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

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 of shock

PATHOPHYSIOLOGY

Perfusi jaringan terganggu

SHOCK

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

Pe↑ kontraktilitas

Peningkatan

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!!!

7-17%

Sepsis

400,000

20-53%Severe Sepsis

300,000

Septic

Shock53-63%