DEPARTEMEN ILMU NESTESI

FAKULTAS KEDOKTERAN
UNIVERSITAS KRISTEN INDONESIA
Jl. Mayjen Sutoyo No. 2 Cawang Jakarta 13650
Telp. (021) 95380533

Disusun oleh :

Maria Elly Nobeta Hutabarat, S.Ked

1161050017

KEPANITERAAN ILMU NESTESI

PERIODE 8 MEI 2017 10 JUNI 2017
RSUD CIBINONG
 INTRODUCTION
SHOCK
Shock is a systemic state of low tissue perfusion
which is inadequate for normal cellular respiration.
With insufficient delivery of oxygen and glucose,
cells switch from aerobic to anaerobic metabolism.
If perfusion is not restored in a timely fashion, cell
death ensues.
Oxygen delivery can be increased by :
a. increasing cardiac output
b. Increasing hemoglobin concentration or
c. Increasing oxyhemoglobin concentration.

Clinical interventions to decrease oxygen demand :

a. Intubation (to support the work of breathing)
b. Sedation
c. Analgesia and
d. Treatment fever
Pathophysiology Of Shock
Cellular level

Hypoxia

Anaerobic metabolism

Lactic acidosis

Cell wall damage

Sodium and calcium enter the cell

Potassium leaks out of the cell

Causes hyperkalaemia, hyponatraemia and hypocalcaemia

Intracellular lysosomes break down releasing powerful enzymes
which destroy own cell
General criteria of shock
a. Systolic arterial BP < 80 mmHg or a
reduction > 40 mmHg
b. Oliguria
c. Metabolic acidosis
d. Poor tissue perfusion

Cinical manisfestation of organ hypoperfusion

a. Mental status changes
b. Oliguria
c. Lactic acidosis
SYOK HIPOVOLEMIK
 Syok hipovolemik terjadi karena
volume intravaskuler berkurang akibat
perdarahan, kehilangan cairan akibat diare, luka
bakar, muntah, dan third space loss, sehingga
menyebabkan pengiriman oksigen dan nutrisi ke
sel tidak adekuat.
4 Beberapa perubahan hemodinamik
yang terjadi pada kondisi syok hipovolemik
adalah CO (cardiac output) , BP (blood pressure) ,
SVR (systemic vascular resistance) , dan CVP (central
venous pressure) .
HYPOVOLAEMIC SHOCK
ETIOLOGY
Haemorrhage
Burns (>10% surface)

Vomiting/diarrhoea
HAEMORRHAGE VOLUME EFFECTS
120

100

80
Loss 10%: no effect 60

40
Loss 25%: hypovolaemic symptoms 36hrs 20

0
Loss 50%: coma. death. Normal 10% 25% 50%
BLOOD LOSS

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Dehidrasi
 Terapi syok hipovolemik bertujuan untuk restorasi volume
intravaskuler, dengan target utama mengembalikan tekanan darah, nadi,
dan perfusi organ secara optimal. Bila kondisi hipovolemia telah teratasi
dengan baik, selanjutnya pasien dapat diberi agen vasoaktif, seperti
dopamine, dobutamine.

Penanganan syok hipovolemik

1.Tentukan defisit cairan

2. Atasi syok: cairan kristaloid 20 mL/kgBB dalam - 1 jam, dapat diulang
3. Sisa defisit: 50% dalam 8 jam pertama, 50% dalam 16 jam berikutnya
4. Cairan RL atau NaCl 0,9%
5. Kondisi hipovolemia telah teratasi/ hidrasi, apabila produksi urin: 0,5 1
mL/ kgBB/jam
SYOK KARDIOGENIK
Definition

