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Syok Pada Anak Haryson Tondy Winoto,dr.,Msi.Med.,Sp.A Bag. Anak UWKS

Syok Pada Anak UWKS

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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

    6

  • 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

    9

    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

    10

  • Oxygen delivery (DO2) DO2 = CO x CaO2

    11

    Critical DO2: consumption

    depends on delivery

  • Oxygen delivery DO2 = CO x CaO2

    12

    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

    17

  • 18

    Initial Assessment

    Goals

    Immediate identification of life-threatening conditions

    Rapid recognition of circulatory compromise

    Early classification of the type and cause of shock

  • 19

    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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