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%
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