Review Pediatrik

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    Review kardiologi anak 

    Debora

    FAKULTAS KEDOKTRAN N

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    Children are not little adults Adults are not big chi

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    DIAGNOSIS PENYAKIT JANTUNG

    1. Diagnosis Kausal

    2. Diagnosis Anatomis

    3. Diagnosis Fungsional

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    DIAGNOSA KAUSAL

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    DIAGNOSIS KAUSAL

    Penyakit Jantung pada Anak TIDAK SAMA dengan Pe

    Jantung pada Dewasa

    Penyebab : 80 % bawaan (kongenital)

    Gejala : sangat tidak jelas

    Tatalaksana : 75 % surgical intervention

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    Etiologic Basis of Congenital Heart

    Diseases

    1. Primary genetic factors 10%

    1) Chromosomal 5-10%

    2) Single mutant gene 3%

    2. Genetic-environmental interaction 90%

    1) Multifactorial inheritance (majority)

    2) Risks to offspring of an affected parent

    3) Environmental contribution

    Drugs

    Infections

    Maternal conditions

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       A   N   S   I   T   I   O   N

       A   L   C   I   R   C   U

       L   A   T   I   O   N

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    DIAGNOSIS ANATOMIS

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    ATRIAL SEPTAL DEFECT

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    COARCTATION OF THE AORTA PULMONIC STENOSIS AORTIC S

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    DIAGNOSIS FUNGSIONAL

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    CHD

    ACYANOTIC

    ↑Pulmonary Blood

    Flow

    ASD,

    VSD,

    PDA

    Obstruction to

    blood flow fromventricles

    Coartation ofaorta,

    Aortic stenosis,Pulmonic Stenosis

    CYANOTIC

    ↓ Pulmonaryblood flow

    ToF,Trikuspid atresia

    Mixed bloodflow

    TGA,Truncus arteriosus

    Hipoplastic left hea

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    Diagnosa Fungsional

    PINKShunts ( L to R) :

    • ASD

    • VSD

    • PDAStenosis:

    • AS

    • PS

    • Coarctation

    • HLHS

    BLUE

    • TOF

    • TGA

    • Tricuspid atresia

    • Truncus

    • TAPVR

    •   Ebstein’s

    • Single ventricle

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    Presentation of CHD

    1. Shock like symptoms

    2. Cyanosis

    3. Congestive symptoms

    4. Exercise intolerance

    5. Asymptomatic heart murmur 

    6. Abnormality in routine chest PA

    7. Chest pain

    8. Syncope/ seizure/ fainting

    9. Airway obstruction/ dysphagia

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    CARDIAC CYANOSIS

    1. Kebiruan mukosa mulut, lidah, kelopak mata,ya

    bertambah jelas saat menangis.

    2. Tidak timbul segera setelah lahir 

    3. Takipnea tanpa distres pernafasan

    4. Suhu tetap hangat.

    5. Tes hiperoksia positip

    AWAS : anemia, pigmen kulit, hipotermi,asfiksia

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    PEMERIKSAAN FISIK

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    CARDIAC AUSCULTATION AREAS

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    HEART SOUND

    • Ejection click = AS or PS

    • Loud S2 = Pulmonary HTN

    • Single S2 = one semilunar valve (truncus), anterior aorta (TGA), pulmo

    • Fixed, split S2 = ASD, PS

    • Gallop (S3)  – may be due to cardiac dysfunction/ volume overload

    Muffled heart sounds and/or a rub = pericardial effusion ± tamponad

    Types of Murmurs

    • Systolic Ejection Murmur (SEM) = turbulence across a semilunar valve

    • Holosystolic murmur = turbulence begins with systole (VSD, MR)

    • Continuous murmur = pressure difference in systole and diastole (PDA

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    FOTO POLOS DADA

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    ELEKTROKARDIOGRAFI

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    8 STEP IN ECG

    Step 1 : Rate

    Step 2 : Rhythm

    Step 3 : Axis

    Step 4 : Precordial leads

    Step 5 : Hyperthrophy

    Step 6 : Block 

    Step 7 : Ischemia, injury etc

    Step 8 : Miscelaneous

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    KEGAWATAN JANTUNG

    PADA BAYI DAN ANAK

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    PEDIATRIC

    CARDIAC

    EMERGENCY 

    PROBLEMS

    DYSRHITHMIA 

    HYPERTENSIVE

    CRISIS

    TAMPONADE

    THROMBO

    EMBOLIC

    CYANOTIC

    SPELS

    SHOCK 

    HEART FAILURE

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    PRESENTASI KLINIS YG SELALU ADA PADAGAWAT JANTUNG

    1. Takipnea

    2. Sianosis3. Renjatan

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    GAGAL JANTUNG

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    Pemahaman gagal jantung

    Gagal jantung bukanlah suatu keadaan klinis

    hanya melibatkan satu sistem tubuh melainka

    SINDROMA KLINIK akibat kelainan jantung yan

    ditandai dengan suatu bentuk respons hemod

    ginjal, syaraf dan hormonal yang nyata.

