MANAJEMEN SYOK

Dhadi G. Daradjat
 KASUS
• Laki-laki , 65 tahun, penurunan kesadaran
TD : 80/60 mmHg RR : 35 x/m
Nadi : 126 x/m Akral hangat
• Laki-laki, 34 tahun, riwayat trauma
TD : 80/60 mmHg RR : 26 x/m
Nadi : 42 x/m Akral dingin
• Wanita, 25 tahun, nyeri perut
TD : 80/60 mmHg RR : 40 x/m
Nadi : 126 x/m Akral dingin
SYOK

• Kondisi yang mengancam nyawa

• Gangguan perfusi jaringan
• Tekanan darah tidak cukup adekuat untuk
menghantarkan oksigen dan nutrisi untuk
mendukung fungsi sel tubuh.
Pompa jantung
Sistem sirkulasi Hipoksia selular
Kematian
Volume Kerusakan organ
intravaskular
Pathophysiology Systemic Level
Hasil akhir syok seluler :
Asidosis laktat
Penurunan kontraktilitas jantung
Penurunan tonus vaskular
KLASIFIKASI (HINSHAW DAN COX)
• Syok hipovolemik
• Syok kardiogenik
• Syok obstruktif
• Syok distributif
FISIOLOGI
HEMODINAMIK TEKANAN
DARAH

CARDIAC RESISTENSI
OUTPUT X PERIFER
(CO) (SVR)

HEART STROKE
RATE X VOLUME
(HR) (SV)

PRELOAD (VOLUME INTRAVASKULAR)

KONTRAKTILITAS JANTUNG
AFTERLOAD
 GAMBARAN HEMODINAMIK
BERDASARKAN TIPE SYOK
VOLUME KONTRAKTILITAS RESISTENSI DENYUT
TIPE SYOK
DARAH JANTUNG PERIFER JANTUNG

HIPOVOLEMIK

KARDIOGENIK

OBSTRUKTIF

DISTRIBUTIF

NEUROGENIK
 PRINSIP MANAJEMEN SYOK
• Mengembalikan stabilitas hemodinamik dan
menangani penyebab syok
– Mengembalikan volume intravaskular
– Obat support hemodinamik untuk
mengembalikan tonus vasomotor dan fungsi
jantung
– Mengoptimalkan penghantaran O2
• Meningkatkan saturasi O2 ≥ 95%
• Meningkatkan Hb > 10 gr/dl
– Support nutrisi
 TERAPI CAIRAN
• Terapi inisial dan target awal untuk
semua jenis syok
• Kristaloid 10 – 20 cc/kgBB dalam 30 menit
 hati-hati pada pasien dengan dugaan syok
kardiogenik
• Resusitasi cairan agresif  edema paru
 OBAT SUPPORT HEMODINAMIK

• Medication agent for the acute management :

– Vasopressor (Noradrenalin, Adrenalin, Dopamin)
– Inotropic (Dobutamin, Digoxin)
– Vasodilator (Nitrogliserin, ISDN)

No one vasoactive agent or combination of agent has

been demonstrated to be superior in managing shock
 MONITORING
– ECG  HR and rhytm
– Tekanan darah
– Pulse Oxymetri
– Central Venous Catheter  indicator of
PRELOAD
– ScvO2  keseimbangan O2
– Kateter urine indikator perfusi ginjal ( 0.5 – 1
mL/kg/jam)
– Lactate  keseimbangan O2
1. Dopamine

• Vasoactive  inotropic and vasopressor

• Doses : 1 – 20 ug/kg/min
2. Norepinephrine
• Potent α – adrenergic vasopressor also has been β-
adrenergic
inotrpic and chronotropic effect.
Doses : 0,05 ug/kg/min and is titrated to desired
effect.
• CO may decrease as afterload and BP increased.
• Increases renal blood flow in pt with adequat volume
resusc.
• An increase in heart rate is uncommon with use of
norepinephrine
3. Epinephrine

• α-adrenergic and β-adrenergic  potent inotropic and

chronotropic effect, at higher doses  vasopressor effect.
• Doses : 0,1 uk/kg/min.  can be titrated to desired effect.
• Increase myocardial oxygen consumption, especially in the
presence of coronary artery desease.
•  mesenteric ischemia.
4. Vasopressin

• Potent vasopressor (similar to the effect of norepinephrine)

• Doses : 0,01 – 0,04 units/min.
• Higher doses  ischemic events.
• To be considered for use in hypotensive shock refractory to
other agent and fluid resuscitation.
5. Dobutamine

• β-adrenergic agonist with inotropic effects.

• Doses : 1 – 20 ug/kg/min  increase in CO.
• Arterial blood pressure may remain unchanged, decrease or
increase slightly.
• Inadequat intravascular volume replacement, blood pressure
can drop precipitously and tachycardia may be problematic.
• Variable chronotropic effects.
A. Hypovolemic Shock
Etiologi :
- hemorrhage
- dehydration
- third space fluid loss  interstitial fluid redistribution
- burn injury, trauma, pancreatitis, any severe form of
shock
PATHOPHYSIOLOGY

DECREASED IN BLOOD VOLUME

DECREASE IN VENOUS RETURN

DECREASE IN STROKE VOLUME

DECREASED IN CARDIAC OUTPUT

DECREASE IN TISSUE PERFURION

B. Distributive Shock
• Is characterized by vasodilation  loss of peripheral vascular
tone.
Etiologi :
- septic shock
- neurogenic shock
- anaphylactic shock
Pathophysiology:

vasodilation decreased stroke

volume

maldistribution of decreased cardiac

blood volume output

decreased tissue
decreased venous
perfusion
return
C. Cardiogenic Shock
• Forward blood flow is inadequate :
– Cardiac pump failure ( ischemia, cardiomyopathy)
– A mechanical or structural defect (valvular failure, septal defect)
– Arrhytmia
Most commonly  acute myocardial infarction (MI).
Clinincal Manifestation :
- Distended jugular veins
- pulmonary edema
- S3 gallop
 Decreased cardiac contractility

Decreased stroke volume and

Cardiac output

Ineffective ventricular
emptying

Pulmonary congestion

Decreased systemic tissue

Decreased coronary artery
perfusion
perfusion
D. Obstructive Shock
• Obst. Shock 
- impaired cardiac filling
- excessive after load
- cardiac tamponade
- constrictive pericarditis
- tension pnemothorax
- massive pulmonary emboli
SUMMARY
– Shock is characterized by impaired tissue oxygenation and
hypoperfusion
– The 4 major categories of shock : hypovolemic, distributive,
cardiogenic and obstructive.
– The clinical manifestation  inadequat tissue oxygenation and
perfusion, compensatory responses and the specific etiology.
– Intervention to restore perfusion  adequat BP, increasing CO
optimizing the Oxygen content of blood, and/or decreasing
oxygen demand.
– The initial therapy  replacement intravascular volume
(crystalloid or colloid solutions).
TERIMAKASIH