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
Hypovolemic
Distributive

Primary Insult
Decreased circulating
blood vol
Vasodilation -> venous
pooling -> decreased preload

Obstructive

Obstruction of cardiac
filling/out flow

Cardiogenic

Decreased contractility

Dissociative

O2 not released from

hemoglobin

Common Causes
Dehydration, hemorrhage,
capilarry leaks
Sepsis, anaphylaxis,
drug intoxication,
spinal cord injury
Cardiac tamponade, tension
pneumothoracx, pulmonary
embolus
Congenital heart disease,
myocarditis, dysritmia
CO poisoning,
methemoglobinemia
3

FUNGSI SISTEM SIRKULASI

JANTUNG

PEMB. DARAH

VOL. DARAH O2 DELIVERY

CURAH JANTUNG

METABOLISME

ALIRAN DARAH

ADEKUAT

JARINGAN

METABOLIT

ELIMINASI

DO2 = CO x CaO2
DI ORGAN= (1,34
PEMBUANGAN
CaO2
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

Blood pressure

Distribution of CO & VO2

in a Healthy Resting Normal Subject
% Total
Organ
CO
GI tract and liver
24
Skeletal muscle
21
Kidney
19
Brain
13
Skin
9
Heart
4
Other organs
10

AVDO2
vol %
4.1
8.0
1.3
6.3
1.0
11.4
3.0

% Total
VO2
25
30
7
20
2
11
5
7

Adapted from Wade OL, Bishop JM: Cardiac output and regional blood flow, Oxford, Blackwell, 1

Extracel. Fluid
Low Output Cardiac Failure
Volume Pericardial Tamponade Oncotic Pressure
Constrictive Pericarditis Capillary Permeability

Intra vasc. Vol. due to

CARDIAC OUTPUT
Activation receptor of ventricular & arterial
Non-osmotic
Vasopressin
Stimulation

Stimulation of
Sympathetic Nervous
System

RENAL WATER
RETENTION

PERIPHERAL & RENAL

ARTERIAL VASC. RESISTANCE

MAINTENANCE OF EFFECTIVE
ARTERIAL BLOOD VOLUME

Activation of the
Renin-AngiotensinAldosterone System

RENAL SODIUM
RETENTION

FRANK STARLING`S LAW

5

STROKE VOLUME

SYMPATHOMIMETIC
AMINES

POSITIVE
INOTROPY

XANTHINES
GLUCAGON

CARDIAC GLYCOSIDES
3

C
B

NEGATIVE
INOTROPY

HYPOXEMIA
ACIDOSIS

HYPOGLYCEMIA

VOLUME INFUSION

ENDOTOXEMIA
0

10

CENTRAL VENOUS PRESSURE (Toor)

DRUG TOXICITY

Oxyhemoglobin saturation

The Oxygen-hemoglobin Dissociation Curve

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 depressant factor
- endogeneous catecholamines
- adenine nucleotides

11

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 DARAH

TAKIPNU
PERFUSI PERIFER
ASIDOSIS (+)
OLIGURI (+)
TINGKAT KESADARAN

14

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

Blood loss (%) Up to 25

25 - 40 > 40

Heart rate

Tachycardia +

Tachycardia ++

Systolic BP

Plummeting

N or falling

Pulse volume N/
Capillary refill
Skin

N/

Tachy/bradycardia

++

+ ++

Cool, pale Cold, mottled

Cold, deathly pale

Respiratory rate Tachypnoea + Tachypnoea ++

Mental state

Irreversible

Sighing rsp.

Mild agitation Lethargic Reacts only to pain

Uncooperative or unresponsive

16

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 AWAL
RESUSITASI

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

18

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
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

IMPROVEMENT

ESTABLISH ETIOLOGY
CONFIRM SOURCE
OF FLUID LOSS

CVP > 5 Torr

1. CORRECT
ACIDOSIS

NO IMPROVEMENT

2. Co. GLUCOSE

ABG, HT, NaK, GLUC Ca,

SWAN GANZ CATHETER
CO, RAP, PAP, POAP

3. INTROPIC
SUPPORT

STROKE VOLUME

CVP < 5 Torr

CRYSTALLOID INFUSION
UNTIL CVP - 5 Torr

ESTABLISH ETIOLOGY,
ETIOLOGY,
OBSERVATION

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
nadi kecil, lemah CVP koagulopati
HR , Oliguria
Smv O2
hipoglikemi
shallow breathing
pe kesadaran
MOSF bergantung sistem
Koma
GI bleeding/DIC
organ failure

asidosis metab

sesuai yang terkena ARDS, CHF, RF jenis

23

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

SIRKULASI & HEMODINAMIK

WHEEZING NEBULASI ADRENALIN/SALBUTAMOL

OBSTRUKSI INTUBASI/SURGICAL AIRWAY
VASOPRESOR
FLUID LOADING

: ADRENALIN (10 g/kg BB)

: 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

25

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

KOREKSI PENYEBAB PRIMER

26

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
27

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