE (Toor)
 The Oxygen-hemoglobin Dissociation Curve
Oxyhemoglobin saturation

H+
2,3-DPG
CO2
Pi

H+
2,3-DPG
CO2
Pi

PaO2 10
 Shock

Hypotension

 Preload

Cellular hypoxia

 Intravasculer volume  Myocardial contractility

Anaerobic metabolism

 Membrane permeability

Metabolic by-
products:
- lactic acid
- myocardial
11
depressant factor
 STADIUM SYOK

 KOMPENSASI
 DEKOMPENSASI
 IREVERSIBEL (PRETERMINAL)
PERJALANAN KLINIS BERSIFAT PROGRESIF

12
 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 >>13
 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 DARAH14
 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

15
 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. 16
Mental state Mild agitation Lethargic Reacts only to pain
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

17
 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)
18
 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 19
 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

20
 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

21
 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

STROKE VOLUME
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
22
 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
23
pe  kesadaran
 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
24
 TATALAKSANA SYOK
ANAFILAKTIK
 STOP ALERGEN PENYEBAB + ADRENALIN (IM)
 AIR WAY & RESPIRATION ADEKUAT
 WHEEZING  NEBULASI
ADRENALIN/SALBUTAMOL
 OBSTRUKSI  INTUBASI/SURGICAL AIRWAY
 SIRKULASI & HEMODINAMIK
 VASOPRESOR : ADRENALIN (10 µg/kg BB)
 FLUID LOADING : KRISTALOID (20 ml/kg BB/IV-IO)
 RE ASSESSMENT ABC RESUSITASI
 WHEEZING (+)  NEBULASI SALBUTAMOL
BILA PERLU (+) HIDROKORTISON (IV)
(+) AMINOPILIN/SALBUTAMOL
25
DRIP
 TATALAKSANA SYOK
KARDIOGENIK
 OKSIGENASI 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
26
 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 27
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 28