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SYOCK PADA ANAK
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Syok Pada Anak
Haryson Tondy Winoto,dr.,Msi.Med.,Sp.A
Bag. Anak UWKS
2
Definition
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
3
Definition
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
Types of Shock
Type Pathophysiology Signs & Symptoms
Hypovolemic PRELOAD: CO, SVR,
intravascular volume loss
HR, pulses, delayed cap
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
Pathophysiology
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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Pathophysiology
O2 supply < O2 demand
O2 delivery < O2 consumption
DO2 < VO2
7
Hemodynamic response to hemorrhage model for cardiovascular response to hypovolemia from hemorrhage (based on normal data). Adapted from Schwaitzberg SD, Bergman KS, Harris BH. A pediatric trauma model of continuous hemorrhage. J Pediatr Surg. Jul 1988;23(7):605-9.
Blood Pressure and Volume
% blood loss % BP
25% Normal
50% 60% o
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BP drops quickly after reaching 50% blood loss
CO follows BP closely
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) DO2 = CO x CaO2
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Critical DO2: consumption
depends on delivery
Oxygen delivery DO2 = CO x CaO2
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Cardiac Output
Heart Rate Stroke volume
Preload Afterload Contractility
Oxygen delivery DO2 = CO x CaO2
CO = HR x SV
HR is independent
Neonates depend on HR (cant 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
Treatment
20
Increase O2 delivery
Decrease O2 demands
Increase O2 contents
Increase cardiac output
Increase blood pressure
Early intubation
Sedation
Analgesia
Treatment: Inotropes
25
Agent Site of Action Dose
Mcg/kg/min
Effects
Dopamine Dopaminergic
Beta
Alpha > Beta
1-3
5-10
11-20
Renal vasodilation
Inotrope/vasoconstriction
Increase perip. Vasc. resistance
Dobutamine Beta 1 & 2 1-20 Inotrope
Vasodilation
Epineprhine Beta > alpha 0.05 1.0 Inotrope, vasoconstriction
Tachycardia
Norepinephrine Alpha > beta 0.05 1.0 Profound vasoconstriction
inotrope
Milranone Phosphodiesterase
inhibitor
0.5 0.75 Inotrope
vasodilation
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