7 - Syok Hipovolemik-S.gaus
7 - Syok Hipovolemik-S.gaus
7 - Syok Hipovolemik-S.gaus
Syafruddin Gaus
Final
Final Common
Common Pathway!
Pathway!
Patofisiologi
Perfusi jaringan yang tidak adekuat
berakibat :
hipoksia seluler
kegagalan metabolisme seluler
kerusakan jaringan
kegagalan organ
kematian
Aerobic Metabolism
6 CO2
6 O2
6 H2O
METABOLISM
GLUCOSE 36 ATP
2 LACTIC ACID
Inadequate
Inadequate
Cellular
Cellular
Oxygenation
Oxygenation
Inadequate
Inadequate Anaerobic
Anaerobic Lactic
LacticAcid
Acid
Energy
Energy Metabolism
Metabolism Production
Production
Production
Production
Metabolic
Metabolic Metabolic
Metabolic
Cell
CellDeath!
Death!
Failure
Failure Acidosis
Acidosis
Suplai Oksigen
JANTUNG
PEMBULUH VOLUME
DARAH DARAH
Respon syok
Syok Hipovolemik
Etiologi:
Kehilangan cairan intravasculer
atau ekstraselluler
Penyebab terbanyak:
Perdarahan
Dehidrasi
Hypovolemic Shock
Fluid (blood or
plasma) is lost from
the intravascular
space.
Hypovolemic Shock
Trauma: GI Tract:
Solid organ injury Esophageal varices
Pulmonary parenchymal Ulcer disease
injury Gastritis/esophagitis
Myocardial Mallory-Weiss tear
laceration/rupture Malignancies
Vascular injury Vascular lesions
Retroperitoneal Inflammatory bowel
hemorrhage disease
Fractures Ischemic bowel disease
Lacerations Infectious GI disease
Epistaxis Pancreatitis
Burns
Hypovolemic Shock
GI Tract: Reproductive Tract:
Infectious diarrhea Vaginal bleeding
Vomiting Malignancies
Miscarriage
Vascular: Metrorrhagia
Aneurysms Retained products of
Dissections conception
AV malformations Placenta previa
Ectopic Pregnancy
Ruptured ovarian cyst
Syok Hipovolemik
Ekstrasel
Intrasel Interstitiel IV
DEHIDRASI PERDARAHAN
Kehilangan Cairan Eksternal
Kehilangan darah:
trauma: tumpul dan penetrasi
DARAH YANG TAMPAK
DARAH YANG TIDAK TAMPAK
Konsekuensi Syok Hipovolemik
fluid volume
preload
preload
contractility
contractility
(Starlings
(Starlings Law)
Law)
blood
blood pressure
pressure cardiac
cardiac
output.
output.
Stages of Shock
Compensated
The bodys compensatory mechanisms are able to
maintain some degree of tissue perfusion.
Decompensated
The bodys compensatory mechanisms fail to
maintain tissue perfusion (blood pressure falls).
Irreversible
Tissue and cellular damage is so massive that the
organism dies even if perfusion is restored.
Clinical Findings
What is the first physiological factor in the
development of shock?
VO2 < MRO2
So, what are the first symptoms you would
expect to find?
respiratory rate
heart rate
Clinical Findings
What is often the second physiological
response to the development of shock?
Peripheral vasoconstriction
What symptoms would you expect to see?
pale skin
cool skin
weakened peripheral pulses
Clinical Findings
As shock progresses, what physiological
effects are seen?
End-organ perfusion falls
What symptoms would you expect to see?
altered mental status
decreased urine output
Clinical Findings
As compensatory mechanisms fully
engage, what signs and symptoms would
you expect to see?
tachycardia
tachypnea
pupillary dilation
decreased capillary refill
pale cool skin
Clinical Findings
When compensatory mechanisms fail,
what signs and symptoms would you
expect to see?
hypotension
falling SpO2
bradycardia
loss of consciousness
dysrhythmias
death
Respon Tubuh terhadap
Syok Hipovolemik
1. Respon Simpatis:
- denyut jantung
- kontraktilitas
- preload
- vasokonstriksi ( SVR/afterload)
Respon sistem RAA, ADH: retensi air
2. Pergeseran Cairan dari ISF ke IVF
Renin-Angiotensin-Aldosterone
Plasma
Plasma
volume
volume Kidney
Kidney
Detected by (juxtaglomerular
(juxtaglomerular
and/or apparatus)
apparatus)
[Na+]
[Na+] Releases
Via ACE
(Angiotensin
Renin
Renin
Converting
Enzyme)
Converts
Angiotensin
AngiotensinII
II
Angiotensin
AngiotensinI
I Angiotensinogen
Renin-Angiotensin-Aldosterone
vasoconstriction
vasoconstriction PVR
PVR
Angiotensin
AngiotensinII
II
thirst
thirst
ADH
ADH
(anti-diuretic Fluid
Fluid
(anti-diuretic BP!
BP!
hormone) volume
volume
hormone)
Releases Na+
Adrenal
Adrenal Na+
cortex Aldosterone
Aldosterone reabsorption
cortex reabsorption
Gejala Umum Syok Hipovolemik
Intrasel Interstitiel IV
Kompensasi Akibat Perdarahan
Resusitasi
Intrasel Interstitiel IV
Transfusi atau Transfusi + RL ?
Hasil :
Kelompok yang hanya mendapat transfusi saja,
80% hewan coba mati
Kelompok yang mendapat transfusi + RL hanya
30% hewan coba mati
A B
Intrasel Interstitiel IV
Dext 5%
RL / Na
Cl 0,9 %
Colloids
/ Blood /
Plasma
Petunjuk Transfusi Darah
British Journal of Hematology 2001, 113, p24-31
Conclusions:
Early resuscitation of haemorrhagic shock with NS or LR has little
impact on oxygenation when resuscitation volume is less than 250
ml/kg. LR has more favourable effects than NS on EVLWI, pH and
blood pressure but not on oxygenation.
25.0 Viscocity
Hb 7-15
120 Centipoise
Relative Oxygen Transport Capacity
100 20.0
80
15.0
Kompensasi tubuh:
(Percent)
60
Lebih mentoleransi
10.0
anesia normovolemi
40 dibanding hipovolemik
Viscocity
5.0
20
0 0
20 40 60 80
Hematocrit
Kecukupan Transport Oksigen
Peningkatan permeabilitas
membran kapiler
Penurunan tekanan osmotik koloid
(ruang ketiga)
Mekanisme Hemodilusi
Tujuan utama:
Mengembalikan volume IVF & ISF secepat
mungkin agar shock & hipoperfusi tidak
berlangsung lama
Konsekuensi Terapi Hemodilusi :
- Anemia (masih aman 5-8 gm/dl)
- Hipoalbuminemia (masih aman bila 2,5 g/dl)
Perubahan Hemodinamik karena
Kehilangan Volume
CO rendah
Penurunan RAP Preload
Penurunan PAP, PAWP
Peningkatan tahanan perifer
(SVR) Afterload
KET, datang syok berat
Ny.S/ MRS OP POSTOP
Tensi 80 110 120
Nadi 148 108 100
Perfusi DBP DKP HKP
Hb ? 7.0 6.5
RL 1500 RL 2000