DISTRIBUTIVE SHOCK

Dr. WIGNYO SANTOSA, SpAn, KIC, FIPM

Anesthesiology Department
Medical Faculty of Unissula
 SHOCK
• Sindrom klinis akibat kegagalan
sirkulasi dalam memenuhi
kebutuhan oksigen jaringan tubuh

ATAU

• Inadekuat perfusi jaringan &

hipofungsi sel
 Pathophysiology of shock

Impaired tissue perfusion occurs when

an imbalance develops between
cellular oxygen supply and cellular
oxygen demand.

All Types of shock eventually result in

impaired tissue perfusion & the development
of acute circulatory failure or shock
syndrome.
PATHOPHYSIOLOGY
 SHOCK

Perfusi jaringan terganggu

Disfungsi sel

KEMATIAN SEL
 Macam-macam Shock
• Shock hipovolemik
• Shock distributif
• Shock obstruktif
• Shock kardiogenik
 Tahapan Syok
• Tahap awal/kompensasi
– MAP turun 10-15 mmHg
– Aktivasi simpatis vs. parasimpatis
• Ditandai oleh vasokonstriksi selektif: ginjal, otot, kulit dan
splanknik  menperbaiki sirkulasi otak dan jantung
– Penurunan aliran darah koroner  metabolisme anaerob &
dilatasi arteri
– Ginjal  pelepasan hormon
• Epinefrin, norepinefrin
• Glikokortikoid
• Renin – angiotensin – aldosteron
– Pituitari anterior: sekresi ADH

 Pe↑ produksi energi

 Pe↑ volume sirkulasi Peningkatan
 Pe↑ kontraktilitas CO
 Tahapan Syok
• Tahap lanjut/intermediate/progresif
– MAP turun > 20 mmHg
– Bila kompensasi awal gagal:
• Vasokonstriksi berlanjut dengan pe↓ MAP  perfusi
jaringan tidak adekuat & hipoksia
– Metabolisme anaerob sistemik  produksi asam
laktat  asidosis metabolik
– Pe↓ produksi ATP  ggn transpor membran 
edema sel, ruptur sel
– Respon renal berlanjut
– Perburukan fungsi jantung

Penurunan CO
 Tahapan Syok
• Tahap Irreversible
– Kompensasi tidak mampu mempertahankan
perfusi otak & jantung
– Depresi fungsi miokard berlanjut
– Iskemia otak  depresi fungsi neuron 
kehilangan mekanisme kompensasi neuronal
sentral
– Vasokonstriksi mikrosirkulasi  pe↓
venous return
 Kompensasi tubuh

1. Takikardi

2. Vasokonstriksi
↓ Cardiac output

3. Tekanan Nadi
turun
↓ aliran darah
A type of distributive shock that
results from widespread systemic
allergic reaction to an antigen

 This
hypersensitive reaction is
LIFE THREATENING
 Early Recognition, treat aggressively
 AIRWAY SUPPORT
 IV EPINEPHRINE (open

 Antihistamines

 Corticosteroids

 IMMEDIATE WITHDRAWAL OF ANTIGEN

IF POSSIBLE
 PREVENTION
 Judicious crystalloid administration
 Vasopressors to maintain organ
perfusion
 Positive inotropes

 Patient education
Pathophysiology of Neurogenic Shock
MEDICAL
MANAGEMENT
 Goals of Therapy are
to treat or remove the
cause & prevent
cardiovascular
instability, & promote
optimal tissue
perfusion
SEPSIS
SEPSIS WITH:
 Microorganisms enter body

Mediator Release

Activation of Complement, kallikrein / kinin/ coagulation
& fibrinolytic factors platelets, neutrophils &
macrophages>>damage to endothelial cells.
ORGAN DYSFUNCTION
Clinical Manifestations
 Late hypodynamic state

Decrease UOP
Decrease CO
Metabolic &
respiratory acidosis
with hypoxemia
MANAGEMENT

 Maximize O2
delivery Support
 Nutritional Support
 Comfort &
Emotional support
 Sequelae of Septic Shock

The effects of the bacteria’s endotoxins

can continue even after the bacteria is
dead!!!
 Sepsis
400,000 7-17%

Severe Sepsis 20-53%

300,000

Septic
53-63%
Shock