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    Adaptation in heart failure

    BP = CO x SVR

    BP = SV x HR x SVR

    Frank-Starling

    Remodelling

    SA system

    SA system SA system

    RAAS

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    Kompetensi

    katup

    Preload  Afterload

    Kontraktilita

    Heart rate

    Sinergistik

    Kontraktilitas

    viskositas darah

    endotel

    CONTRACTILITY

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    STROKEVOLUME

    PRELOAD

    CONTRACTILITY

    AFTER

    -SYNERGISTICCONTRACTION

    -VALVULARCOMPETENCE

    HEARTRATE

    CARDIACOUTPUT

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    HEMODYNAMICSMyocardiContracti

     Stroke Volume Preload

      Cardiac Output Afterload

      Blood  Pressure Heart Rate

      Systemic Vascular   Resistance

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    presents immediately at birthanemia, acidosis, hypoxia, hypoglycemia, hypocalcemia, sep

    presents at 1 day (congenital)PDA in premature infants

    presents in first month (congenital)HPLV, aortic stenosis, coarctation, VSD presents later

    presents later (acquired)myocarditis, cardiomyopathy (dilated or hypertrophic), SVT, serheumatic fever 

    The causes of CHF depend on “the ag

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    Neonatal congestive heart failure

    Dysfunction• Myocarditis

    • Cardiomyopathy — think inborn error of metabolism

    • Coronary artery anomaly

    • Arrhythmias

    Volume

    Unrestrictive ventricular septal defect(s)• Truncus arteriosus

    Pressure — think ductal-dependent left-sided obstruction

    • Hypoplastic left heart syndrome

    • Critical aortic stenosis

    • Critical coarctation of the aorta

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    Hypertension, Anemia, sepsis

    Bronchoplumonary dysplasia in premature

    Acute corpulmonle due to airway obstruction

    Toxins: digitalis, calcium channel blockers, Beta blockers

    Pediatric CHF  – Non Cardiac Etiology

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    KLINIS

    infants:

    irritable, poorfeeding (earlyfatigue), failure tothrive, respiratorysymptoms

    *always considerin patients withrespiratorysymptoms

    LABORATORY

    -CBC: anemia orinfection

    -Blood gas:respiratoryalkalosis ormetabolicacidosis

    -Renal and

    hepatic function

    Thorax RÖ

    -Cardiomegaly isalmost alwayspresent-Increasedpulmonary bloodflow

    PENUNJANG

    ECG

    ECHO

    Pulse oxymetri

    Hyperoxia test

    2. Block the

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    Activates the

    RAAS

    Sympathetic NervousSystem

    salt & fluidretention

    workload weakness of heart muscle

    Inssuficientblood pump

     blood vesselsContractility

    workload

    1. Increase force

    of contraction

    3. Block the SNS

    RAAS

    4. Increase urine

    production

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    CARDIAC CYANOSIS

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    Central Cyanosis vs. Acrocyanosis

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    Newborn Problems - Cyanosis

    Cardiac Cyanosis

    Does not respond to oxygen

    Does not respond to ventilation

    Usually no respiratory distress

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    Differential Diagnosis of cyanosis

    1. Not enough oxygen in

    Apnea : neurologic and drugs

    Diffusion barrier : RDS, aspiration, pneumonia

    Obstruction: pneumothorax, head position

    2. Oxygen “mal-absorption” Shunting lesions : cardiac

    non-cardiac : PPHN, Hematologic

    Methemoglobinemia : carboxyhemoglobinemia

    3. Too much oxygen out

    sepsis

    low flow, high extraction

    acrocyanosis

    hyperviscosity/polycythemia

    extravasated (e.g. bruising)

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    squating

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    Treatment of CYANOTIC SPELLS

    Knee-chest or squatting positioning (increases afterload thus

    decreasing R to L shunting)

    Manual external aortic compression be low level of renal art

    Morphine, 0.1-0.2 mg/kg IV or SC (to treat hyperpnea and

    decrease systemic catecholamines)

    Oxygen (perhaps limited value)

    Intravenous volume expansion, 10 cc/kg isotonic

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    Treatment of CYANOTIC SPELLS

    Sodium bicarbonate 1-2 mEq/kg/dose

    Propanolol, 0.15-0.25 mg/kg IV over 2-5 minutes(to block be

    in infundibulum therefore lessening RV outflow obstruction

    Phenylephrine, 0.1 mg/kg IM or SC(increases afterload there

    decreasing R to L shunt)

    General anesthesia (if severe/prolonged spells)

    interim prophylactic treatment with propranolol while await

    Knee chest

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    Knee chest

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    Thank You