mapping skenario 1

7/27/2019 Mapping Skenario 1

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Case Mapping

Anamnesis:SesakBatukBB sulit naik

Pemeriksaan FisikKeadaan umum : lemah, tampak distress nafas

GCS 456, Nadi 176x/menit, RR 74x/menit, t axiler 38,7C TD 100/70 mmHg, JVP

Anemia +St. Antropometri: malnutrisi/underweightJantung: murmur sistolik punctum maksimum di ICS III PSL (parasternal line) kiri, gallopParu-paru : ronki + (seluruh lap baru)Ekstremitas :edema non pittingEKG :CT scan Brachicephalli SkullChest X rayProminence pulmonary artery segmentIncreased pulmonary vascular markingBronchopneumoni

Ekokardiografi: Ventrikular SeptalDefect grade sedang berat

Gagal Jantung Akut dengan ec Ventricular Septal Defect dgn Bronchopneumoni, Down Syndrome, Brachicephalli, Gizi kurang

PenatalaksanaanO2 headbox 8 liter per menitPlugCefotaxime 3x 100mg (iv)Amikacine 2x30 mg (iv)Furosemide 3x5mg (iv)Captopril 2x1,2 mg (po)Digoxin 2x0,02mg (po)Pamol 3x0,4cc (po)

Multivit sirup 1xcth (po)ZnSO

41x1 mg (po)

Diet per NGT 12 x 25 ccKebutuhan cairan 340 cc restriksi 20% menjadi 320 ccTransfusi PRC I 20 cc selama 24 jam kemudian PRC II 20 ccNebulizer PZ ditambah Ventolin, suction tiap 4 jamEvaluasi distress nafas


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Mapping Konsep

PDA with PHTetralogy Fallot non cyanoticInnosent murmur

Preventif

Pemeriksaan PenunjangPemeriksaan laboratoriumPemeriksaan radiologi thorax (Apex downward,Prominence pulmonary artery segment,Increased pulmonary vascular markingPemeriksaan ElektrokardiografiPemeriksaan Ekokardiografi

Embriology AnatomyThe heart is forming during the first 3 weeks offetal development. It begins as a hollow tube,then partitions within the tube develop thateventually become the septa (or walls) dividingthe right side of the heart from the left.Ventricular septal defects occur when thepartitioning process does not occur completely,

leaving an opening in theVentricularseptum

Penyebab dan patomekanismeGenetikLingkungan (radiasi, rokok, obat-obatan

(thalidomide), infeksi maternal (rubella PDA), umur ibu (muda, tua),geografis daerah ketinggian (O2 ),

gangguan metabolisme (DM)

Anamnesis :AsimtomatikSimtomatik (sesak nafas, kesulitan

mengisap susu, infeksi paru berulang,gagal tumbuh kembang, gagal jantung)

Fisik Diagnostik :

Inspeksi, palpasi, perkusi, auskultasi.

Normal 1st HS or loud , Widely splitand fixed 2nd HS, Ejectionsystolic murmur)

Pemeriksaan Gangguan TumbuhKembang

VENTRIKULAR SEPTAL DEFECT

Epidemiologi

Prevalensi & Insidens

Inciden 20% PJBgejala timbul pada usia 2-6minggu kehidupan50% meninggal pada bulanpertama kehidupanINDONESIA : 200 jutapenduduk --- 30.000 bayiPJB

Rehabilitasi

Promotif

Surgery:Recent treatment: withtranscatheter closureSupportif (Medikamentosa, nutrisi)

Penatalaksanaan

Pengendalian


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hypoxic hypoxia (anoxic anoxia), in which the PO2 of the arterial blood is reduced;

Venous-to-Arterial Shunts

When a cardiovascular abnormality such as an inter-atrial septal defect permits large amounts of unoxygenated venous blood to

bypass the pulmonary capillaries and dilute the oxygenated blood in the systemic arteries ("right-to-left shunt"), chronic hypoxichypoxia and cyanosis (cyanotic congenital heart disease) result. Administration of 100% O2 raises the O2 content of alveolar air andimproves the hypoxia due to hypoventilation, impaired diffusion, or ventilation-perfusion imbalance (short of perfusion of totally

unventilated segments) by increasing the amount of O2 in the blood leaving the lungs. However, in patients with venous-to-arterialshunts and normal lungs, any beneficial effect of 100% O2 is slight and is due solely to an increase in the amount of dissolved O2 in

the blood.

Table 33-7. Simplified summary of pathogenesis of major findings in

congestive heart failure

Abnormality Cause

Weakness, exercise

intolerance

"Foward failure " of left ventricle; cardiac output

inadequate to perfuse muscles; especially, failure ofoutput to rise with exercise.

Ankle, sacral edema "Backward failure " of right ventricle increased

venous pressure increased fluid transudation.

Hepatomegaly Increased venous pressure increased resistance to

portal flow.

Pulmonary congestion "Backward failure " of left ventricle increased

pulmonary venous pressure pulmonary venousdistention and transudation of fluid into air spaces.

Dyspnea on exertion failure of left ventricular output to rise during

exercise increased pulmonary venous pressure.

Paroxysmal dyspnea,pulmonary edema

Probably sudden failure of left heart output to keepup with right heart output acute rise in pulmonary

venous and capillary pressure transudation of fluid


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into air spaces.

Orthopnea Normal pooling of blood in lungs in supine positionadded to already congested pulmonary vascular

system; increased venous return not put out by leftventricle. (Relieved by sitting up, raising head of bed,

lying on extra pillows.)

Cardiac dilation Greater ventricular end-diastolic volume.

mapping skenario 1

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