Mk Icu Slide Shock

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    SHOCK

    Emergency pediatric PICU division

    Pediatric Department

    Medical Faculty, University of Sumatera Utara H. Adam Malik Hospital

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    Definition

    Shock is an acute, complex state of

    circulatory dysfunction that results in

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    oxygen and other nutrients to meet tissue

    metabolic demands

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    Pathophysiology

    Delivery of Oxygen (DO2):

    DO2 = Cardiac output (CO) x Arterial oxygen content (CaO2)

    CO = Heart Rate (HR) x Stroke Volume (SV)

    CaO2= Hb x SaO2 x 1,39

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    CO

    SV

    Preload

    Myocard

    Contractility

    Pressure AfterloadHRSVR

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    CO = Cardiac OutputSVR = Systemic Vascular resistance

    SV = Stroke VolumeHR = Heart Rate

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    Clinical Manifestation

    Clinical Sign Compensated Uncompensated Irreversible

    Heart rateSystolic BP

    Pulse volumeCapillary refill

    Tachycardia +Normal

    Normal/reducedNormal/increased

    Tachycardia ++Normal or falling

    Reduced +Increased +

    Tachycardia/bradicardia

    PlummetingReduced ++

    Three phases: compensated, uncompensated, irreversible

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    SkinRespiratory rateMental state

    Cool,paleTachypnoea +Mild agitation

    Cool,mottledTachypnoea ++Lethargic

    Uncooperative

    Increased ++Cold,deathly paleSighing respiration

    React only to pain orunresponsive

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    Management

    Intubation & mechanical ventilation

    Fluid resuscitation

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    FUNCTIONAL CLASSIFICATION

    Hypovolemia Cardiogenic

    Obstructive

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    Distributive Septic

    Endocrine

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    HYPOVOLEMIC SHOCK

    A decrease in intra vascular blood volume to such an extent thateffective tissue perfusion can not be maintain

    Most common cause of shock in infants & children Etiology:

    Hemorrhage

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    asma oss Fluid & electrolyte loss

    Hypovolemia preload SV CO

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    CLINICAL MANIFESTATION:

    Tachycardia

    Skin mottling

    Prolonged capillary refill

    Cool extremities

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    Hypotensive

    Lethargy / comatose

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    THERAPY

    Adequate oxygenation and ventilation

    Rapid volume replacement reestablish circulation: Crystalloid: 20 ml/kg shock persist 20 ml/kg

    Hemorrhagic: transfusion

    10Continuous monitoring of HR, arterial BP, CVP, UOPContinuous monitoring of HR, arterial BP, CVP, UOP

    Shock (+)Shock (+)

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    CVP:

    < 10 mmHg fluid infusion until preload is reach >10 mmHg indication: flow-direct thermo dilution

    pulmonary artery catheter and/or echocardiogram

    Ventricular fillin ressure rises without evidence of im rovement

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    in cardiovascular performance

    Discontinue fluid resuscitation

    Inotropic agent (+)

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    REFRACTORY SHOCK:

    Unrecognized pneumothorax / pericardial effusion

    Intestinal ischemia Sepsis

    Myocardial dysfunction

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    Adrenal cortical insufficiency Pulmonary hypertension

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    CARDIOGENIC SHOCK

    The pathophysiologic state in which abnormality of cardiacfunction is responsible for the failure of the cardiovascular

    system to meet the metabolic needs of tissue

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    epresse Etiology: Heart rate abnormalities, Cardiomyopathies/carditis,

    Congenital heart disease, Trauma

    Myocardial dysfunction is frequently a late manifestation ofshock of any etiology

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    CLINICAL MANIFESTATION Tachycardia

    Hypotensive

    Diaphoretic Oliguria

    Acidotic

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    oo ex rem es

    Altered mental status

    Hepatomegaly

    Jugular venous distension

    Rales

    Peripheral edema

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    THERAPY

    Tissue oxygen supply

    Tissue oxygen requirements

    Correct metabolic abnormalities

    Preload should be o timized

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    Myocardial contractility: inotropic agent cathecholamine:norepinephrine, epinephrine, dopamine & dobutamine

