management of shock

1. 1
S Y O K
APRC 7/1/2023

2. DEFINISI SYOK
SINDROM KLINIS AKIBAT KEGAGALAN SISTEM
SIRKULASI UNTUK MENCUKUPI :
 NUTRISI PASOKAN METABOLISME
 OKSIGEN UTILISASI JARINGAN TUBUH
FASE: KOMPENSASI
DEKOMPENSASI
IREVERSIBEL DEFISIENSI O2 SELULER

3. 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

4. FUNGSI SISTEM SIRKULASI
 JANTUNG CURAH JANTUNG METABOLISME
 PEMB. DARAH ALIRAN DARAH ADEKUAT JARINGAN
 VOL. DARAH O2 DELIVERY
METABOLIT
ELIMINASI
DI ORGAN
PEMBUANGAN
DO2 = CO x CaO2
CaO2 = (1,34 x Hb x sat O2) + (0,003 x PaO2)

5. Pengaturan curah jantung dan tekanan darah
Preload Contractility Afterload
Heart rate Stroke volume
Cardiac output Systemic vascular resistance
Blood pressure

7. 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

8. 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

9. FRANK STARLING`S LAW
SYMPATHOMIMETIC
AMINES
XANTHINES
GLUCAGON
CARDIAC GLYCOSIDES
HYPOXEMIA
ACIDOSIS
HYPOGLYCEMIA
ENDOTOXEMIA
DRUG TOXICITY
VOLUME INFUSION
4
2
3
1
5
0 5 10
CENTRAL VENOUS PRESSURE (Toor)
A
D
B
C
POSITIVE
INOTROPY
NEGATIVE
INOTROPY

10. Oxyhemoglobin
saturation
H+
2,3-DPG
CO2
Pi
H+
2,3-DPG
CO2
Pi
PaO2
The Oxygen-hemoglobin Dissociation Curve

11. 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

12. STADIUM SYOK
 KOMPENSASI
 DEKOMPENSASI
 IREVERSIBEL (PRETERMINAL)
PERJALANAN KLINIS BERSIFAT PROGRESIF

13. 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 >>

14. 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 

15. 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

16. 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

17. 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

18. 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

19. 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

20. 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

21. 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

22. 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
UNTIL CVP - 5 Torr
IMPROVEMENT ABG, HT, NaK, GLUC Ca,
SWAN GANZ CATHETER
ESTABLISH ETIOLOGY CO, RAP, PAP, POAP
CONFIRM SOURCE
OF FLUID LOSS
CENTRAL VENOUS PRESSURE
1. CORRECT
ACIDOSIS
2. Co. GLUCOSE
3. INTROPIC
SUPPORT

23. 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 sesuai
yang terkena ARDS, CHF, RF jenis
GI bleeding/DIC organ failure

24. 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

25. 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 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

26. 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

27. 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

28. 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