AFTERLOAD
O2 CONSUMPTION
MEKANISME KOMPENSASI
S aO2 Hb
O2 CONTENT
O2 DELIVERY
PRELOAD AFTERLOAD
INOTROPY
CARDIAC
STROKE VOLUME OUTPUT
AFTERLOAD
O2 CONSUMPTION
KOMPENSASI DAN TANDA KLINIS
Ginjal Oiguria
Peningkatan tahanan vaskular
renal dan splanknik
Saluran cerna Vomiting, ileus
SYOKTERKOMPENSASI
Te kanan darah P 5
SYOKHIPOTENSIF
<1 60
1-10 70 + ( 2n)
> 10 90
KLASIFIKASI KLINIS
TIPE PATOGENESIS PENYEBAB
Sianosis
BEHAVIOUR
DIURESIS Menurun
TUJUAN TERAPI
• Sedasi-analgesia
MENURUNKAN KEBUTUHAN OKSIGEN • NIVatau MV
• Antipiretik
AKSES VASKULAR
RESUSITASI CAIRAN
PEMERIKSAAN PENUNJANG
OBAT-OBATAN
KONSULTASI AHLI
LANGKAH-LANGKAH TERAPI ( 1)
PRINSIP METODE
POSITIONING
• Stabil: posisi nyaman bersama pengasuh
• Tidak stabil: posisi supine
• Menentukan etiologi
PEMERIKSAAN PENUNJANG
• Evaluasi disfungsi organ
• Menilai kelainan metabolik
• Evaluasi terapi
TIPE METODE
Non-Hemoragik • 20 ml/kg RL/NS bolus, ulang bila perlu
• Pertimbangkan koloid
HIPOVOLEMIK • Kontrol perdarahan
Hemoragik • 20 ml/kg RL/NS bolus, ulang bila perlu
• Transfusi PRCsesuai indikasi
Septik • Sesuai algoritme syok septik
• IMepinefrin 0.01 mg/kg 1:1000 (atau autoinjektor)
• 20 ml/kg RL/NS bolus, ulang bila perlu
Anafilaktik • Albuterol inhalasi
DISTRIBUTIF • Antihistamin, kortikosteroid
• Infus epinefrin 0,05-0,5 mcg/kg/mnt
Neurogenik
• 20 ml/kg RL/NS bolus, ulang bila perlu
• Vasopressor
TERAPI SPESIFIKBERDASARKAN TIPE SYOK( 2)
TIPE METODE
Bradi-/ Takiaritmia • Sesuai algoritme gangguan irama
KARDIOGENIK • 5-10 ml/kg RL/NS bolus, ulang bila perlu
Non-aritmia • Vasoaktif (terutama inotropik)
• Konsul kardiologi
Obstruksi LV ( DDL)
• Prostaglandin E1
• Konsul kardiologi
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EVALUASI TERAPI CAIRAN