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    OBSTRUCTIVE SHOCK

    Caused by inability to produce adequate CO despite normal

    intravascular volume & myocardial function Causative factor:

    Acute pericardial tamponade

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    Tension pneumothorax Pulmonary / systemic hypertension

    Congenital / acquired outflow obstruction

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    CARDIAC TAMPONADE

    Hemodinamically significant cardiac compression accumulation

    pericardial contents that evoke & defeat compensatory mechanism

    Physical examination:

    Pulsus paradoxus

    Narrowed pulse pressure

    Pericardial rub

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    Jugular venous distension

    Definitive treatment: removed pericardial fluid or air surgical drainage /

    pericardiocentesis

    Medical management: Blood volume expansion maintain venoarterial gradients

    Inotropic agent

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    DISTRIBUTIVE SHOCK

    Results from maldistribution of blood flow to the tissue

    May be seen with anaphylaxis, spinal / epiduralanesthesia, disruption of spinal cord, inappropriate

    administration vasodilatory medication

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    Treatment: Reversal underlying etiology

    Vigorous fluid administration

    Vasopressor infusion

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    SEPTIC SHOCK

    Contains many elements of the other types of shock discussed

    previously (hypovolemic, cardiogenic, and distributive shock)

    SIRS (Systemic Inflammatory Response Syndrome): non specificinflammatory response

    Modified criteria for SIRS:

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    Temp. >38,5 C or < 36 C Tachycardia

    Tachypnea

    WBC / or >10% immature neutrophils

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    Sepsis: SIRS + documented infection Severe sepsis: Sepsis + end organ dysfunction

    Se tic shock: Se sis with h otension des ite ade uate fluid

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    resuscitation

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    MANAGEMENT:

    Early recognition

    Antibiotics appropriate with microbiological examination

    Initial fluid resuscitation 20 ml/kg boluses over 5-10minutes up to 40-60 ml/kg in the first hour

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    Mechanical ventilation refractory shock

    Hydrocortisone

    Glycemic control

    Blood transfusion

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    Catecholamine-resistant shock resistant

    Observe in PICUTitrate epinephrine for cold shock, norepinephrine for warm shock to

    Normal MAP-CVP difference for age and SVCO2 saturation > 70%

    Establish central venous access, begin dopamine orDobutamine therapy and establish arterial monitoring

    Push 20 cc/kg isotonic saline or colloid boluses up to andOver 60 cc/kg correct hypoglycemia and hypocalcemia

    Fluid responsive*

    15 min

    Recognize decreased mental status and perfusion.Maintain airway and establish acces according to PALS guidelines

    0 min5 min

    Fluid refractory-dopamine/dobutamine resistant shock

    Fluid refractory shock**

    ECMORefractory shockStart cardiac output measurement and direct fluid, inotrope, vasopressor, vasosilator,and hormonal therapies to attain normal MAP-CBP and CI > 3.3 and < 6.0 L/min/m2

    Persistent Catecholamine-resistant shock

    Add vasodilator or type III PDE

    inhibitor with volume loading

    Normal Blood Pressure Cold Shock

    SVC O2 Sat < 70%

    Low Blood Pressure Cold Shock

    SVC O2 Sat < 70%

    Titrater volume resuscitation

    and epinephrine

    Low Blood Pressure Warm Shock

    SVC O2 Sat < 70%

    Titrater volume and

    norepinephrine

    60 minDraw baseline cortisol level

    Then give hydrocortisone

    Draw baseline cortisol level or perform

    ACTH stim test. Do not give hydrocortisone

    Not at risk ?At risk of adrenal insufficiency ?

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    THANK YOUTHANK YOUTHANK YOUTHANK YOU

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