Cardiogenic shock (CS) is a clinical condition of inadequate

tissue(end organ) perfusion due to cardiac dysfunction
Hypotension (SBP < 80-90 mmHg) or MAP 30 mmHg
below baseline
Reduced cardiac index(<1.8 L/min per m2) <2.0-2.2
L/min per m2 with support
Adequate or elevated filling pressures
Signs and Symptoms
Hypotension
Absence of hypovolemia
Tachycardia
Clinical signs of poor perfusion (ie oliguria, cyanosis, cool
extremities, altered mentation)
Dopamine, doses :
2-3 g/kgBB/mt has modest inotropic and chronotropic effects
(acts on the dopaminergic receptor in the kidney)
4-10 g/kgBB/mt has primarily inotropic effects
10 g/kgBB/mt has significant agonist effect related
vasoconstriction
25 g/kgBB/mt no advantage over NE

Dobutamine
Is a adrenergic agonist
Doses of 5-20 /kg/BB/mt is a potent inotropes increase CO
Norepinephrine (NE)
Is a potent adrenergic vasopressor agent.
Also has adrenergic, inotropic, and chronotropic effects.
Dose ranges start at 0,05 g/kgBB/mt titrated to desired
effects

Epinephrine (E)
Has both and adrenergic effects
Potent inotrope and chronotrope
Increase in myocrdial oxygen consumption
Dose ranges start at 0,1 g/kgBB/mt titrated to desired
effects
SYOK SEPTIK
 Syok septik adalah sepsis yang disertai
hipotensi (tekanan sistolik <90 mmHg) dan
tanda-tanda hipoperfusi meskipun telah
dilakukan resusitasi cairan secara adekuat. Syok
septik merupakan salah satu penyebab kematian
utama pada unit perawatan intensif.
Patofisiologi: Vasodilatasi akibat
menurunnya SVR Kebocoran kapiler difus
disebabkan peningkatan permeabilitas
endotelial vaskuler yang menyebabkan
penurunan preload bermakna, sehingga berdampak
perburukan perfusi jaringan
Systemic inflamatory response syndrome (SIRS)
The SIR to a variety of severe clinical insults.
The respon in manifested by two or more of the following
conditions :
- Temperature > 38o C or < 36o C
- Heart rate > 90 x/mt
- RR > 20 x/mt or PaO2 < 4,3 kPa (< 3,2 Torr)
-White blood cell count > 12.000 cells/mm3, or >10 %
immature (band) forms

Sepsis
Defined as SIRS as a result of infection.
Severe Sepsis
Sepsis that is associated with organ dysfunction,
hypoperfusion, or hypotension.

Septic Shock
Sepsis with hypotension, despite adequate fluid resuscitation,
a long with the presence of perfusion abnormalities.

Multiple organ dysfunction (MOF) syndrome

Presence of alterated organ function in an acutely ill patient
such that homeostasis can not be maintained without
intervention.
Penanganan syok septik antara lain:
1. Pemberian antibiotik, umumnya dengan golongan spektrum luas
2. Perbaiki dan mempertahankan hemodinamik dengan terapi
berikut:
a. Terapi cairan: Meskipun syok septik tergolong dalam syok
hiperdinamik (terjadi hipovolemi relatif akibat vasodilatasi dan
hipovolemi absolut akibat kebocoran kapiler), cairan yang
direkomendasikan tetap cairan kristaloid
b. Vasopressor: Norepinephrine
c. Inotropik: Dobutamine
d. Oksigen
SYOK ANAFILAKTIK
ANAPHYLACTIC SHOCK:
AETIOLOGY

Histamine release from blood basophils

Drugs e.g. penicillin
Stings
Foods e.g. Shellfish, Peanuts

Vasodilatation - blood pressure

drops

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ANAPHYLACTIC SHOCK:
MECHANISM

Antigen, for example wasp venom

accesses specific IgE on blood
basophils. IgE dimerises at the cell
surface and the basophil releases
histamine by degranulation:
vasodilatation causes the blood
pressure to drop.

Clinical features of shock develop

rapidly.

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 ANAPHYLACTIC SHOCK: MECHANISM
37
ANAPHYLACTIC SHOCK:
TREATMENT

Adrenaline and hydrocortisone are

given in the acute phase. The patient
may recover without further specific
treatment.

If not, full support in an intensive care

unit will be required.

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TERIMAKASIH