SYOK PADA ANAK

DEFINI
TION
• Failure of delivery oxygen and substrates to
meet the metabolic demands of the tissue beds
SUPPLY < DEMAND
Oxygen delivery < Oxygen Consumption
DO2 < VO2
• Failure to remove metabolic end-products
• Result of inadequate blood flow and/or oxygen
delivery

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 DEFINI
TION
• COMMON PATHWAY
– FAILURE TO DELIVER SUBSTRATES 
CONVERSION TO ANAEROBIC
METABOLISM
• REVERSIBLE IF RECOGNIZED EARLY
• IRREVERSIBLE ORGAN DAMAGE AT THE LATE STAGE
– PROGRESSIVE ACIDOSIS AND
EVENTUALLY CELL DEATH
• EARLY RECOGNITION IS KEY
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 TYPES OF
SHO
CK
Type Pathophysiology Signs & Symptoms
Hypovolemic ↓ PRELOAD: ↓CO, ↑ SVR, ↑HR, ↓ pulses, delayed cap
intravascular volume loss refill, dry skin, sunken eyes,
oliguria
Distributive ↓ AFTERLOAD (SVR)
Anaphylactic ↑ CO, ↓ SVR Angioedema, low BP,
wheezing, resp. distress
Spinal Normal CO, ↓ SVR Low BP without tachycardia;
paralysis, h/o trauma
Cardiogenic ↓ CO, variable SVR Normal to ↑ HR, ↓ pulses,
delayed CR, JVD, murmur or
gallop, hepatomegaly
Septic Variable More to come
 PATHOPHYSI
OLOGY
• Children
– Higher % body water
– Higher resting metabolic rate
– Higher insensible losses
– Lower renal concentrating ability
– Subtle signs/symptoms
• Higher risk for organ hypo-perfusion

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 PATHOPHYSI
OLOGY

O2 supply < O2 demand

O2 delivery < O2 consumption
DO2 < VO2

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BLOOD PRESSURE
AND VOLUME

% blood loss % BP
25% Normal
50% 60% o

•BP drops quickly after

reaching 50% blood loss
•CO follows BP closely

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 OXYGEN
DELIVERY (DO2)
• DO2 = CO x CaO2
– DO2 : oxygen delivery
– CO : Cardiac output
– CaO2: arterial oxygen content
• CO = HR x SV
– HR: heart rate
– SV: stroke volume
• CaO2 = HgB x SaO2 x 1.34 + (0.003 x PaO2)
– Oxygen content = oxygen carried by HgB + dissolved
oxygen

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 OXYGEN
DELIVERY
DO2 = CO X
CAO2
Cardiac
Output

Stroke
Heart Rate
volume

Preload Afterload Contractility

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 OXYGEN
DELIVERY
DO2 = CO X
• CO = HR x SV CAO2
• HR is independent
– Neonates depend on HR (can’t increase SV)
• SV depends on
– Pre-load: volume of blood
– After-load: resistance to contraction
– Contractility: force
 OXYGEN
DELIVERY
DO2 = CO X
CAO2
• CaO2 = HgB x SaO2 x 1.34 + (0.003 x PaO2)
• Normal circumstance: CaO2 is closely associated
with SaO2
• Severe anemia or in the presence of abnormal HgB
(i.e. CO poisoning) - CaO2 is strongly affected by
PaO2
 HYPO-
PERFUSION
• Poor perfusion of a vital organs leads to organ dysfunction
– Decreased urine output
– Altered mental status
– Elevated LFTs, bilirubin
• Switches to anaerobic metabolism  Lactate
• Activates inflammatory cascade
– Activates neutrophils, releases cytokines
• Increases adrenergic stress response
– Increases lipolysis/glycogenolysis (also increases lactate)
– Releases catecholamine and corticosteroid
 EVALUATION &
TREATMENT

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 INITIAL
ASSESSMENT
• Goals
–Immediate identification of life-
threatening conditions
–Rapid recognition of circulatory
compromise
–Early classification of the type and
cause of shock
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 INITIAL
ASSESSMENT

• Airway
– Mental status: can the patient maintain the
airway
• Breathing
– ?impending respiratory failure
• Circulation
– Heart rate, pulses, blood pressure
– Capillary refills - perfusion
• Dextrose 19
 TREATM
ENT

Decrease O2 Increase O2
demands delivery

Early
Increase O2 contents intubation
Increase cardiac Sedation
output Increase blood Analgesia
pressure
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TREATMENT:
INOTROPES

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TERIMA KASIH